Module 7
Nervous and Sensory Systems
a. Neurons: The Communication Specialists
The nervous system detects information about external and internal conditions. It
then integrates those inputs and selects or controls muscles and glands that carry out
responses.
Three types of neurons carry out the functions of the nervous system. Sensory
neurons collect information about stimuli such as light or touch. They usually signal an
interneuron. Interneurons, which are located in the brain and spinal cord, are go-betweens
that receive signals from and send signals to other neurons. They may signal another
interneuron or a motor neuron. Motor neurons control muscles and glands. Muscles and
glands are called effectors because their response to the motor neuron’s signal produces
the final effect.
Neurons have a large cell body that contains the cell’s nucleus and other
organelles. Cytoplasm, which send out and receive signals. For example, all neurons have
an axon, an extension that transmits electrical signals along its length and releases
chemical signals at its terminals. Motor neurons and interneurons also have dendrites,
which are cytoplasmic extensions that receive chemical signals from other neurons.
Sensory neurons don’t receive signals from other neurons, so they don’t have dendrites.
One end of their axon has receptor endings that detect a particular type of stimulus; the
other end has signal-sending axon terminals.
Where different events occur in a motor neuron. The dendrites and cell body are
an “input zone” where the neuron receives arriving chemical signals and converts them to
electrical signals. The part of the axon nearest the cell body (sometimes called an axon
“hillock,” meaning little hill) is a “trigger zone” where an arriving electrical signal
triggers signals along the conducting portion of the axon to the axon terminals. These
terminals are the neuron’s “output zone”: They release signaling molecules that serve as
messages to other cells.
Recall from that roughly 90 percent of your nervous system consists of cells
called glia (neuroglia). Glia help maintain the proper concentrations of vital ions in the
fluid around neurons and assist in the formation of connections between brain neurons.
Some physically support and protect neurons. Others provide insulation that allows
signals to move along sensory and motor neurons with lightning speed.
Neurons are suited for communication partly because they are excitable—that is,
a neuron can respond to certain stimuli by producing an electrical signal. Described how
the plasma membrane’s lipid bilayer prevents charged substances—such as ions of
potassium (K1) and sodium (Na1)—from freely crossing it. Even so, ions can cross the
membrane through channel proteins that span the bilayer. Some channels are always
open, so that ions can steadily “leak”—by diffusion—in or out. Other channels open like
gates under the proper circumstances. These controls mean that the concentrations of an
ion can be different on either side of the plasma membrane.
For several reasons, on balance the cytoplasm next to the membrane is more
negative than the fluid just outside the membrane. Electrical charges may be measured in
millivolts, and for many neurons, the steady charge difference across the plasma
membrane is about 270 millivolts. The minus indicates that the cytoplasm side of the
membrane is more negative than the outer side of the membrane. This difference is called
resting membrane potential. The term means that the charge difference has the potential
to do physiological work in the body. That “work” is the launching of a nerve impulse.
Various kinds of signals occur in the nervous system, but not all of them spark
nerve impulses. Only a signal that is strong enough when it reaches a resting neuron’s
input zone may spread to a trigger zone. When a strong enough signal does arrive,
however, it can cause the voltage difference across the plasma membrane to reverse, just
for an instant. In the following section, we see how these reversals produce nervous
system signals.
b. Nerve Impulses = Action Potentials
When a signal that is strong enough reaches a resting neuron’s input zone, a
change occurs in the membrane. Sodium gates in it open, and Na1 rushes into the neuron.
Sodium ions have a positive charge, so as they flow in, the cytoplasm next to the plasma
membrane becomes less negative. Then, more gates open, more sodium enters, and so on
—an example of positive feedback. When the voltage difference across the neuron
plasma membrane shifts by a minimum amount called the threshold, the result is a nerve
impulse or action potential.
The threshold for an action potential can be reached where a neuron’s plasma
membrane has voltage-sensitive gated channels for sodium ions. When the threshold
level is reached, the opening of more sodium gates doesn’t depend any longer on the
strength of the stimulus. The gates open on their own.
Keep in mind that an action potential occurs only if the stimulus to a neuron is
strong enough. A weak stimulus— say, pressure from a tiny insect walking on your skin
—that arrives at an input zone may not upset the ion balance enough to cause an action
potential. This is because input zones don’t have gated sodium channels, so sodium can’t
flood in there. On the other hand, a neuron’s trigger zone is packed with sodium
channels. If a stimulus that reaches an input zone is strong enough to spread to the trigger
zone, an action potential may “fire.”
To transmit messages within the body, action potentials must spread to other
neurons or to cells in muscles or glands. Each action potential propagates itself, moving
away from its starting point. This self-propagation occurs in part because the changes in
membrane potential leading to an action potential don’t lose strength. When the change
spreads from one patch of a neuron’s plasma membrane to another patch, about the same
number of gated channels open.
When a signal triggers an action potential in the trigger zone of a neuron, a series
of complex events unfold within the cell's plasma membrane. This trigger zone, typically
located at the axon hillock, is crucial for initiating the electrical impulse that travels along
the neuron. The process begins with the arrival of neurotransmitters or other stimuli at the
dendrites or cell body of the neuron. These signals generate local depolarizations known
as graded potentials.
As these graded potentials propagate towards the trigger zone, they integrate, and
if the threshold potential is reached, an action potential is initiated. The threshold is the
minimum membrane potential that must be reached to trigger an action potential. Once
this threshold is surpassed, voltage-gated sodium channels open, allowing an influx of
sodium ions into the cell. This influx further depolarizes the membrane, leading to the
rapid opening of more sodium channels and a rapid increase in membrane potential,
known as the rising phase of the action potential.
Following the rising phase, voltage-gated potassium channels open, allowing
potassium ions to leave the cell. This efflux of positively charged potassium ions
repolarizes the membrane, bringing it back towards its resting membrane potential.
During this repolarization phase, the neuron becomes refractory to further stimulation.
This refractory period is essential because it prevents the neuron from responding to
additional signals until it has fully recovered.
The refractory period consists of two stages: the absolute refractory period and the
relative refractory period. During the absolute refractory period, the neuron is completely
unresponsive to additional stimuli, regardless of their strength. This period coincides with
the time when voltage-gated sodium channels are either already open or inactivated,
preventing the generation of another action potential. Following the absolute refractory
period, the neuron enters the relative refractory period, during which it is possible to
trigger another action potential, but only with a stronger-than-usual stimulus. This stage
occurs as voltage-gated sodium channels recover from inactivation and the membrane
potential approaches but has not yet reached, its resting state.
The restoration of the resting membrane potential is crucial for the neuron to be
able to receive and process new signals effectively. This period of repolarization and
refractoriness ensures that the neuron can transmit signals in a controlled and reliable
manner, preventing excessive firing and maintaining the integrity of neural
communication within the nervous system.
