Di3PR1&2

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· What are the parts of the neuron? 

· A neuron contains three main parts: dendrites, an axon, and a cell body or soma

· What is the synapse and what happens there?

· The synapse is where the neurons communicate to other neurons at the junction. Synapses can be chemical, which most are and communicate via chemical messengers (neurotransmitters). The other marginal synapses are electrical synapses.

· How does one neuron send signals to other neurons?

· A neuron sending a signal (i.e., a presynaptic neuron) releases a chemical called a neurotransmitter, which binds to a receptor on the surface of the receiving (i.e., postsynaptic) neuron. 

· Neurons may communicate through electric synapses as well, this signal may occur differently and much quicker than chemical transmission, as there is a direct physical connection between the presynaptic neuron and the postsynaptic neuron. This connection takes the form of a channel called a gap junction, which allows current ions to flow directly from one cell into another.

· How do neurotransmitters go from one neuron to another?

· The process of neurotransmission, occurs through the neurotransmitters crossing the synapse and binding to special molecules on the other side, called  receptors. Receptors are located on the dendrites. Receptors receive and process the message. A neurotransmitter binds to a receptor in much the same way a key fits into a lock. After transmission has occurred, the neurotransmitter is either broken down by an enzyme (a chemical that speeds up some of the body’s processes) or is reabsorbed into the neuron that released it. The reabsorbed neurotransmitters can be reused at a later time. 

· Discuss the degradation and reuptake of neurons at the synapse?

· After neurotransmitters have been released into the synaptic cleft, they act upon postsynaptic receptors. That action must be terminated in order for proper neuronal communication to continue. This is accomplished mainly through two processes: neurotransmitter transport and/or degradation. Transport physically removes the neurotransmitter molecule from the synaptic cleft. Degradation breaks down the neurotransmitter molecule by enzyme activity.

. Acetylcholine action is terminated by acetylcholinesterase, an enzyme present in the synaptic cleft. Acetylcholinesterase degrades acetylcholine into choline and acetate molecules. Choline is then transported back into the presynaptic terminal and used in the synthesis of new acetylcholine.

. Glutamate action is terminated by two mechanisms. Reuptake of glutamate molecules into the presynaptic terminal can occur, or glutamate can be transported into nearby glial cells. The excitatory amino acid transporters are sodium co-transporters and use the sodium electrochemical gradient to drive neurotransmitter transport. Within glial cells, glutamate is converted into glutamine by glutamine synthetase. Glutamine is then transported out of the glial cell and back into the presynaptic terminal for use in future glutamate synthesis. If glutamate is transported back into the presynaptic terminal, it can be repackaged in synaptic vesicles.

. GABA and glycine action are terminated by either reuptake into the presynaptic terminal and packaging in synaptic vesicles or through transport into glial cells where breakdown can occur. The GABA and glycine transporter also use the sodium electrochemical gradient to drive the movement of the transmitter across the membrane.

. Dopamine action is terminated by reuptake into the presynaptic terminal via the dopamine transporter (DAT). Once inside the cell, dopamine is either degraded via the actions of either monoamine oxidase (MAO) or catechol-O-methyltransferase (COMT), or it is repackaged into vesicles.

. Norepinephrine follows the same pathway as dopamine. Reuptake into the presynaptic terminal occurs via the norepinephrine transporter (NET), and then the transmitter is either degraded within the cell by MAO or COMT or repackaged into synaptic vesicles.

. Like the other monoamines, serotonin is transported back into the presynaptic terminal via the serotonin transporter (SERT). The difference between serotonin and the catecholamines dopamine and norepinephrine is that monoamine oxidase is the only enzyme used for degradation.

· How do SSRI mechanisms of action?

· SSRIs have their basis on increasing deficient serotonin that researchers postulate as the cause of depression in the monoamine hypothesis. SSRIs exert action by inhibiting the reuptake of serotonin, thereby increasing serotonin activity. They inhibit the serotonin transporter (SERT) at the presynaptic axon terminal. By inhibiting SERT, an increased amount of serotonin (5-hydroxytryptamine or 5HT) remains in the synaptic cleft and can stimulate postsynaptic receptors for a more extended period. 

· What is MAOIs mechanism of action?

· Monoamine oxidase inhibitors are responsible for blocking the monoamine oxidase enzyme. The monoamine oxidase enzyme breaks down different types of neurotransmitters from the brain: norepinephrine, serotonin, dopamine, and tyramine. MAOIs inhibit the breakdown of these neurotransmitters thus, increasing their levels and allowing them to continue to influence the cells that have been affected by depression.

· What is TCAs mechanism of action?

· Tricyclic antidepressants act on approximately five different neurotransmitter pathways to achieve their effects. They block the reuptake of serotonin and norepinephrine in presynaptic terminals, which leads to increased concentration of these neurotransmitters in the synaptic cleft. The increased concentrations of norepinephrine and serotonin in the synapse likely contribute to its anti-depressive effect. TCA’s additionally act as competitive antagonists on post-synaptic alpha cholinergic (alpha1 and alpha2), muscarinic, and histaminergic receptors (H1). TCAs structure greatly influences the affinity of the TCA for each of these receptors.

· How do antipsychotic mechanisms of action?

·

· The first-generation antipsychotics work by inhibiting dopaminergic neurotransmission; their effectiveness is best when they block about 72% of the D2 dopamine receptors in the brain. They also have noradrenergic, cholinergic, and histaminergic blocking action. Second-generation antipsychotics work by blocking D2 dopamine receptors as well as serotonin receptor antagonist action. 5-HT2A subtype of serotonin receptor is most commonly involved.

· Difference between neurogenesis and apoptosis

Neurogenesis is the formation of neurons  de novo—the hallmark of a developing brain. It has been proposed that human neurogenesis takes place in subgranular zone (SGZ) of the DG closer to its hilum, which maintains a neurogenic stem cell (NSC) niche. Neurogenesis in the adult human DG has been postulated to play a role in memory and learning systems, as well as in protecting the brain from stress-induced attrition

Apoptosis is a mode of cell death in which the cell plays an active role in its own demise. Neuronal apoptosis and survival are tightly controlled processes that regulate cell fate during the development of the central nervous system and its homeostasis throughout adulthood. Apoptosis is triggered by two principal pathways: the intrinsic (or mitochondrial) pathway and the extrinsic (or death receptor) pathway. 

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