Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neurobiology > Lecture 4+5 > Flashcards

Lecture 4+5 Flashcards

1
Q

What are gap junctional intercellular channels formed from?

A

connexins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are oligo connexins?

A

connexins that make “reflexive” junctions to shorten pathway of diffusion (found in spatial buffering)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

___ has the smallest single- channel conductance and pore size – perfect for electrical conductance.

A

Cx36

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

allow ionic current to flow passively from one neuron to another; very fast, bidirectional transmission

A

electrical synapses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the advantages of electrical synapses?

A
  • rapid,synchronized communication between cells

- relatively fail-safe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the disadvantages of electrical synapses?

A
  • difficult to modulate gating of channels

- can’t change the “sign”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where are electrical synapses found?

A
  • during early embryonic stages
  • interneurons in the cerebral cortex, thalamus, cerebellum, etc.
  • brainstem neurons – generate rhythmic electrical activity that underlies breathing
  • retinal neurons (photoreceptors, bipolar cells, horizontal cells, amacrine cells, ganglion cells)
  • “escape reflex” in many organisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when Cx36 is disabled/eliminated?

A
  • loss of synchronous activity among interneurons
  • retinal deficits (e.g., total night blindness)
  • EEG abnormalities
  • slower motor-coordination learning (Firsch et al., 2005)
  • deficits in circadian behavior
  • loss of ocular dominance plasticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

communication between neurons that involves a rapid release and diffusion of a chemical signal secreted from the presynaptic membrane of one cell

A

chemical synapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

site of NT release receptors release on presynaptic cell

A

active zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

site containing NT receptors on postsynaptic cell

A

postsynaptic density

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

space between synapse and dendrite

A

synaptic cleft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

the theory that the neurotransmitter is released in multimolecular “packets” of a fixed size

A

quantal hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

the theory that synaptic vesicles are the structural basis of quanta – they contain neurotransmitter, which they release by fusion with the presynaptic membrane

A

vesicle hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

the theory that voltage-dependent calcium entry couples stimulation (i.e., the action potential) to secretion

A

calcium hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

the theory that interactions between SNARE proteins on the vesicle and the presynaptic membrane, modulated by calcium, lead to vesicle fusion

A

SNARE hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

spontaneous change in potential even in the absence of an action potential; same shape as EPP but smaller

A

MEPP (miniature end plate potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the characteristics of a MEPP?

A
  • size declines with distance from NMJ -> arise at synapse
  • disappear when nerve is removed -> come from nerve
  • blocked by Ach inhibitors -> due to NT action
  • correspond to ~5-10,000 molecules of ACh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How are MEPPs and EPPs related?

A

The EPP is made up of many MEPPs (i.e., quanta) released simultaneously

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

average number of vesicles released upon stimulation;

A

quantal content (M)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

If a perturbation (drug, stimulation pattern, disease, etc.) affects quantal number, the effect is likely _____.

A

presynaptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how many receptors does one vesicle activate (measured by EPP size)

A

Quantal size (Q)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

If a perturbation (drug, stimulation pattern, disease, etc.) affects quantal size, the effect is likely ____.

A

postsynaptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

A presynaptic alteration will show _____ in MEPP amplitude but ____ in EPP/MEPP.

A

no change

change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

A postsynaptic alteration will show ____ in MEPP amplitude but _____ in EPP/MEPP.

A

change

no change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

There are _____ molecules of NT per vesicle.

A

~10,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

discharge of the contents of a single synaptic vesicle

A

quanta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens during the calcium hypothesis for neurotransmitter release?

A

1) An action potential arrives at presynaptic terminal and depolarizes it.
2) Voltage-gated calcium channels open.
3) Calcium enters the presynaptic terminal.
4) Calcium influx triggers fusion of synaptic vesicles. 5) Neurotransmitter is released.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What happens if Ca+2 is absent from the extracellular space?

A

no postsynaptic response; amount of NT released is sensitive to the exact amount of Ca2+ that enters the presynaptic terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happens during the SNARE hypothesis of neurotransmitter release?

A

• Neurotransmitters are actively transported into synaptic vesicles (1)
• Vesicles cluster at the active zone (2), dock (3), and are primed (4) to ready
them for Ca2+-triggered fusion (5).
• After NT is released, vesicles are endocytosed (6) and recycled.
• Vesicles are refilled with NT directly (7) or after passing through an endosomal intermediate (8).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

SNAREs found on synaptic vesicles

A

Synaptobrevin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

SNAREs found on vesicle, acts as Ca2+ sensor

A

Synaptotagmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

SNAREs found on presynaptic plasma membrane

A

Syntaxin and SNAP-25

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What happens during priming of SNARE NT release?

