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9 Cards in this Set
- Front
- Back
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List the characteristics of excitatory and inhibitory synapses |
-Excitatory synapses: Excitatory postsynaptic potentials (EPSPs) depolarize the postsynaptic membrane; smaller than an end plate potential; produced by activation of an excitatory receptor by excitatory NTs; the excitatory receptors increase permeability to Na+ and K+ ions; graded potentials.
-Inhibitory synapses: inhibitory postsynaptic potentals (IPSPs)-hyperpolarizing or stabilization of membrane potential; produced by activation of an inhibitory receptor by inhibitory NTs; increase permeability to K+ or Cl- ions; graded potentials. |
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List types of summation and describe their mechanism |
-Spatial: multiple synapses producing EPSPs simultaneously
-Temporal: a single axon with a high frequency of APs producing a train of EPSPs. |
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Describe how APs are initiated in neurons |
APs are initiated at the axon hillock due to high concentration of VG Na+ and K+ channels. Depolarizing current from the graded potentials produced at the dendrites and cell body must flow to the axon hillock to bring it to threshold potential. Summation of multiple EPSPs is required to bring the axon hillock to threshold. |
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Describe mechanisms for presynaptic inhibition and potentiation |
Presynaptic modulation--produced by axo-axonic synapses
-Presynaptic inhibition: decreased cytosolic Ca2+, decreased neurotransmitter release.
-Presynaptic facilitation: increased cytosolic Ca2+, increased neurotransmitter release |
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Describe differences between a neurotransmitter and a neuromodulator |
-Neurotransmitter: primary effector at a synapse
-Neuromodulator: secondary effector which fine tunes post-synaptic cell's response to NT; they're co-released with NTs. |
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List steps involved in neurotransmitter synthesis and elimination |
-Synthesis: 1. NT precursors are taken up into the synaptic terminal. 2. NT is synthesized by enzymes in nerve terminals. 3. NT is packaged in synaptic vesicles. 4. NT released into the synaptic cleft by fusion of the synaptic vesicle. 5. NT binds to receptors on the postsynaptic membrane
-Elimination: 6. NT is metabolized by enzymes in the synaptic cleft. 7. NT and or its metabolites are taken up into the synaptic terminal. 8. NT may be metabolized by enzymes in the nerve terminal. 9. NT not taken up into the nerve terminal diffuses away. |
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List the biogenic amine neurotransmitters, excitatory amino acid neurotransmitters and inhibitory amino acid neurotransmitters and examples of neuropeptides |
1. Biogenic amino acid NTs: -Catecholamines (dopamine, norepinephrine, epinephrine) -Indolamines (5-HT aka serotonin)
2.Excitatory amino acid NTs: |
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Describe synthesis and metabolic pathways for ACh, biogenic amines, and nitric oxide |
1. ACh: -Synthesis in nerve terminal: choline + AcetylCoA (choline acetyltransferase)--> ACh + CoA -Metabolism in synaptic cleft: Acetylcholine (acetylcholine esterase)--> choline + acetic acid
2. Biogenic amines: -Synthesis: Tyrosine--> L-Dopa --> Dopamine --> norepinephrine --> epinephrine -Elimination: reuptake into the nerve terminal
3. Nitric Oxide: -Synthesis: arginine (nitric oxide synthase)--> NO. NO is a gas and diffuses into adjacent cells and cGMP is produced. It is synthesized and released on demand and is NOT stored in synaptic vesicles.
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Describe mechanisms of modulation of neurotransmission and examples of drugs that act by these mechanisms |
1. Inhibition: -Blockade of APs: local anesthetics (lidocaine) -Inhibition of NT synthesis -Inhibition of NT release: botox -Receptor antagonism: curare, atropine, propranolol
2. Potentiation (enhances effects of NTs): -Inhibition of NT metabolism [elimination] (increases NT levels at the synaptic cleft): organophosphates inhibit acetylcholine esterase; MAO inhibitors increase NE and 5-HT levels; COMT inhibitors used for Parkinson's disease. -Blockade of NT reuptake (increases NT levels in the synaptic cleft): cocaine blocks dopamine reuptake; fluoxetine (prozac) blocks serotonin uptake. -Allosteric modulation of receptor (drugs bind to sites on receptor independent of the NT binding site and modulate [increase or decrease] the activity of the NT): diazepam (valium) binds to GABA receptors and potentiates the GABA stimulated chloride conductance. -Agonists: administration of exogenous agonists phenylephrine-a-adrenergic agonist -Precursors: administration of NT precursors e.g. L-DOPA for parkinson's patients (L-DOPA is converted to dopamine) |
