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Anatomy 403 > Synaptic Transmission > Flashcards

Synaptic Transmission Flashcards

1
Q

types of synapses

A
  • electrical

- chemical

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2
Q

electrical synapse

A

gap junctions

  • direct cell to cell contact
  • cytoplasmic continuity
  • conduct electrical signals very rapidly (no delay)
  • 2-4 nm gap
  • 2 way conductance
  • diameter on the protein pores = 1.5 nm
  • –> only ions/small molecules can pass
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3
Q

electrical synapse location

A
  • immature neurons
  • glacial cells to neurons
  • cardiac muscle
  • smooth muscle
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4
Q

chemical synapse

A
  • synaptic cleft (10-20 nm gap) between 2 neurons
  • AP in presynaptic neuron stimulates neurotransmitter release
  • NT release across cleft (.2 msec delay) to bind to receptors on postsynaptic cleft
  • one way flow
  • amount of NT can be modified
  • number of receptors for NT can be modified
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5
Q

level of excitability of a postsynaptic cellar any moment depends on:

A
  1. the number of synapses active at one time
  2. number the are excitatory
  3. number that are inhibitory
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6
Q

complexity altered by:

A
  1. number of neurons

2. number of synapses

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7
Q

plasticity

A

constantly making new synapses, basis for learning

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8
Q

excitatory postsynaptic potentials (EPSPs)

A

depolarizing graded potentials

- neuron more likely to generate action potential

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9
Q

NT’s that generate EPSPs

A
  • Ach
  • glutamate
  • NE
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10
Q

EPSPs caused by:

A

Na+ flows in

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11
Q

inhibitory postsynaptic neuron (IPSPs)

A

hyper polarizing graded potenitals

- less likely to generate action potential

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12
Q

NT’s that generate IPSPs

A
  • GABA

- glycine

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13
Q

IPSPs caused by:

A
  • Cl- flow in
  • K+ flow out
    • most will K+ channels, Cl- doesn’t have much of an effect by itself
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14
Q

NT removal options

A
  1. diffuse away (glutamate)
  2. reuptake (serotonin)
  3. degradation by an enzyme (AchE –> degrade Ach)
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15
Q

summation

A

local potentials are small: need about 20 EPSPs to reach voltage (.5 mV)

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16
Q

temporal summation

A

multiple inputs in rapid success ion from one synapse

17
Q

spatial summation

A

input from multiple different synapses arriving at the same time

18
Q

convergence

A

many different presynaptic neurons can affect a single postsynaptic cell

19
Q

divergence

A

a single presynaptic neuron that can affect many postsynaptic cells

20
Q

presynaptic facilitation

A

increased number of Ca+ channels open on presynaptic neuron, increasing the quanta of NT released, increase the postsynaptic response

21
Q

presynaptic inhabitation

A

decreased number of Ca+ channels open in presynaptic neuron, decreasing the quanta of NT released, decreasing the postsynaptic response (decreasing local potential)

22
Q

desensitization

A

with persistent stimulus, receptor fails to respond (tolerance to drugs)

23
Q

neuromodulation

A

modify the postsynaptic cells response to a specific NT (amplifying or dampening its effectiveness)

24
Q

Ligand-gated ion channels

A
  • ionotropic
  • cellular response = local potential
  • rapid response
25
Q

ionotropic

A

receptor forms ion channel

26
Q

G-protein coupled receptors

A
  • metabotropic
  • cellular response = activation of second messenger cascade
  • slower response
  • change in gene transcription, enzyme activity, etc.
27
Q

metabotropic

A

change “metabolism”

28
Q

metabotropic receptors

A
  • usually small molecules, co-released with NT
  • bind to receptors on pre- or postsynaptic membrane
  • activate 2nd messenger signaling cascades –> have longer term effects
  • ex: NTs, neuropeptides, nitric oxides, ATP
29
Q

neuromodulators

A
  • alter synthesis, release, uptake or metabolism of NT at the presynaptic cell
  • increase or decrease the effectiveness of a NT at the postsynaptic cell
  • are associated with longer term effects
30
Q

Botulism Toxin mechanism of action

A
  • prevents exocytosis of synaptic vesicles –> no NT released
  • specific for excitatory neurons
31
Q

Botulims Toxin consequence

A
  • decrease in muscle contraction

- can paralyze respiratory muscles (fatale)

32
Q

dystonia

A

too much muscle contraction

33
Q

sarin (nerve gas) mechanism of action

A
  • inhibits AchE

- increases Ach in synapse

34
Q

sarin consequence

A
  • uncontrolled muscle contraction
  • desenitization –> paralysis
  • respiratory arrest –> most common death
35
Q

SSRI

A

selective serotonin reuptance inhibitor

36
Q

Paxil (SSRI) mechanism of action

A
  • prevents reuptake

- increases serotonin

37
Q

Paxil consequence

A
  • build up of serotonin in synaptic cleft

- stabilizes mood

38
Q

xanax, valium, ethanol mechanism of action

A
  1. stimulate GABA-R

2. block Glut-R

39
Q

xanax, valium, ethanol consequence

A
  1. decrease anxiety and increase sleep (GABA-R)

2. decrease mental processing (learning) and decrease sensory / motor (Glut-R)

Anatomy 403 (13 decks)

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