Brainscape's Knowledge GenomeTM

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


See full index

Bio 222 Cell/Molec Neuroscience > Exam 3 > Flashcards

Exam 3 Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Lashley’s experiment

A

Lesioned different parts of the brain:

-learning/remembering maze was not impaired by local cortical legion anywhere

BUT: larger the lesion, greater the impairment (engram is everywhere)

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

Kandel’s initial research

A

made first intracellular recordings of APs from hippocampal neurons (in cats)

ended up working with aplysia later on with Tauc

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

characteristics of aplysia

A
  • abdominal ganglion has only about 300 neurons
  • neuron cell bodies are big
  • identical organization of nervous system in all aplysia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Kandal and Tauc’s initial experiment: what did they do? initial conclusions?

A

intracellular recordings from neurons

found ones that got EPSP when they stimulated nerve 1, but not when stimulated nerve 2

conclusions: a cell w/ an axon in nerve 1 makes excitatory synapse on test nuron; no neurons w/ an axon in nerve 2 directly synapse onto test neuron

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

Kandal and Tauc’s major experiment: what did they do?

A

stimulate nerve 2 repetitively for a few seconds

test to see if amplitude of response to stimulating nerve 1 was larger or smaller (was larger)

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

homosynaptic facilitation and depression

A

repetitive stimulation of anueron leads to either transient increase (facilitation) or decrease (depression) in response amplitude

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

hetersynaptic facilitation

A

repetitive stimulation of one neuron changes the response to stimulation of another neuron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

simple behaviors mediated by the aplysia abdominal ganglion

A

gill and siphon: respiratory organis

gentle tap to siphon causes gill to withdraw

repetitive taps causes less and less response (habituation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

sensitization in aplysia

A

behavioral event analogous to heterosynaptic facilitation

gentle tap to siphon causes gill to withdraw

give electrical shock to tail

responses to sphon tap is larger, more rapid, longer lasting gill withdrawal

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

cells involved in gill withdrawal

A

sensory neurons respond to siphon tap

motor neurons cause gill to withdraw

tail sensory neurons contact interneuron 5-HT

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

where is the locus of non-associative learning

A

habituation occurs at sensory motor synapses

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

how does habituation and facilitation work on molecular level?

A

habituation: decrease in release probability of NT release
sensitization: increase in release probability

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

short term and long term sensitization

A

single shock produces short term sensitization only

multiple shocks gives changes that are larger and persist for days

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

what do interneurons in aplysia release and what does it do

A

L29 facilitator interneuron releases serotonin

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

adding what 3 molecules can cause synaptic facilitation

A

serotonin (5-HT), cAMP, PKA

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

how does PKA increase transmitter release

A

PKA phosphorylates voltage independent “leak” K channel (gKs) and shuts it off, slowing spike repolarization

calcium channels stay open longer so more calcium enters

more transmitter is release, thus sensitization

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

whats the easiest way to study long term sensitization

A

motor neuron and one or more sensory neurons in a cell culture

directly apply serotonin with a pipette

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

long term sensitization requires what

A

new protein synthesis

protein synthesis inhibitor Anisomycin prevents long term sensitization to serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Kelsey Martin’s long term sensitization experiment

A

single sensory neuron innervates 2 motor neurons

apply 5 pulses of 5-HT only near MN2

only SN-MN2 synapses facilitated (something beyond transcription/translation required for sensitization)

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

2 models to explain synapse specificity observed in Martin’s experiment

A

synpases that see 5x serotonin are marked:

1) RNA/protein synthesis are near nucleus, but the new protein is only incorportated into synapses that were marked by 5HT
2) RNA synthesis is in the nucleus, but protein synthesis occurs in marked-presynaptic terminals, not in cell body (CORRECT)

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

experiment by Martin to determine why synapse specificity occurs

A

put photoswitchable tag on newly translated proteins

initally glows green, turns red w/ UV light (all pre-existing protein glows red)

look for where the new green proteins are

RESULT: only branches that saw 5-HT make new protein, even though mRNA is in all branches

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

how did they find the first learning mutant drosophila (5 steps)

A

forward genetics

  1. feed EMS to male flies (random mutations)
  2. cross to WT females
  3. outcross offspring separately (offspring each carry different mutations)
  4. make inbred lines of new mutations
  5. test for any phenotype of interest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how did they measure defect in learning in drosophila mutants

A
  • before odorant-shock pairing, flies have no preference for odor A or B
  • associate odor A with electric shock
  • WT flies choose odor A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

fruit flies odor learning: performance index

A

-performance index = (flies avoiding odor A - flies avoiding odor B)/total flies

index = 1: learning; index = 0: no learning

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

what is the first learning mutant fly called, what does it do

A
  • dunce*:
  • do not learn well, forget rapidly (index closer to 0)
  • dunce gene encodes phosphodiesterase enzyme that hydrolyzes cAMP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

after dunce, what learning mutant was discovered

A
  • rutabega:* encodes an enzymes that catalyzes cAMP synthesis
  • decrease in performance index
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does the fly brain process odor cues

A

sensilla: have sensory neuron dendrites in them

odor molecules bind odor receptors on the dendrites of olfactory sensory neurons (OSNs)

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

axel and buck

A

nobel prize for discovering odor receptors and the organization of the olfactory system

in rats

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

axel and buck assumptions regarding olfactory receptor genes that led to discovery:

A

1) odor receptors should resemble rhodopsin receptors in eye
2) ORs belong to large family of related proteins
3) must be expressed only in rat’s olfactory epithelium

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

mammalian vs insect olfactory receptors (ORs)

A

mammalian ORs are GPCRs

insect ORs are ligand gated ion channels

both have 7 transmembrane domains

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

how is odor information relayed to the brain: first destination in brain

A

OSN axons go to antennal lobes in brain

each antennal lobe made up of 50 distinct glomeruli

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

olfactory sensory neurons (OSNs) of the same type….

A

(express same odor receptor) project their axons to the same glomerulus in the antennal lobe

OSNs connect w/ olfactory projection neurons in antennal lobe

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

each olfactory projection neuron

A

carries information from a single odor receptor

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

overview: odor to behavior steps

A

odor → olfactory sensory neuron → olfactory projection neuron → kenyon cells in mushroom body → mushroom body output neurons → learned behaviors

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

mushroom body

A

learning and memory center of drosophila

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

projection neuron axons terminate in the

A

mushroom body and the lateral horn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

connections between projection neurons and kenyon cell

A

each kenyon cell gets input from 3-10 projection neurons

kenyon cells combine information about multiple olfactory cues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how can projection neuron inputs to kenyon cells be mapped out

A

1) label a single kenyon cell (using photoactivable-GFP)
2) label the presynaptic partners of that kenyon cell
3) identify what projection neuron type is labeled
5) repeat this for all the KC dendrites
5) repeat this for all KCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

___ is the key to plasticity in the mushroom body

A

dopmaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

kenyon cell to behavior?

A

kenyon cells transmit odor information to mushroom body output neuron (MBON), which transmits this information to other brain areas

dopaminergic neuron (DAN) also transmits information about the context/experience to MBON (DA only released during learning)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

facilitation, augmentation, potentiation, long term potentiation

A

facilitation: very short lasting form of enhancement (few ms)

augmentation: enhancement lasting a few seconds

potentiation: enhancement lasting longer than a few seconds

LTP: lasting at least half an hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

basic hippocampal circuitry: 3 excitatory connections

A

synapse 1: perforant path (from entorhinal cortex) to granule cells of dentate gyrus

synapse 2: granule cell axons (mossy fibers) to CA3 cells

synapse 3: CA3 cell axons (Schaffer collaterals) to CA1 cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

different ways of studying hippocampus

A

intact animals

hippocampal slice preparations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

hippocampus and dissociated cell culture

A

hippocampal neurons survive well in dissociated cultures:

  • need secreted materials from astrocytes
  • during dissociation, dendrites/axon torn off, but eventually grow back in culture
  • allows for good access to synapses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

problem of studying hippocampal neurons in culture

A

don’t know where hippocampal neurons originated from

mechanism of LTP is not the same at all synpases of the hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Neher and Sakmann

A

discovered how to record electrical activity of single channels in isolation with a patch clamp

invented whole cell recordings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

patch clamp recording method used to study hippocampus:

cell attached recording

A

glass pipette mounted on micromanipulator, bring in contact w/ plasma membrane of a cell, form tight seal, feedback amplifier controls potential across membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

patch clamp recording method used to study hippocampus:

whole cell recording

A

can apply pulse to destroy membrane at the tip but leave seal intact and do whole cell recording

samples activity of all channels, not single channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

patch clamp recording method used to study hippocampus:

excised patch recording

A

pull pipette off cell w/ seal intact

can be outside out or inside out

matters bc changing solution is easier on the face exposed to the outside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

measuring synaptic responses in hippocampus: stimulus is usually ___ and you control ______