To understand how the resting potential is restored, remember that a neuron’s
resting membrane potential is due in part to the different concentrations of Na1 and K1
on either side of the plasma membrane. Remember also that the inside of the cell is a bit
more negative than the outside. Negatively charged proteins in the cytoplasm help create
this electric gradient. Together these factors mean that sodium is always leaking into the
neuron (down an electrochemical gradient), and potassium is always leaking out (down
its concentration gradient).
A neuron can’t respond to an incoming signal unless the proper concentration and
electric gradients across its plasma membrane are in place. Yet the Na1 and K1 leaks
never stop, opening the possibility that an imbalance might develop in the necessary
gradients. This imbalance doesn’t develop, however, because a resting neuron uses
energy to power a pumping mechanism that maintains the gradients. Carrier proteins
called sodium–potassium pumps span the neuron’s membrane. With energy from ATP,
they actively transport potassium into the neuron and transport sodium out.
There is no such thing as a “weak” or “strong” action potential. Every action
potential in a neuron spikes to the same level above threshold as an all-or-nothing event.
That is, once the positive-feedback cycle of opening sodium gates starts, nothing will
stop the full spiking. If threshold is not reached, the disturbance to the plasma membrane
will fade away as soon as the stimulus is removed.
Each spike lasts for about a millisecond. At the place on the membrane where the
charge reversed, the gated sodium channels close and the influx of sodium stops. About
halfway through the action potential, potassium channels open, so potassium ions flow
out and restore the original voltage difference across the membrane. Sodium–potassium
pumps restore the ion gradients. After the resting membrane potential has been restored,
most potassium gates are closed and sodium gates are in their initial state, ready to be
opened again when a suitable stimulus arrives.
c. How Neurons Communicate
Action potentials can stimulate neurons to release the chemical signals called
neurotransmitters. These molecules diffuse across a chemical synapse, a narrow gap
between a neuron’s output zone and the input zone of a neighboring cell. Some chemical
synapses occur between neurons, others between a neuron and a muscle cell or gland cell.
At a chemical synapse, one of the two cells stores neurotransmitter molecules in
synaptic vesicles in its cytoplasm. This is the presynaptic cell. The cell’s plasma
membrane has gated channels for calcium ions, and they open when an action potential
arrives. There are more calcium ions outside the cell, and when they flow in (down their
gradient), synaptic vesicles fuse with the plasma membrane, discharging their content.
Neurotransmitter molecules now pour into the synapse, diffuse across it, and bind with
receptor proteins on the plasma membrane of the postsynaptic, or receiving, cell. Binding
changes the shape of these proteins, so that a channel opens up through them. Ions then
diffuse through the channels and move into the receiving cell.
How a receiving cell responds to a neurotransmitter depends on the type and
amount of a neurotransmitter, the kinds of receptors the cell has, and some other factors.
Exciting signals help drive the membrane toward an action potential. Inhibiting signals
have the opposite effect.
One neurotransmitter, acetylcholine (ACh), can excite or inhibit different target
cells in the brain, spinal cord, glands, and muscles. Neuromuscular junction chemical
synapse between a motor neuron and a muscle cell. ACh released from the neuron
diffuses across the gap and binds to receptors on the muscle cell membrane. It excites this
kind of cell, triggering the action potentials that cause skeletal muscle contractions.
Epinephrine and norepinephrine prepare the body to respond to stress or
excitement. Dopamine acts in fine motor control and influences some type of learning.
GABA inhibits the release of other neurotransmitters. Serotonin acts on brain cells that
govern emotional states, sleeping, sensory perception, and regulation of body
temperature. Some neurons secrete nitric oxide (NO), a gas that controls blood vessel
dilation. It is not stored in synaptic vesicles but instead is manufactured as needed. As an
example, a sexually aroused male has an erection when NO calls on blood vessels in his
penis to dilate, allowing blood to rush in.
Neuromodulators can magnify or dampen the effects of a neurotransmitter. These
substances include natural painkillers called endorphins. Endorphins inhibit nerves from
releasing substance P, which conveys information about pain. In athletes who exercise
beyond normal fatigue, endorphins can produce a euphoric high.
At any moment, many signals are washing over the input zones of a receiving
neuron. All of them are graded potentials (their magnitude can be large or small), and
they compete for control of the membrane potential at the trigger zone. The ones called
EPSPs (for excitatory postsynaptic potentials) depolarize the membrane—they bring it
closer to threshold. On the other hand, IPSPs (inhibitory postsynaptic potentials) may
hyperpolarize the membrane (drive it away from threshold) or help keep the membrane at
its resting level.
Synaptic integration tallies up the competing signals that reach an input zone of a
neuron at the same time—a little like adding up the pros and cons of a certain course of
action. This process, called summation, is how signals arriving at a neuron are
suppressed, reinforced, or sent onward to other cells in the body.
Integration occurs when neurotransmitter molecules from more than one
presynaptic cell reach a neuron’s input zone at the same time. Signals also are integrated
after a neurotransmitter is released repeatedly, over a short time period, from a neuron
that is responding to a rapid series of action potentials.
The flow of signals through the nervous system depends on the rapid, controlled
removal of neurotransmitter molecules from synapses. Some of the neurotransmitter
molecules diffuse out of the gap. Enzymes cleave others in the synapse, as when
acetylcholinesterase breaks down ACh. Also, membrane transport proteins actively pump
the neurotransmitter molecules back into presynaptic cells or into neighboring neuroglia.
Certain drugs can block the reuptake of particular neurotransmitters. For example,
some antidepressant drugs elevate a depressed person’s mood by blocking the reuptake of
serotonin. Others shift the balance of a combination of neurotransmitters, such as
serotonin and norepinephrine.
d. Information Pathways
Nerves are communication lines between the brain or spinal cord and the rest of
the body. A nerve consists of nerve fibers, which are the long axons of sensory neurons,
motor neurons, or both. Connective tissue encloses most of the axons like electrical cords
inside a tube. In the central nervous system (the brain and spinal cord) nerves are called
nerve tracts.
Each axon has an insulating myelin sheath, which allows action potentials to
propagate faster than they would otherwise. The sheath consists of glial cells that wrap
around the long axons like jelly rolls. Exposed node, or gap, separates each cell from the
next one. There, voltage-sensitive, gated sodium channels pepper the plasma membrane.
In a manner of speaking, action potentials jump from node to node (a phenomenon that
sometimes is called saltatory conduction, after a Latin word meaning “to jump”). The
sheathed areas between nodes hamper the movement of ions across the plasma
membrane, so stimulation tends to travel along the membrane until the next node in line.
At each node, however, the flow of ions can produce a new action potential. In large
sheathed axons, action potentials propagate at a remarkable 120 meters (nearly 400 feet)
per second!
In the intricate network of the nervous system, the role of glial cells extends far
beyond mere structural support. Among these specialized cells, oligodendrocytes and
Schwann cells stand out for their crucial contributions to the transmission of nerve
impulses through the formation of myelin sheaths.