A

Prepare for rapid triggering of exocytosis
• vesicle must be primed and ready to fuse in <0.5 msec
• Ca2+ channel binds syntaxin
• synaptotagmin is the calcium sensor
• prepare for fusion: ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What happens during vesicle fusion of SNARE NT release?

A
  • Ca2+-induced, fast neurotransmitter release

- released NTs diffuse across the synaptic cleft and interact with receptors in the post- synaptic membrane

36
Q

____ affects SNARE proteins involved in vesicle fusion; impairs NT release.

A

Botulinum toxin (botox)

37
Q

loss of voltage- gated calcium channels

A

Lambert-Eaton myasthenic syndrome

38
Q

impaired vesicle recycling

A

Congenital myasthenic syndrome

39
Q

What are the advantages of chemical synapses?

A
  • can be modulated (at one of many steps)

* change signs by release of inhibitory neurotransmitter

40
Q

What are the disadvantages of chemical synapses?

A
  • multiple steps are required for NT release and receptor activation  time delay
  • directional(presynaptic –> postsynaptic only)
41
Q

What are the major differences between electrical and chemical synapses?

A

electrical: gap junction channels composed of connexins, cytoplasmic continuity, flow of ions, 3.5 nm distance between pre- and postsynaptic membrane, brief or no delay, bidirectional transmission
chemical: presynaptic vesicles and postsynaptic receptors, no cytoplasmic continuity, chemical transmitters, 20-40 nm distance between pre- and postsynaptic membrane, 1-5 ms synaptic delay, unidirectional transmission

42
Q

Botulism prefers a ___ pH, _______ environment. The toxin passes through bloodstream to reach ___ and cleaves ____. This results in _____ and _____. This is ____.

A 
low
anaerobic
NMJ
syntaxin and SNAP25
no ACh release
no muscle contraction
irreversible
43
Q

Tetanus travels to ___, binds irreversibly, cleaves ____ to block release of ____ neurotransmitters
–> body cannot ____.

A

CNS
SNARES (synaptobrevin)
inhibitory
prevent muscle contraction

44
Q

What are some symptoms of tetanus?

A

lockjaw, difficulty swallowing, continuous muscle spasms throughout the body, including breathing

45
Q

Alpha- latrotoxin toxin affects what part of the NT release pathway?

A

promotes Ca2+-dependent vesicle fusion; promotes vesicle exocytosis instead of blocking it

46
Q

receptors that let ions flow through; fast and direct; voltage- or -ligand gated

A

ionotropic

47
Q

receptors that change metabolism; slow and indirect; G-protein coupled

A

metabotropic

48
Q

Name the 7 small molecule NTs.

A
  • acetylcholine
  • dopamine
  • GABA
  • glycine
  • glutamate
  • norepinephrine
  • serotonin
49
Q

derived from larger proteins (up to 36aa); exclusively use GPCRs

A

neuropeptides

50
Q

What is Dale’s rule?

A

all terminals of a neuron release the same neurotransmitter(s); very common to release both a small molecule and a neuropeptide (separate vesicles)

51
Q

breaks down ACh in synaptic cleft; cleaves 5000 molecules/sec

A

acetylcholinesterase

52
Q

___ is a ligand- gated ion channel for ACh

A

nicotinic acetylcholine receptor (nAChR)

53
Q

component of venom from elapid snakes that blocks the acetylcholine receptor

A

alpha bungarotoxin

54
Q

There are __ ACh binding sites per receptor. The receptors are ___ than voltage-gated channels and __ ion specific.

A

2
larger
less

55
Q

What is the structure of nAChR?

A

• 5 subunits (a2, b, d, g)
• each subunit has 4 membrane-spanning
domains (TM1-TM4)
• TM2 lines the pore
• 3 rings of negatively charged amino acids around TM2: selects for cations
• poor selectivity compared to potassium or sodium channels: allows K+, Na+, and Ca2+

56
Q

potential at which current flow through AChR channel is 0; inward and
outward currents are equal and opposite

A

reversal potential (Erev)

57
Q

What ions flow through AChR

A

cation channel (K+, Na+, and some Ca2+)

58
Q

What is Erev for AChR (which Eion)?

A

Erev for the AChR is not at the equilibrium potential of a single ion - lies between EK and ENa

59
Q

In AChR, because ___ are similar, current depends on ____ for each ion.

A

permeabilities

driving force

60
Q

When muscle is at rest and AChR opens, __ rushes in an very little __ rushes out, depolarization leads to __.

