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week 1 > kenyon neurotransmission 1 > Flashcards

kenyon neurotransmission 1 Flashcards

1
Q

gap jxn allow __(be specific)__ to move between cells

A

ions (and really small molecules according to the book)

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2
Q

“electrically coupled.” what does that mean?

A

this term refers to cells that are connected by GAP jxns and, therefore, have the same membrane potential

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3
Q

gap jxn structure

A

connexons that span both the presynapatic and postsynaptic neuron membranes

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4
Q

hallmarks of electrical transmission

A
  • gap jxns
  • bidirectional conduction
  • can be either positive or -negative
  • allows for SYNCRONIZATION
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5
Q

three examples of neurons that connect through electrical transmission

A
  • cardiac m
  • smooth m
  • some CNS neurons, like those that release hormones in the hypothalamus
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6
Q

define synaptic vesicles

A

organelles!
membrane bound
MUST contain 1 or more NTs

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7
Q

synaptic cleft space parameter

A

wide but narrow

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8
Q

chemical neurotransmission… up the where NT is released into cleft

A
  • NT packed vesicles chill
  • AP depolarizes terminal, causing opening of voltage gated Calcium channels
  • calcium then rushes through these channels
  • calcium increase causes vesicles to fuse w/ presynaptic membrane
  • NT is released into synaptic cleft
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9
Q

chemical neurotransmission after NT release into cleft

A
  • NT binds to receptors on postsynaptic membrane
  • ^^binding of NT will open OR close postsynpatic channels
  • the post synaptic current will cause inhibitory or excitatory change in electric potential
  • then NT gets removed by uptake or enzymatic degradation
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10
Q

lidocain

A

Na+ channel inhibitor, so it blocks the AP

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11
Q

Lambert-eaton

A

autoimmune disease where the body makes INHIBITORY antibodies against the voltage gated calcium receptors on the presynaptic membrane

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12
Q

conotoxin

A

a type of neuropeptide that inhibits voltage gated calcium channels on the presynaptic membrane

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13
Q

botulin and tetanus toxins

A

block vesicle release

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14
Q

curare

A

irreversibly binds and inhibits the nicotinic ACh receptor on neuromuscular junctions

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15
Q

benzodiazepine

A

binds to GABA receptor and inhibits it

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16
Q

myasthenia gravis

A

antibodies bind to ACh receptors at neuromuscular jxns.

similar effect to curare!

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17
Q

physostigmine

A

blocks acetylcholinesterase

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18
Q

prozac

A

serotonin reuptake inhibitor

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19
Q

slow axonal transport

A

FOR SMALL MOLECULE NT synthesis!!!

  • enzymes are synthesized in the cell body
  • enzymes travel down slowly along axon
  • synthesis and packaging of NT happens at the presynaptic terminal
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20
Q

fate of small molecule NTs

A

usually, they precursor gets recycled by coming directly back into the terminal

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21
Q

fast axonal transport

A

FOR NEUROPEPTIDES:

  • neuropeptides are synthesized and pre-packaged into vesicles of cell body
  • these “loaded” vesicles are transported to the terminal
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22
Q

fate of neuropeptides

A

usually, they get degraded/diffused away

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23
Q

unconventional NT synthesis

A

the whole new school sequence: NT etiology, calcium FXN, and receptor location

just remember that the enzymes are synthesized in the cell body and then transported to terminal

24
Q

list the three unconventional NTs

A

NO, C02, endocannabinoids

25
Q

NT location: old schools vs new school

A

old: substance must be present in presynaptic vesicles

new (unconventional NTs): substance can be synthesized on demand–like in the case of unconventional NTs

26
Q

calcium fxn: old school vs new school

A

old: release of substance MUST be triggered by an increase in [Ca++]presynaptic

new (unconventional NTs) … calcium-activated enzymes can synthesize NTs upon increase in presynaptic calcium; then these NTs diffuse out

27
Q

receptors: old school vs new school

A

old: specific receptors must be present on postsynaptic membrane

new (unconventional receptors): specific receptors present, instead, on CYTOPLASM of postsynaptic cells

28
Q

vesicle cycling

A
  • vesicles originate off an endosome and are filled w/ NTs
  • upon Ca++, vesicles bind to the plasma membrane
  • and then these same vesicle membranes are retrived by clathrin-mediated ENDOcytosis
  • then the clathrin comes off (uncoating)
  • and finally the vesicles are at a position where they can return to the endosome
29
Q

kiss and run

A

vesicles may transiently open pores to the synaptic space. this opening is very transient and only releases a small amount of contents. in kiss and run releases, vesicle does not have to get reabsorbed