Within the central nervous system (CNS), which includes the brain and spinal
cord, oligodendrocytes take center stage in the creation of myelin sheaths. These sheaths
consist of multiple layers of lipid-rich membrane wrapped around the axons of neurons,
providing insulation and facilitating the rapid conduction of electrical impulses.
Oligodendrocytes are adept at forming and maintaining these myelin sheaths, which play
a pivotal role in the efficient transmission of information within the CNS.
On the other hand, in the peripheral nervous system (PNS), comprising the nerves
outside the CNS, Schwann cells take on the responsibility of sheath formation. These
specialized glial cells are highly versatile, performing a range of functions essential for
the proper functioning of peripheral nerves. One of their primary roles is to envelop
axons with myelin sheaths, enhancing the speed and efficiency of signal propagation
along these nerve fibers.
The distinction in myelin sheath formation between oligodendrocytes in the CNS
and Schwann cells in the PNS reflects the intricate specialization and organization of the
nervous system. While oligodendrocytes can myelinate multiple axons simultaneously,
extending their processes to ensheath segments of different neurons, Schwann cells
typically myelinate a single axon segment. This fundamental difference underscores the
diverse strategies employed by glial cells to support and regulate neuronal function in
different regions of the nervous system.
Moreover, the formation and maintenance of myelin sheaths by oligodendrocytes
and Schwann cells are subject to dynamic regulation and intricate molecular signaling
pathways. Various factors, including neuronal activity, developmental cues, and
pathological conditions, can influence the production, structure, and stability of myelin
sheaths. Understanding these regulatory mechanisms is essential for unraveling the
complexities of neural circuitry and addressing neurological disorders characterized by
dysregulated myelination, such as multiple sclerosis.
In essence, the collaboration between oligodendrocytes in the CNS and Schwann
cells in the PNS exemplifies the remarkable cellular diversity and functional
specialization within the nervous system. Their collective efforts in forming myelin
sheaths contribute not only to the efficient transmission of nerve impulses but also to the
maintenance of neural integrity and the adaptation of neuronal circuits to changing
physiological demands.
Sensory and motor neurons of certain nerves take part in automatic responses
called reflexes. A reflex is a simple, programmed movement in response to a stimulus.
Reflexes are always the same and do not involve the brain. In the simplest ones, sensory
neurons synapse directly on motor neurons. In most reflex pathways, however, the
sensory neurons also interact with several interneurons. These excite or inhibit motor
neurons as needed for a coordinated response.
The stretch reflex contracts a muscle after gravity or some other load has
stretched the muscle. Suppose you steadily hold out a bowl as someone loads peaches
into it, adding weight to the bowl. When your hand starts to drop, the biceps muscle in
your arm is stretched. This stretching activates receptors in muscle spindles. These are
sensory organs in which specialized cells are enclosed in a sheath that runs parallel with
the muscle. The receptor endings are the input zones of sensory neurons whose axons
synapse with motor neurons in the spinal cord. Axons of the motor neurons lead back to
the stretched muscle. Action potentials that reach the axon endings trigger the release of
ACh, which triggers contraction. As long as receptors continue to send messages, the
motor neurons are excited. This allows them to send signals to muscles that maintain
your hand’s position. This type of reflex is often called a spinal reflex. The pathway
neural signals travel to generate a reflex is called a reflex arc.
During the early stages of human development, infants display a fascinating array
of reflexes that serve critical functions in their survival and development. These reflexes
are innate, automatic responses to specific stimuli, and they play a vital role in the
interaction between the infant and its environment. One such reflex is the "rooting"
reflex, a remarkable behavior observed in newborns that gradually diminishes as the
nervous system matures.
The rooting reflex is a primitive yet essential response that aids in the infant's
ability to locate a source of nourishment, typically the mother's breast, for feeding. When
the infant's cheek or mouth is gently stroked or touched, it triggers a reflexive turning of
the head toward the stimulus. This automatic movement facilitates the positioning of the
mouth and facilitates the initiation of breastfeeding. The rooting reflex is crucial during
the early stages of infancy when the infant is learning to feed and establish a bond with
the primary caregiver.
As the nervous system undergoes maturation and refinement, many of these
primitive reflexes, including the rooting reflex, gradually disappear or become integrated
into more sophisticated voluntary movements. This process, known as
neurodevelopmental maturation, involves the pruning of redundant neural connections
and the strengthening of neural circuits that underpin higher-order cognitive and motor
functions.
The gradual disappearance of the rooting reflex parallels the infant's increasing
ability to coordinate voluntary movements and to engage in purposeful behaviors. As the
infant gains greater control over its head movements and becomes more adept at feeding,
the need for the rooting reflex diminishes. Instead, the infant learns to suckle and feed in
response to hunger cues, guided by learned behaviors and the establishment of feeding
routines.
While the rooting reflex fades over time, its transient presence in newborns
underscores the intricate interplay between genetic programming and environmental
stimuli in shaping early developmental milestones. Moreover, the observation of these
reflexes provides valuable insights into the integrity of the nervous system and can serve
as indicators of neurological health and functioning in newborns.
In conclusion, the rooting reflex exemplifies a fascinating aspect of early human
development, highlighting the dynamic interplay between innate reflexes and the
maturation of the nervous system. While this reflex serves a crucial role in facilitating
feeding and nurturing behaviors in newborns, its eventual disappearance reflects the
progressive refinement and specialization of neural circuits during infancy and early
childhood.
In your nervous system, sensory nerves relay information into the spinal cord,
where they form chemical synapses with interneurons. The spinal cord and brain contain
only interneurons, which integrate the signals. Many interneurons synapse with motor
neurons, which carry signals away from the spinal cord and brain.
In the brain and spinal cord, blocks of hundreds or thousands of interneurons are
parts of interacting circuits. Each block receives signals—some that excite, others that
inhibit—and then integrates the messages and responds with new ones. For example, in
some regions of the brain the circuits diverge—the processes of neurons in one block fan
out to form connections with other blocks. Elsewhere signals from many neurons are
funneled to just a few. And in still other brain regions, neurons synapse back on
themselves, repeating signals among themselves. These “reverberating” circuits include
the ones that make your eye muscles twitch as you sleep.
e. Overview of the Nervous System
Humans have the most intricately wired nervous system in the animal world. The
brain alone contains at least 100 billion neurons, and many more form part of the nerves
that branch throughout the rest of the body. To simplify this complexity we divide the
nervous system into two main parts, the central nervous system, abbreviated CNS, and
the peripheral nervous system, abbreviated PNS.
The central nervous system consists of the brain and spinal cord. All the neurons
in these structures are interneurons. Nerves that carry sensory information to the central
nervous system sometimes are called afferent (“bringing to”) nerves. Nerves that carry
motor messages away from the central nervous system to muscles and glands may be
termed efferent (“carrying outward”) nerves.
The peripheral nervous system consists of thirty-one pairs of spinal nerves that
carry signals to and from the spinal cord and twelve pairs of cranial nerves that carry
signals to and from the brain. At certain places in the PNS, cell bodies of several neurons
occur in knotlike clusters called ganglia (singular: ganglion). The central and peripheral
nervous systems both also have glial cells, such as oligodendrocytes (in the CNS) and
Schwann cells (in the PNS).
When a nerve is “pinched” (compressed) or irritated by inflammation, painful
disorders may result. A fairly common example is the stabbing pain or persistent aching
of trigeminal neuralgia (TN). TN develops due to damage to the trigeminal nerve, a
sensory nerve serving the face and head. Dental work, a blow to the face, and other
“insults” may trigger the disorder, which can recur throughout a sufferer’s life.
Compression of nerves where they exit the spine in the neck (cervical), lower back
(lumbar), or “tailbone” (sacral) can cause mild to severe pain. The disorder known as
sciatica results when the root of the sciatic nerve is affected.
Our remarkable nervous system integrates the array of body functions in ways
that help maintain homeostasis. With this introduction, we now turn to a closer look at
the two major parts of the human nervous system.
f. Major Expressways: Peripheral Nerves and the Spinal Cord
Nerves of the PNS are grouped by function. To begin with, the cranial and spinal
nerves are subdivided into somatic and autonomic categories. Somatic nerves carry
signals related to movements of the head, trunk, and limbs. Autonomic nerves carry
signals between internal organs and other structures.
In somatic nerves, sensory axons carry information from receptors in skin,
skeletal muscles, and tendons to the central nervous system. Their motor axons deliver
commands from the brain and spinal cord to skeletal muscles. In the autonomic category,
motor axons of spinal and cranial nerves carry messages to smooth muscle, cardiac
(heart) muscle, and glands.
Unlike somatic neurons, single autonomic neurons do not extend the entire
distance between muscles or glands and the central nervous system. Instead,
preganglionic (“before a ganglion”) neurons have cell bodies inside the spinal cord or
brain stem, but their axons travel through nerves to autonomic system ganglia outside the
CNS. There, the axons synapse with postganglionic (“after a ganglion”) neurons, which
make the actual connection with effectors—the body’s muscles and glands.
Autonomic nerves are divided further into parasympathetic and sympathetic
groups. Normally these two sets of nerves work antagonistically—the signals from one
oppose those of the other. However, both these groups of nerves carry exciting and
inhibiting signals to internal organs. Often their signals arrive at the same time at muscle
or gland cells and compete for control. When that situation arises, synaptic integration
leads to minor adjustments in an organ’s activity.
The autonomic nervous system, comprised of the sympathetic and
parasympathetic divisions, plays a crucial role in regulating physiological processes that
are largely involuntary and essential for maintaining homeostasis in the body. While both
divisions work in concert to respond to changing environmental demands, they often
exhibit opposing effects on target organs and tissues.
During periods of relaxation and low stress, the parasympathetic nervous system
predominates, orchestrating a cascade of physiological responses geared towards
promoting rest, recovery, and digestion. Often referred to as the "rest and digest" system,
the parasympathetic division is instrumental in conserving energy and facilitating
essential bodily functions necessary for sustaining life.
One of the hallmark features of parasympathetic dominance is the promotion of a
state of calmness and relaxation. Activation of parasympathetic nerves leads to a decrease
in heart rate and blood pressure, promoting a sense of tranquility and well-being.
Additionally, parasympathetic stimulation results in the dilation of blood vessels
supplying the digestive organs, facilitating optimal blood flow to support digestion and
nutrient absorption.
Moreover, parasympathetic activity stimulates the secretion of digestive enzymes
and enhances gastrointestinal motility, promoting the efficient breakdown and absorption
of nutrients from ingested food. This aspect of parasympathetic function underscores its
role in promoting metabolic efficiency and nutrient utilization, essential for sustaining
cellular energy production and overall health.
Furthermore, the parasympathetic division regulates other essential bodily
processes during periods of relaxation, such as promoting bronchoconstriction to
facilitate optimal gas exchange in the lungs and stimulating salivary gland secretion to
aid in the initial digestion of food.
The intricate balance between sympathetic and parasympathetic activity ensures
adaptive responses to varying physiological demands and environmental stressors. While
the sympathetic division prepares the body for "fight or flight" responses during times of
perceived danger or stress, the parasympathetic division promotes relaxation and
restoration, allowing the body to recuperate and replenish its energy reserves.
In summary, the parasympathetic nervous system plays a pivotal role in
orchestrating physiological responses that promote relaxation, digestion, and metabolic
efficiency during quiet, low-stress situations. By diverting energy towards basic bodily
housekeeping tasks and facilitating restorative processes, the parasympathetic division
contributes to overall health and well-being in the face of daily challenges and demands.
Sympathetic nerves dominate at times of danger, stress, excitement, or strenuous
physical activity. Among other effects, their signals increase the force and rate of the
heartbeat, elevate blood pressure by constricting arterioles, increase the breathing rate,
and dilate the pupils of the eyes so that more light can enter. This physiological shift is
called the “fight–flight response” because it primes the body to respond to rapid-fire
physical demands that might arise in an emergency (such as fighting hard or running
away). The response suppresses activities that are less important during an emergency,
such as digestion.
The spinal cord carries signals between the peripheral nervous system and the
brain. It threads through a canal made of bones of the vertebral column. Most of the cord
consists of nerve tracts (bundles of myelinated axons). Because the myelin sheaths of
these axons are white, the tracts are called white matter. The cord also contains gray
matter that consists of dendrites, cell bodies of neurons, interneurons, and glial cells. The
cord lies inside a closed channel formed by the bones of the vertebral column. Those
bones, and ligaments attached to them, protect the soft nervous tissue of the cord. So do
the coverings called meninges.
Besides carrying signals between the brain and the peripheral nervous system, the
spinal cord is a control center for reflexes that were described. It also contributes to
autonomic reflexes that deal with internal functions such as bladder emptying.
g. Disorders of the Nervous System
A blow to the head or neck can cause a concussion, one of the most common
brain injuries. Blurred vision and a brief loss of consciousness result when the blow
temporarily upsets the electrical activity of brain neurons. Damage to the spinal cord can
lead to lost sensation and muscle weakness or paralysis below the site of the injury.
Immediate treatment is crucial to limit swelling. Although cord injuries usually have
severe consequences, intensive therapy during the first year after an injury can improve
the patient’s long-term prognosis. Using nerve growth factors or stem cells to repair
spinal cord injuries is a major area of medical research.
Brain injury, birth trauma, or other assaults can cause various forms of epilepsy,
or seizure disorders. Sometimes the trigger is an inherited predisposition. A seizure
results when the brain’s normal electrical activity suddenly becomes chaotic. Worldwide,
thousands of people develop recurrent seizures either as children or later in life. All but
the most difficult cases usually respond well to drug therapy.
