Ch 3 - synapses and synaptic transmission Flashcards

1
Q

Local depolarization is an

A

excitatory postsynaptic potential

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2
Q

Local hyperpolarization is an

A

inhibitory postsynaptic potential

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3
Q

Presynaptic facilitation

A

more NT is released

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4
Q

Presynaptic facilitation occurs when

A

a presynaptic axon releases a NT that slightly depolarizes the axon terminal of a second neuron, facilitating release of more NT into the cleft “priming effect”

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5
Q

Presynaptic inhibition

A

less NT is released

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6
Q

Presynaptic inhibition occurs when

A

an axon releases a NT that slightly hyperpolarizes the axonal region of a second neuron so less than neormal NT is released into the cleft

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7
Q

NT act directly on

A

postsynaptic ion channels or activates proteins inside the postsynaptic neuron

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8
Q

neuromodulators are released into

A

extracellular fluid and adjust the activity of many neurons

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9
Q

Two types of NT

A

fast acting and slow acting
Fast - act directly (less than 1/1000 of a s)
Slow - act indirectly (1/10 of a sec to min)

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10
Q

Neuromodulators effects last

A

minutes to days

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11
Q

Specific fast acting NT and NM

A

Acetylcholine - usually +

Amino acids - glutamate Excit, GABA Inhib

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12
Q

Specific slow acting NT and NM

A

Amines, Peptides, NO

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13
Q

Receptors are typically named for

A

transmitter/modulator to which they bind

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14
Q

Synaptic receptors act directly when

A

the receptor and ion channel make up a single functional unit

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15
Q

Synaptic receptors act indirectly whe

A

using a cascade of intracellular molecules to activate ion channels or cause other changes within the postsynaptic neuton

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16
Q

Postsynaptic receptors use three mechanisms to transduce signals

A

direct, indirectly, cascade

17
Q

Agonists are drugs that

A

bind to the receptor and mimic the effects of naturally occurring NTs

18
Q

Antagonists are drugs that

A

prevent the release of NTs or bind to the receptor and impede the effects of a naturally occuring transmitter

19
Q

Lambert Eaton Syndrome

A

disease in which antibodies destroy voltage gated Ca2+ channels in the presynaptic terminal

20
Q

Myasthenia gravis

A

disease in which antibodies attack and destroy nicotinic receptors on mm cells

21
Q

Channelopathy

A

disease that involves dysfunction of ion channels

cause some cases of epilepsy and migraine headaches

22
Q

What can serve as postsynaptic cell of a synapse

A

smooth muscle cell
hepatocyte
neuron in thalamus
mm cells of triceps

23
Q

How does botox produce paresis

A

inhibits the release of Ach from presynaptic terminal at neuromuscular junction

24
Q

Myesthenia gravis is an autoimmune disease that

A

destroys Ach receptors on postsynaptic membrane of mm and interferes with binding for repetitive mm contractions

25
Q

First step in sequence of actions in G protein receptr activity

A

NT bidns with receptor

26
Q

when an AP arrives at preasynaptic terminal

A

voltage gated Ca channels are activated and intracellular Ca stores are released

27
Q

the binding of Ach at neuromuscular junction results in

A

ESPS

28
Q

PTSD associated with

A

hyperactivity of NE system

29
Q

what meds used to treat myesthenia gravis

A

inhibit breakdown of Ach

30
Q

Antagonist drug acts by

A

preventing release of NT