A

extracellular (gives info about large # of synapses)

control amplitude and stimulus frequency (as amplitude goes up, recruit more and more axons, target cell response increases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

whole cell recording: downward deflections means what

A

voltage clamp cell to cause inward current, depolarization, EPSP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

paired whole cell recordings

A

initiate AP in one cell, record from nearby cell, see if there is EPSP (rapid inward current)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Bliss and Lomo

A

discovered LTP in rabbits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Bliss and Lomo’s experiment

A

extracellular stimulating electrode onto perforant path, extracellar recording electrode onto dentate gyrus

brief high frequency stimulus causes increased amplitude of EPSP, eventually LTP lasted few hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

differences in LTP in 3 major excitatory synapses in hippocampus

A

synapse 1 (entorhinal cortex to dentate gyrus) and synapse 3 (CA3 to CA1): use classic mechanism

synapse 2 uses alternative mechanism (granule neurons to CA3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is hippocampal excitator NT

A

glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

properties of classical LTP in CA1 and dentate gyrus

A

cooperative: need minimum number of activated synapses to get LTP

synapse specific: inactive synapse is not potentiated

associative: LTP occurs when activity in weak input is paired w/ activity in strong one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

manipulating postsynaptic membrane potential: results

A
  • pairing weak presynaptic stimulus w/ properly timed postsynaptic AP (elicited by passing current) is sufficient to produce LTP
  • strong presynaptic stimulus won’t produce LTP if postsynaptic cell is hyperpolarized with current
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

voltage clamp of AChR responses

A

change voltage, measure current

slope of IV relation is linear

ACh increases conductance, I follows conductance (g) bc driving force is constant

conductance of cys-loop receptor (ACh receptor) is voltage independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

voltage clamp of glutamate responses

A

voltage clamp (vary postsynaptic current) postsynaptic, stimulate presynaptic

slove of IV curve is J shaped

response of synapse using glutamate receptors is voltage dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

4 classes of glutamate receptors

A

ionotropic: AMPA, Kainate, NMDA

metabotropic: mGluR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

expression cloning approach: steps

A
  1. Demonstrate that Xenopus oocytes don’t respond to glutamate
  2. Demonstrate that injecting polyA+ RNA for glutamate receptors results in responses to glutamate in oocytes
  3. Make cDNA library of clones
  4. Find a single responsive clone
  5. Sequence DNA and study gene receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

CNQX

A

antagonist of AMPA and kainate receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

kainate agonist for what receptors

A

activate kainate receptors at low concentrations

activate AMPA receptors at high concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

NMDA agonist

A

needs 2 agonists: glutamate + glycine

or NMDA + glycine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ionotropic glutamate receptor structure

A
  • 4 subunits (can be homo or heterotetramers)
  • each unit has 3 transmembrane helices
  • 4 agonist binding sites
  • LBD: binds agonists, works like pacman
  • ATD: binds multiple modulators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

NMDA receptors are inhibited by

A

APV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

activated NMDA receptors

A

produce prolonged responses to brief application of glutamate

have J shaped IV relation

highly calcium permeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

AMPA receptors produce ____ and are inhibited by ____

A

-brief responses

inhibted by CNQX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

AMPA: IV curve and calcium

A

in majority of CNS neurons

linear IV curve

calcium impermeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what does outward rectification mean

A

there is more outward current than inward current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

inhibitory interneuron AMPA receptors

A

inwardly rectifying (unlike non-rectifying AMPA receptors)

highly calcium permeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

CA1 neurons express:

A

both NMDA and AMPA recptors

AMPA receptors: inward rectification in those that rectify, but most don’t rectify

NMDA receptors: outward rectification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

different types of AMPA receptor genes

A

GluA1, GluA2, GluA3, GluA4

homotetramers: A1, A2, A4 large current w/ strong inward rectification; A2 doesn’t conduct current

heterotetramers: 2+1, 2+3, 2+4 gives large glutamate activated current; all combos of 1,3,4 give large inward rectifying currents

A2 alone doesn’t allow rectification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

in all AMPA receptor genes, what is identical and what do ion substitution experiments show