Parkinson’s disease, or PD, is a degenerative brain disorder. In PD, neurons in
parts of the thalamus begin to die. Those neurons make neurotransmitters (dopamine and
norepinephrine) required for normal muscle function, so PD symptoms include muscle
tremors and balance problems, among others. Multiple factors contribute to the
development of PD. A head injury or exposure to pesticides in drinking water may
increase the risk. There is no cure, but surgery and treatments that help replace absent
neurotransmitters may relieve some symptoms.
Like PD, Alzheimer’s disease involves the progressive degeneration of brain
neurons. At the same time, there is an abnormal buildup of amyloid protein, leading to
the loss of memory and intellectual functions. Alzheimer’s disease is associated with
advancing age, and we consider it again in our discussion.
Meningitis is an often fatal disease caused by a bacterial or viral infection.
Symptoms—headache, a stiff neck, vomiting—develop when the meninges in the central
nervous system become inflamed. Encephalitis is inflammation of the brain. It is usually
caused by a viral infection, such as by the West Nile virus or a herpes virus. Encephalitis
can be extremely dangerous. Early symptoms include fever, confusion, and seizures.
In cancer, cells divide much more often than normal. Neurons generally do not
divide, so cancer does not develop in them. Glial cells do divide, however, and glial
cancers, called gliomas, can have extremely destructive effects in the nervous system. An
aggressive form called glioblastoma multiforme usually strikes males and kills within a
year of the diagnosis. Most cases of spinal cancer are metastases, meaning that the cancer
has spread to the spine from a primary cancer elsewhere in the body.
Some people are concerned that the radio waves emitted by cell phones could
cause tumors. Although to date research hasn’t shown increased brain tumor incidence
related to cell phone use, studies have shown increased metabolic activity in cells near
the phone. Some health officials recommend using a headset to keep the radiation
emitting part of the phone farther from the brain.
In young adults, the most common nervous system disease is multiple sclerosis
(MS). It is an autoimmune disease that may be triggered by a viral infection in
susceptible people. MS involves progressive destruction of myelin sheaths of neurons in
the central nervous system. The symptoms develop over time and include muscle
weakness or stiffness, extreme fatigue, and slurred speech. A disorder called Guillain-
Barre syndrome produces similar symptoms in the peripheral nervous system. It is caused
by a viral or bacterial infection and usually is temporary.
There aren’t any sensory nerves in the brain, so it doesn’t “feel pain.” Instead,
headache pain typically is due to tension (stretching) in muscles or blood vessels of the
face, neck, and scalp. Migraine headaches are infamous for being extremely painful and
lasting for up to 3 days. In the United States alone, 28 million people suffer from
migraines, which can be triggered by hormonal changes, fluorescent lights, certain foods
(such as chocolate)—even changes in the weather.
Tension headaches and migraines are thought to be part of a continuum, and both
are treated with drugs ranging from aspirin to prescription painkillers and drugs that act
as neuromodulators to reduce the sensitivity of affected brain neurons to stimuli that
trigger the headache. Cluster headaches produce a piercing pressure in one eye and may
recur several times a day for weeks or months. Some sufferers have found the pain so
unbearable that they have committed suicide.
People affected by ADHD, or attention deficit hyperactivity disorder, have trouble
concentrating, tend to fidget, and may be unusually impulsive. A lower than normal level
of dopamine may be involved, and drugs used to treat ADHD increase brain dopamine
levels.
The mental state we call “mood” results at least in part from the interactions of
several neurotransmitters, including serotonin and dopamine. Medications that adjust the
levels of these substances in the brain are used to treat mood disorders such as bipolar
disorder and depression. By some estimates, depression affects up to 17 percent of adults
at some time in their lives. A clinically depressed person feels sad all the time and can’t
experience pleasure. Several widely prescribed antidepressants increase the amount of
serotonin in the brain by preventing its reuptake. Antidepressants that prevent serotonin
reuptake are also used to treat people who have anxiety disorders—feelings of extreme
worry or panic in situations most people would consider normal.
Autism spectrum disorders are forms of persistent developmental disorders
(PDDs) that usually show up in childhood. Affected youngsters experience mild to severe
problems in thinking, language skills, and the capacity to relate to others. Research
suggests that a family of “autism genes” may underlie PDDs. In some cases, affected
children show major improvement with intensive behavioral therapy.
Disrupted thinking is a key sign of schizophrenia. Patients have paranoid
delusions and often “hear voices” (auditory hallucinations). Holding a job and normal
social relationships often are impossible. Medicines can help control symptoms.
h. Sensory Receptors and Pathways
A stimulus (plural: stimuli) is a form of energy that activates receptor endings of a
sensory neuron. That energy is converted to the electrochemical energy of action
potentials—the nerve impulses by which the brain receives information and sends out
commands in response. This basic response in the brain is a sensation, which is conscious
awareness of a stimulus. Higher-level processing in the brain produces a perception—an
understanding of what the sensation means.
There are three basic forms of sensory receptors. Those called free nerve endings
are present in the epidermis and many connective tissues. They detect touch, pressure,
heat, cold, or pain. An encapsulated receptor is an organ in which a capsule of epithelial
or connective tissue encloses nerve endings of a sensory neuron. The third basic type of
sensory receptor is formed by a cell that synapses with a sensory neuron.
We organize sensory receptors based on the type of stimulus each detects.
Photoreceptors detect visible light. Chemoreceptors detect chemicals dissolved in the
fluid around them. Mechanoreceptors detect changes in pressure, position, or
acceleration. Thermoreceptors respond to heat or cold. Receptors for pain, called
nociceptors, detect damage to tissues. Osmoreceptors detect changes in water volume
(solute concentration) in a body fluid. Regardless of their differences, all sensory
receptors convert the stimulus to nerve impulses (action potentials).
Nerve impulses that move along sensory neurons are all the same. So how does
the brain know what sort of sensory event has occurred? It assesses which nerves are
carrying nerve impulses, the frequency of the nerve impulses on each axon in the nerve,
and the number of axons that responded to the stimulus. Let’s consider the steps involved
in this processing.
First, specific sensory areas of the brain can interpret action potentials only in
certain ways. That is why you “see stars” when your eye is poked, even in the dark. The
mechanical pressure on photoreceptors in the eye triggers signals that travel along the
optic nerve. The brain always interprets signals from an optic nerve as “light.” In fact,
the brain has a detailed map of the sources of different sensory stimuli.
Second, a strong signal makes receptors fire nerve impulses more often and
longer than a weak one does. So, while the same receptor in your ear can detect the
sounds of a whisper and a screech, the brain senses the difference through variations in
the signals each sound produces.