A

Na+
K+
EPSP (EPP)

61
Q

ligand-gated ion channel open too long (i.e., too much neurotransmitter) -> channel closes

A

Desensitization

62
Q

What is succinylcholine and how does it work?

A

muscle relaxant in surgery because it causes desensitization; succinylcholine not easily cleaved by acetylcholinesterase

63
Q

Nearly all excitatory CNS neurons are ____. ___ is most common precursor – converted in presynaptic terminal; retrieved from synapse by transporters in both neuron and glia. Too much ___ can kill (__)

A

glutamatergic
Glutamine
glutamate
excitotoxicity

64
Q

Glutamate has ionotropic receptors that are non-selective ___ channels. It also has metabotrpic receptors that activate ____.

A

cation

GPCRs

65
Q

Glutamate binds to the ionotropic __ receptors, allows __ and ___ ions through; evoke EPSPs that are __ and ___.

A 
AMPA
sodium
potassium
large
fast
66
Q

Glutamate binds to the iontotropic ____ receptor, which allows flow of Ca2+ in addition to Na+ and K+. Increased Ca+2 can act as a ____. It evokes EPSPs that are ___ and ___.

A

NMDA
second messenger
slow
long-lasting

67
Q

NMDA channels are blocked by __ in pore. Block is removed by ___; requires either multiple cells to fire or a single cell to fire repeatedly.

A

Mg2+
depolarization

NOTE: no Mg2+, no block – channel is always open

68
Q

inhibitory NT that is everywhere (cortex, midbrain, etc.); most important inhibitory NT in brain

A

GABA

69
Q

inhibitory NT that is in the spinal cord, brainstem, retina (evolutionarily older); low levels in other areas

A

Glycine

70
Q

Inhibitory NT activate ligand-gated ion channel selective for __, which flows into the cell; cell becomes more __.

A

Cl-

hyper polarized

71
Q

In metabotropic (GPCRs), NT binds receptor extracellular domain. Intracellular domain binds a set of 3 proteins – α,β,γ - together, called __. ___ is hydrolyzed– ___ splits off an binds to effector protein and activates/inactivates.

A

G proteins
GTP
α

72
Q

Cyclic AMP (cAMP) is generated from ATP by ____. cAMP activates __, which can activate many proteins, including channels.

A

adenylyl cyclase

protein kinase A (PKA)

73
Q

when a few molecules of NT can have a big effect

A

amplification

74
Q

What are the advantages of GPCRs?

A
  • amplification
  • multiple effects on a single target
  • multiple targets
75
Q

The primary structures and NT involved in depression are?

A

hippocampus and prefrontal cortex

norepinephrine and serotonin

76
Q

___ metabolizes serotonin, noradrenaline, and dopamine - removes them from use by the neuron.
___ are anti-depressants that prevent breakdown - more NT available for release

A

MAO

MAOIs

77
Q

___ block serotonin and noradrenaline transporters (i.e., reuptake pumps). They have no effect on __. They are antagonists of multiple ___ and ___ along with ___ and ___ receptors, which leads to multiple side effects.

A 
TCAs (tricyclic antidepressants)
dopamine
serotonin
noradrenaline
histamine
acetylcholine
78
Q

___ block re-absorption of serotonin - more available at synapses; can be extended/controlled release; generally fewer side effects

A

SSRIs (selective serotonin reuptake inhibitors)

79
Q

Drug with the same concept as SSRIs but with noradrenaline instead of serotonin

A

SNRIs (selective noradrenaline reuptake inhibitors)

80
Q

biochemical imbalance in serotonin/noradrenaline may underlie pathogenesis of depression

A

Monoaminergic hypothesis

81
Q

Many sub-threshold synaptic inputs sum together in the soma

A

intergration

82
Q

second of two closely spaced EPSPs is bigger than the first due to increased quantal content

A

facilitation

83
Q

What is the residual calcium hypothesis of facilitation?

A

Ca2+ enters to trigger transmitter release, then removed; when 2nd stimulus is soon after 1st, not all Ca2+ has been removed from the initial pulse

84
Q

smaller synaptic potentials with repetitive stimulation (often at high frequency) –> depletion of readily available vesicles and decreased quantal conten

A

depression

85
Q

Excitatory synapses generally occur on __ or __. Inhibitory synapses closer to the __.

A

dendritic shafts
spines
axon initial segment

86
Q

What factors affect synaptic integration?

A
  • distance of synapse from initial segment; dendrites are leaky and signals attenuate with distance
  • shunting inhibition: inhibitorysynapselocated between an excitatory synapse and soma can cause EPSP to attenuate to zero before reaching soma
  • temporal and spatial summation: multiple synaptic potentials combine within one postsynaptic neuron

Neurobiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions