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
First step in sequence of actions in G protein receptr activity
NT bidns with receptor
26
when an AP arrives at preasynaptic terminal
voltage gated Ca channels are activated and intracellular Ca stores are released
27
the binding of Ach at neuromuscular junction results in
ESPS
28
PTSD associated with
hyperactivity of NE system
29
what meds used to treat myesthenia gravis
inhibit breakdown of Ach
30
Antagonist drug acts by
preventing release of NT