Third, the stronger a stimulus, the more sensory receptors respond. Gently tap a
spot of skin on your arm and you activate only a few touch receptors. Press hard on the
same spot and you activate more. The increase translates into nerve impulses in many
sensory neurons at once. Your brain interprets the combined activity as an increase in the
intensity of the stimulus.
In some cases the frequency of nerve impulses (how often they occur in a given
period of time) slows or stops even when the stimulus continues at constant strength. For
instance, after you put on a T-shirt, you quickly become only dimly aware of its pressure
against your skin. This diminishing response to an ongoing stimulus is called sensory
adaptation.
The human body is equipped with a diverse array of mechanoreceptors,
specialized sensory receptors that detect mechanical stimuli such as pressure, touch, and
vibration. These receptors play a fundamental role in our ability to perceive and respond
to tactile sensations, enabling us to interact effectively with our environment.
Importantly, mechanoreceptors exhibit varying degrees of adaptation, influencing the
nature and duration of their response to stimuli.
One of the most intriguing aspects of mechanoreceptor function is their capacity
for adaptation, which refers to the ability of these sensory receptors to adjust their
sensitivity over time in response to sustained stimulation. Some mechanoreceptors
demonstrate rapid adaptation, meaning they quickly become desensitized to a sustained
stimulus and only signal when the stimulus initiates or ceases. These rapidly adapting
mechanoreceptors are particularly sensitive to changes in stimulus intensity or onset,
making them well-suited for detecting dynamic changes in the environment. Examples of
rapidly adapting mechanoreceptors include Meissner's corpuscles in the skin, which are
sensitive to light touch and low-frequency vibration, and Pacinian corpuscles, which
respond to deep pressure and high-frequency vibration.
In contrast, other mechanoreceptors exhibit slow or non-adapting characteristics,
maintaining their responsiveness to sustained stimuli over time. These receptors
continuously signal the presence of a stimulus and provide the brain with ongoing
feedback about specific environmental conditions. Slowly adapting mechanoreceptors are
crucial for monitoring prolonged or static stimuli, such as sustained pressure or touch,
ensuring that the brain remains aware of these stimuli even after prolonged exposure.
Merkel cells and Ruffini corpuscles are examples of slowly adapting mechanoreceptors
found in the skin, responsible for detecting sustained pressure and skin stretch.
The diversity in mechanoreceptor adaptation properties reflects the specialized
roles these receptors play in sensory processing and perception. Rapidly adapting
mechanoreceptors excel at detecting changes and initiating rapid responses to dynamic
stimuli, while slowly adapting receptors provide sustained feedback about ongoing
stimuli, allowing for continuous monitoring and adjustment to environmental conditions.
Moreover, the adaptation properties of mechanoreceptors contribute to the
phenomenon of sensory gating, whereby the nervous system filters out repetitive or non-
essential stimuli to focus on relevant sensory information. By adapting to sustained
stimuli, mechanoreceptors prevent sensory overload and ensure that the brain prioritizes
novel or significant sensory inputs.
Understanding the complex dynamics of mechanoreceptor adaptation enhances
our appreciation of the sophisticated mechanisms underlying tactile sensation and
perception. Moreover, insights into the adaptation properties of mechanoreceptors have
implications for various fields, including neuroscience, biomedical engineering, and
clinical medicine, where an understanding of sensory processing is essential for
developing therapies for sensory disorders and enhancing human-machine interfaces.
In the rest of this we explore examples of the body’s sensory receptors. Receptors
that are found at more than one location in the body contribute to somatic (“of the body”)
sensations. Other receptors are restricted to sense organs, such as the eyes or ears, and
contribute to what are called the “special senses.”
i. Somatic Sensations
Receptors for somatic senses are scattered in different parts of the body. Somatic
sensations come about when signals from receptors reach the somatosensory cortex in the
cerebrum. There, interneurons are organized like maps of individual parts of the body
surface, just as they are for the motor cortex. The largest areas of the map correspond to
body parts where sensory receptors are the most dense. These body parts, including the
fingers, thumbs, and lips, have the sharpest sensory acuity and require the most intricate
control.
There are thousands of sensory receptors in your skin, providing information
about touch, pressure, cold, warmth, and pain. Places with the most sensory receptors,
such as the fingertips and the tip of the tongue, are the most sensitive. Less sensitive
areas, such as the back of the hand, have many fewer receptors.
There are several types of free nerve endings in the epidermis and many
connective tissues. As noted, this form of sensory receptor detects touch, pressure, heat,
cold, or pain. Free nerve endings are simple structures. Basically, they are thinly
myelinated or unmyelinated (“naked”) dendrites of sensory neurons. One type coils
around hair follicles and detects the movement of the hair inside. That might be how, for
instance, you become aware that a spider is gingerly making its way across your arm.
Free nerve endings that are sensitive to chemicals such as histamine may be responsible
for the sensation of itching.
The dermis of your skin contains four types of encapsulated receptors. Each bears
the name of its discoverer. One type, Merkel’s discs, adapt slowly and are the most
important receptors for steady touch. In the lips, fingertips, eyelids, nipples, and genitals
there are many Meissner’s corpuscles, which are sensitive to light touching. Deep in the
dermis and in joint capsules are Ruffini endings, which respond to steady pressure.
The Pacinian corpuscles widely scattered in the dermis are sensitive to deep
pressure and vibrations. They also are located near freely movable joints (like shoulder
and hip joints) and in some soft internal organs. Sensing limb motions and changes in
body position relies on mechanoreceptors in skin, skeletal muscles, joints, tendons, and
ligaments. Examples include the stretch receptors of muscle spindles.
Pain is perceived injury to some body region. The term for the body’s most
important pain receptors, “nociceptor,” comes from the Latin word nocere, meaning “to
do harm.” Nociceptors are free nerve endings. Several million of them are distributed
throughout the skin and in all internal tissues except the brain.
Somatic pain starts with nociceptors in skin, skeletal muscles, joints, and tendons.
One group is the source of prickling pain, like the jab of a pin when you stick your finger.
Another contributes to itching or the feeling of warmth caused by chemicals such as
histamine. Sensations of visceral pain, which is associated with internal organs, are
related to muscle spasms, muscle fatigue, too little blood flow to organs, and other
abnormal conditions.
When cells are damaged, they release chemicals that activate neighboring pain
receptors. The most potent of these substances are bradykinins. They trigger the release
of histamine, prostaglandins, and other substances associated with inflammation.
When signals from pain receptors reach interneurons in the spinal cord, the
interneurons release a chemical called substance P. One result is that the hypothalamus
and midbrain send signals that call for the release of endorphins and enkephalins. These
are natural opiates (morphine-like substances) that, like morphine derived from opium
poppies, reduce our ability to perceive pain. Morphine, hypnosis, and natural childbirth
techniques may also stimulate the release of these natural opiates.