30
Q

kiss and run/classic mech effect on membrane

A

has an effect on membrane for sure, but looks smaller than quantal release

31
Q

define cotransmission

A

when one neuron releases more than one NT

32
Q

Differential release in cotransmission

A

preferential release is dictated by frequency of stimulation and concomitant increase in calcium concentration

at low frequency, usually, small molecules are released.
at high frequency, usually, neuropeptides are released

33
Q

snap 25

A

a non-SNAP protein lol. it’s important to serve as a dock for synaptobrevin to syntaxin. it serves to dock the vesicle to the membrane

34
Q

synaptobrevin and syntaxin

A

synaptobrevin (SNARE on vesicle)

syntaxin (SNARE on plasma membrane)

35
Q

synaptotagmin

A

protein located on vesicle membrane.

fxn: once the SNARE complexes dock via SNAP-25, synaptotagmin is primed to accept the calcium.

once calcium binds, synaptotagmin catalyzes the membrane fusion!!!!. How? by binding to itself to SNARES and the plasma membrane

36
Q

nerst equation

A

Ex=[58/z][logXo/Xi]mV

37
Q

permeability effect on membrane potential

A

more permeability = heavier contribution to overall membrane

38
Q

ACh example in terms of permability

A

ACh increased the permeability to a particular ion. NTs can increase or decrease it

39
Q

iontropic

A

deals w/ muscles

40
Q

permeability and gating: two cases–ionotrpoic and metabotropic

basically ionotropic is direct and metabotropic is indirect

A

ionotropic: NT binds to a receptor; that same receptor opens its channel; ions flow through receptor.
metabotropic: NT binds to receptor; G protein sequence; G protein subunits or intracellular messengers modulate the ion channels; ions flow through channels.

41
Q

Suppose: channel opens to allow BOTH Na+ and K+ in. how will membrane potential change?

A

It’ll go somewhere between Ek and ENa

42
Q

Define: Erev

A

the target potential associated w/ the opening of ANY particular channel

when you open more channels for a particular ion, you will be more closer to the Erev

43
Q

effect of opening nonselective channels

A

should be around zero because of the positive and negative summations of Exs, like EK, and ENa

44
Q

The general rule of NTs on membrane potential!

A

NT will drive the POSTsynpatic potential toward Erev for the SPECIFIC ion channel that said NT is activating

always think in terms of changing permeability

45
Q

Types of channels in NT transmission

A

Common: non-selective channels for Na, K, or Ca++

Also common: Selective for Cl- or for Ca++

rare: selective for K+ and Na+

46
Q

are the channels involved in NT different than those in the AP?

A

YES!!!!

as far as i know

47
Q

Define EPSP

A

Erev is more positive than the postsynaptic neuron AP THRESHOLD mark

48
Q

Define IPSP

A

Erev is more negative than the postsynaptic neuron AP THRESHOLD mark

49
Q

Is a IPSP that causes depol more likely to reach threshold than a cell just chillin at resting threshold?

A

NOOO!

Coz the IPSP depol actually stabilizes, sort of electrically buffers, the membrane potential to FOR SURE keep it below the threshold

50
Q

general threshold rules.

A

-Ion channels nonselective for cations or selective for
Ca2+ mediate EPSPs (Erev positive to threshold)

-Ion channels selective for K+ mediate IPSPs (Erev negative to threshold)

  • Ion channels selective for Cl- mediate IPSPs if ECl is negative to threshold or EPSPs if ECl is positive to threshold.
  • Recall the range of ECl given as -88 to -35 mV. See box 6D for gory details..
51
Q

Define the summation phenomenom. what two factors are important too?

A

summation: neuron receives 100s/1000s of inputs and sums them up

location and timing are CRITICAL

52
Q

define EPP

A

EPP=end plate potential, which is when ACh opens ligand gated channels and therefore creates an AP.

(ONLY REQUIRES ONE MOTOR END PLATE–NO SUMMATION NEEDED)

53
Q

Are EPSP and IPSP additive?

A

yes BUT not linearly

54
Q

list examples of NTs involved in retrograde signaling

A

NO, CO, endocannaboids, and prostagladins

55
Q

retrograde mech

A

NT binds to post synaptic neuron; calcium concentration increases; increased calcium pushes endocannabinoid production; then that same endocannabinoid seeps back into the synaptic cleft to bind onto the presynaptic terminal.

good for like a negative feedback effect.

56
Q

presynaptic receptors

A

fxn: receptors on presynaptic terminal serve to regulate release of NTs

source of the NTs that modulate these presynaptic receptors: (1) NT inhibiting itself and (2) NTs from other neurons

week 1 (12 decks)

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