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Action Potentials and Nerve/Brain

Resting membrane potential

 cells inside negative because of 3Na+/2K+ pump (20% of negative charge) and K+ leak channels

(80% of effect)

Action potentials require some graded potential to get to threshold

= opening of voltage-gated Na+ channels, happens at axon hillock

Four phases of action potential after threshold

 depolarization, peak, repolarization, hyperpolarization

Refractory period (absolute and relative)

Propogation of action potentials

 by contiguous (non-myelinated) and saltatory (myelinated) conduction down axons

Neurotransmitter release from terminals

 (AP  voltage gated Ca2+ channels open  vessicles release neurotransmitter)

Nuerotransmitter binds to post-synaptic cell, causes a depolarization (positive charge/excitatory post-

synaptic potential/EPSP) or a hyperpolarization (negative charge/ inhibitory post-synaptic

potential/IPSP)

Brain areas – cerebral hemispheres (higher order functions), cerebellum (autopilot), medulla (cardio and

vent centers), brain stem (some reflexes), spinal cord (parasympathetic and sympathetic by vertebra)

Nervous Tissue Injuries

 Concussions, strokes (CVAs), Alzheimers, Parkinsons, edema, etc.

Senses

Types of sensors (external/internal/proprio) and (chemo/mechano/photo etc)

Afferent (sensory nerves), Efferent (motor to glands and nerves)

Lateral inhibition – in vision and hearing adjacent nerves to a stimuls reduce action potential outputs but

sharpens determination of location

Eye – function of iris and lens, photoreceptors and retina, lacrimal glands (mucous, antibodies)

 Rods and cones, low-light vision vs bright/color vision

Retinene hit by photon of light, Photoreceptors (turns off), bipolar cells spontaneously depolarize (on),

ganglion/optic nerve(on) carries visual information

Taste – five qualities of taste (sweet, sour, salty, bitter, umami)

Skeletal muscle

Structure of muscle – muscle fiber = cell, myofibrils are tubes of sarcomeres within cells/fibers, thick

filament is myosin heavy chain(1, 2a, 2x in humans); thin filament = actin (rope for myosin to pull on),

tropomyosin (covers actin, prevents cross-bridges), troponin (binds Ca2+, controls

relaxation/contraction).

Sarcomere zones dark (A band, thick filament/myosin), light (I band, thin filament), z lines (end of each

sarcomere), m lines (middle of each sarcomere), h zones

Neuromuscular junction

 alpha motor nerves come from spinal cord, continuous to muscle fiber, ends at neuromuscular

junction.

 Releases ACH onto ACH-gated channels, depolarization then opens voltage-gated Na+ channels

to start action potential in muscle (AP).

 AP spreads in ALL directions on muscle, and into the core through transverse (T) tubules.

 This voltage opens DHP receptors, allowing Ca2+ to come out from release channels in

sarcoplasmic reticulum (SR).

 Ca2+ goes to sarcomere, moves tropomyosin and allows contraction. Is pumped back into SR via

smooth endoplasmic reticulum Ca2+ ATPase (SERCA pumps).

Muscle properties

 Motor units – nerve from spinal cord to muscle, one nerve may connecto multiple muscles, each

nerve has only one parent nerve. Recruitment happens when more nerves turn on until 100%

of muscle is turned on.

 Crossbridge cycle – needs ATP and Ca2+, continues as long as those are present. Resetting

myosin = use of energy

 Load-recruitment – more muscle/motor units required for heavier loads

 Force-velocity – contraction fastest with no resistance, stops when weight=max muscle force,

can have lengthening contraction when lowering weights (or walking down stairs etc). Length

tension – muscle force changes with joint motion; biggest force when sarcomere have overlap,

lose force when muscle is too long or too short and cross-bridges not optimum

Muscle fiber type – red, intermediate and white muscle differ in myosin (1, 2a, 2x), myoglobin (red

oxygen-storing pigment), mitochondria, fat/glycogen stores, and many other characteristics