A person’s perception of pain often depends on the brain’s ability to identify the
affected tissue. Get hit in the face with a snowball and you “feel” the contact on facial
skin. However, sensations of pain from some internal organs may be wrongly projected
to part of the skin surface. This response, called referred pain, is related to the way the
nervous system is built. Sensory information from the skin and from certain internal
organs may enter the spinal cord along the same nerve pathways, so the brain can’t
accurately identify their source. For example, a heart attack can be felt as pain in skin
above the heart and along the left shoulder and arm, or between the shoulder blades.
Referred pain is not the same as the phantom pain reported by amputees. Often
people who have lost a body part sense the presence of the missing part, as if it were still
there. In some undetermined way, sensory nerves that were cut during the amputation
continue to respond to the trauma. The brain projects the pain back to the missing part,
past the healed region.
j. Taste and Smell: Chemical Senses
Taste and smell are chemical senses. They begin at chemoreceptors, which are
activated when they bind a chemical that is dissolved in fluid around them. Although
these receptors wear out, new ones replace them. In both cases, sensory information
travels from the receptors through the thalamus and on to the cerebral cortex, where
perceptions of the stimulus form. The input also travels to the limbic system, which can
integrate it with emotional states and stored memories.
The technical term for taste is gustation. Sensory organs called taste buds hold the
taste receptors. About 10,000 taste buds are scattered over your tongue, the roof of your
mouth (the palate), and your throat.
A taste bud has a pore through which saliva and other fluids in the mouth contact
the surface of receptors. The stimulated receptor in turn stimulates a sensory neuron,
which conveys the message to centers in the brain where the stimulus is interpreted.
Every perceived taste is some combination of five primary tastes: sweet, sour, salty,
bitter, and umami (the savory taste associated with meats or aged cheese).
The flavors of most foods are some combination of the five basic tastes, plus
information from olfactory receptors in the nose. Simple as this sounds, scientists now
know that our taste sense involves complex genetic mechanisms. Science Comes to Life
on the facing page examines some of these findings.
The olfactory element of taste is extremely important. In addition to odor
molecules in inhaled air, molecules of volatile chemicals are released as you chew food.
These waft up into the nasal passages. There, the “smell” inputs contribute to the
perception of complex flavors. This is why anything that dulls your sense of smell—such
as a head cold—also seems to diminish food’s flavor.
Olfactory receptors detect substances that dissolve in watery mucus on the surface
of olfactory epithelium in the upper nasal passages. When odor molecules bind to
receptors on olfactory neurons in cells of the olfactory epithelium, the resulting nerve
impulse travels directly to olfactory bulbs in the frontal area of the brain. There, other
neurons forward the message to a center in the cerebral cortex, which interprets it as
“fresh bread,” “pine tree,” or some other substance.
From an evolutionary perspective, olfaction is an ancient sense—and for good
reason. Food, potential mates, and predators give off substances that can diffuse through
air (or water) and so give clues or warnings of their whereabouts. Even with our rather
insensitive sense of smell, we humans have about 10 million olfactory receptors in
patches of olfactory epithelium in the upper nasal passages.
Just inside your nose, next to the vomer bone, is a tiny vomeronasal organ, or
“sexual nose.” (Some other mammals also have one.) Receptors in this organ can detect
pheromones, which are chemicals that influence social interactions in many animal
species. Pheromones can affect the behavior— and maybe the physiology of other
individuals. For instance, one or more pheromones in the sweat of females may account
for the common observation that women of reproductive age who are in regular, close
contact with one another often come to have their menstrual periods on a similar
schedule. Many scientists are not convinced that pheromones operate in humans,
however, and debate on the topic is always lively!
k. Science Comes to Life: Tasty Science
Each taste category such as sweet or sour is associated with particular “tastant”
molecules. When you eat food, however, which taste category (or combination of them)
you ultimately perceive depends on the nature of the triggering chemical and on how it is
processed by the receptor. In each case, some event causes the receptor cell to release a
neurotransmitter that triggers nerve impulses in a nearby sensory neuron.
For example, when you taste “salt,” the receptor cell’s response is due to the flow
of Na1 through sodium ion channels in its plasma membrane. Acidic tastant molecules
release hydrogen ions that block certain ion channels. The blockage causes a receptor to
respond with a “sour” message.
Cells that detect bitter substances may have receptors sensitive to as many as one
hundred different trigger tastants. This diversity probably is a survival tool. Many toxic
chemicals (including plant alkaloids such as nicotine and morphine) taste bitter, an
adaptation that may help protect us from ingesting dangerous substances. Familiar bitter-
tasting alkaloids are caffeine and quinine, the mouth-puckering tastant in tonic water.
And while many “sweet” tastants are sugars, others are amino acids or alcohols. Both
bitter and sweet tastes are detected by specific proteins inside the receptor. The taste
category called umami also is triggered by amino acids, notably glutamate. Its name was
bestowed by the Japanese researcher who identified it.
The intricate sensory system responsible for taste perception, often referred to as
gustation, involves a complex interplay of receptors, neural pathways, and cognitive
processes. At the forefront of this sensory experience are taste buds, specialized
structures located primarily on the tongue but also found in other regions of the oral
cavity and upper throat. These taste buds contain receptors capable of detecting various
chemical compounds, or tastants, that elicit different taste sensations.
Contrary to a once-held belief that each taste bud exclusively responds to a single
taste class (such as sweet, sour, salty, bitter, or umami), research has revealed a more
nuanced understanding. Each taste bud harbors a diverse array of receptors that can detect
tastants from multiple taste classes. This phenomenon is known as taste receptor
polymorphism, where individual taste receptor cells express receptors for more than one
taste quality. Thus, a single taste bud can be responsive to tastants representing two or
more taste classes, allowing for the detection of a broader range of flavors.
Furthermore, the integration of taste with other sensory modalities, such as
olfaction (sense of smell), plays a pivotal role in shaping our perception of flavor. When
we consume food or beverages, volatile compounds released from the substance travel to
the olfactory receptors in the nasal cavity, contributing to our perception of aroma. These
olfactory signals interact with taste sensations, enhancing and enriching the overall flavor
experience. As a result, the perception of flavor is a multisensory process that integrates
taste, smell, texture, temperature, and even auditory cues (such as the sound of food being
chewed) to create a holistic sensory experience.
Moreover, the complexity of flavor perception extends beyond the taste buds and
olfactory receptors to encompass higher-order brain regions responsible for processing
and integrating sensory information. Neuroimaging studies have revealed the
involvement of multiple brain regions, including the primary gustatory cortex in the
insula and frontal operculum, as well as areas involved in olfactory processing, such as
the olfactory bulb and piriform cortex. These brain regions work in concert to analyze
and interpret sensory inputs, ultimately generating our subjective experience of flavor.
The interplay between taste, smell, and other sensory modalities gives rise to an
astonishing diversity of flavor perceptions, allowing us to discern subtle nuances and
distinguish between a myriad of tastes and aromas. From the sweetness of ripe fruit to the
pungency of spicy peppers, our experience of flavor is a testament to the remarkable
complexity of the human sensory system and its capacity for discerning and appreciating
the rich tapestry of culinary delights.
Not all taste receptors are equally sensitive. “Bitter” ones tend to be extremely
sensitive and so can detect tiny amounts of bitter tastants—and thus potential poisons.
Sour tastants are needed in higher concentrations before the stimulus registers. Even
higher levels of sweet and salty substances must be present for the stimulus to register. So
why can relatively small amounts of artificial sweeteners so readily sweeten foods? Their
molecular characteristics make them 150 times (aspartame) to more than 600 times
(saccharin) as potent as plain sucrose.
l. Hearing: Detecting Sound Waves
Sounds are waves of compressed air. They are a form of mechanical energy. If
you clap your hands, you force out air molecules, creating a low-pressure state in the area
they vacated. The pressure variations can be depicted as a wave form, and the amplitude
of its peaks corresponds to loudness. The frequency of a sound is the number of wave
cycles per second. Each cycle extends from the start of one wave to the start of the next.
The sense of hearing starts with vibration-sensitive mechanoreceptors deep in the
ear. When sound waves travel down the ear’s auditory canal, they reach a membrane and
make it vibrate. The vibrations cause a fluid inside the ear to move, the way water in a
waterbed sloshes. In your ear, the moving fluid bends the tips of hairs on
mechanoreceptors. With enough bending, the result will be action potentials sent to the
brain, where they are interpreted as sound.
A human ear has three regions, each with its own role in hearing. The outer ear is
a pathway for sound waves to enter the ear, setting up vibrations. The vibrations are
amplified in the middle ear. The inner ear contains the coiled cochlea, where vibrations of
different sound frequencies are sorted out as they stimulate different patches of receptors.
The inner ear also contains semicircular canals, which are involved in balance.
Hearing begins when the outer ear’s fleshy flaps collect and channel sound waves
through the auditory canal to the tympanic membrane (the eardrum). Sound waves cause
the membrane to vibrate, which in turn causes vibrations in a leverlike array of three tiny
bones of the middle ear: the malleus (“hammer”), incus (“anvil”), and stirrup-shaped
stapes. The vibrating bones transmit their motion to the oval window, an elastic
membrane over the entrance to the cochlea. The oval window is much smaller than the
tympanic membrane. So, as the middle-ear bones vibrate against its small surface with
the full energy that struck the tympanic membrane, the force of the original vibrations is
amplified.
Now the action shifts to the cochlea. If we could uncoil the cochlea, we would see
that a fluid-filled chamber folds around an inner cochlear duct. Each “arm” of the outer
chamber functions as a separate compartment. The amplified vibrations of the oval
window create pressure waves in the fluid within the chambers. These waves are
transmitted to the fluid in the cochlear duct. On the floor of the cochlear duct is a basilar
membrane, and resting on the basilar membrane is a specialized organ of Corti, which
includes hair cells. These cells are the mechanoreceptors that serve as the sensory
receptors for sound.
Slender projections at the tips of hair cells rest against an overhanging tectorial
(“rooflike”) membrane, which is not a membrane at all but a jellylike structure. When
pressure waves in the cochlear fluid vibrate the basilar membrane, its movements can
press hair cell projections against the tectorial membrane so that the projections bend like
brush bristles. Affected hair cells release a neurotransmitter. It triggers action potentials
in neurons of the auditory nerve, which carries them to the brain.
Different sound frequencies cause different parts of the basilar membrane to
vibrate—and, accordingly, to bend different groups of hair cells. Apparently, the total
number of hair cells stimulated in a given region determines the loudness of a sound. The
perceived tone or “pitch” of a sound depends on the frequency of the vibrations that
excite different groups of hair cells. The higher the frequency, the higher the pitch.
Eventually, pressure waves moving through the cochlea push against the round
window, a membrane at the far end of the cochlea. As the round window bulges outward
toward the air-filled middle ear, it serves as a “release valve” for the force of the waves.
Air also moves through an opening in the middle ear into the eustachian tube. This tube
runs from the middle ear to the throat (pharynx), permitting air pressure in the middle ear
to be equalized with the pressure of outside air. When you change altitude (say, during a
plane trip), this equalizing process makes your ears pop.
The human auditory system is exquisitely sensitive, capable of detecting a wide
range of sound frequencies and amplitudes. However, while this sensitivity is
advantageous for perceiving subtle sounds in the environment, it also renders the auditory
system vulnerable to damage from excessively loud sounds. In modern society, exposure
to amplified music at concerts, the roar of jet engines, and other loud noises has become
increasingly prevalent, posing a significant risk to the delicate structures of the inner ear.
At the heart of the auditory system's vulnerability to loud sounds are the hair cells
located within the cochlea, a spiral-shaped structure in the inner ear responsible for
converting sound vibrations into neural signals. These hair cells play a crucial role in
auditory transduction, whereby mechanical stimulation from sound waves is converted
into electrical signals that can be interpreted by the brain. However, prolonged exposure
to high-intensity sounds can result in damage to these hair cells, leading to a condition
known as noise-induced hearing loss (NIHL).
Unlike some other sensory cells in the body, such as photoreceptor cells in the
retina, hair cells of the inner ear have limited regenerative capacity. Once damaged or
destroyed, these cells may not be able to regenerate or repair themselves fully, leading to
permanent hearing loss. Moreover, the evolution of the human auditory system has not
prepared it for the unprecedented levels of noise encountered in modern society, which
far exceed the intensity of sounds encountered in natural environments.
Furthermore, the detrimental effects of loud sounds extend beyond hair cell
damage to include damage to other structures within the auditory system, such as the
auditory nerve fibers and synapses connecting hair cells to auditory neurons. These
structural alterations can disrupt the transmission of neural signals from the cochlea to the
brain, impairing auditory processing and perception.
In addition to noise-induced hearing loss, exposure to loud sounds can also lead to
other auditory problems, such as tinnitus, a persistent ringing or buzzing sensation in the
ears, and hyperacusis, an increased sensitivity to sounds. These conditions can
significantly impact quality of life, affecting communication, social interactions, and
emotional well-being.
Given the growing prevalence of loud sounds in modern society, there is an
urgent need for public awareness campaigns and preventive measures to protect against
noise-induced hearing damage. These may include the use of hearing protection devices,
such as earplugs or earmuffs, limiting exposure to loud environments, and implementing
noise-reduction strategies in occupational and recreational settings.
In conclusion, while the human auditory system is remarkably adept at detecting
and processing sound, it is ill-equipped to withstand the intensity of modern-day noises.
Understanding the mechanisms underlying noise-induced hearing damage and
implementing proactive measures to mitigate its impact are essential for preserving
auditory health and well-being in an increasingly noisy world.