A

in M2 regions, AA sequence is identical except Q/R site

mutate R to Q in GluA2, mutate Q to R in GluA3

→ QR site is necessary position to control rectification

→ linear receptors impermeable to Ca, inward rectifying receptors, Ca permeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what is outward rectification in NMDA receptors (J shaped IV curve) caused by

A

extracellular Mg2+ getting stuck in the pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what causes inward rectification in AMPA receptors

A

intracellular polyamines (such as spermine) cause inward rectification only in AMPA-R with Q in all four subunits

get stuck in pore

R electrostatically repels polyamines, prevents them from getting into pore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what happens to AMPA and NMDA receptors when glutamate concentration is low or high

A

low: few AMPA and NMDA receptors open gates

  • current flows through AMPAR receptors, cell slightly depolarized
  • in NMDAR, pore opens, Mg tries to enter cell, but gets stuck (no Ca can enter)

high: many gates open

  • large currents flow through AMPAR
  • at this more positive potential, Mg doesn’t try to enter cell via NMDAR (Na or Ca can enter, K can exit)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

traditional method of inducing LTP is to…

A

give high frequency stimulation to the presynaptic neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

APV experiment

A

APV (antagonist of NMDA) blocks induction but not maintanence of LTP in CA1

in CA1, induction of LTP is postsynaptic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

role of calcium in LTP

A

LTP requires a rise in postsynaptic intracellular calcium

82
Q

evidence that elevated postsynaptic calcium is necessary and sufficient for LTP

A
  • preventing rise of intracellular calcium postsynaptically prevents LTP (Ca is necessary)
  • elevating postsynaptic calcium w/o presynaptic activity causes LTP (Ca is sufficient): caged calcium introduced to cells, UV pulse uncages it
83
Q

cooperativity explained using properties of NMDA receptors

A

small stimulus only opens calcium impermeable AMPA receptors

large stimulus activates sufficient AMPA receptors to depolarize the cell enough to relieve Mg block from NMDAR, allowing large calcium influx that triggers LTP

84
Q

synapse specificity explained using properties of NMDA receptors

A

at inactive synapses, there is no glutamate, so even a large depolarization produces no calcium entry through NMDAR at these specific synapses

85
Q

associativity explained using properties of NMDA receptors

A

when weak stimulus paired with strong, cooperative mechanism (NMDAR w/o Mg in pore) is activated at both weak and strong synapses

86
Q

what is the target of postsynaptic calcium

A

CaMKII protein highly expressed in CA1 neurons

CaMKII inactive when [Cain] is low

when [Cain] rises, calcium binds to calmodulin (CAM), complex activates CaMKII

when [Cain] is sustained, CaMKII autophosphorylates and stays active

87
Q

evidence for role of CaMKII in LTP

A
  • selective inhibitors of CaMKII prevents LTP induction (CaMKII is necessary for LTP)
    • T286A mutation prevents autophosphorylation and prevents LTP
  • injecting active CaMKII postsynaptically produces LTP (CaMKII is sufficient)
88
Q

if previous LTP has occured and you add CaMKII, what happens?

A

previous LTP occludes the effect of CaMKII (very little addition of LTP)

89
Q

potential mechanisms for expression of LTP: presynaptic changes

A

1) increase release probability
2) increase number of release sites
3) increase number of vesicles

90
Q

potential mechanisms for expression of LTP: postsynaptic changes

A

1) increase receptor sensitivity
2) increase number of functional receptors
3) add more synapses

91
Q

why did Stevens and Tsien think LTP expression locus was presynaptic

A

whole cell recordings, found that the number of responses that are failures goes down greatly after LTP: matches presynaptic theory

92
Q

what causes decrease in the number of failures after LTP

A
  • *silent synapse hypothesis:**
  • failures are due to inability to respond to glutamate, not due to failure to release NT

-LTP adds AMPA receptors onto dendritic spines that initially only have NMDA receptors

93
Q

according to silent synapse hypothesis, what should happen when postsynaptic potential is shifted from -60 to +30

A

at -60mV, NMDA receptors are blocked by Mg

at +30mV, postsynaptic neuron will show synaptic potentials bc Mg block is relieved

94
Q

according to silent synapse hypothesis, what happens when shift postsynaptic potential from -60 to +50 mV

A

the number of failures before and after LTP should be similar

this is observed, so the synapses that show LTP are not NMDAR silent

95
Q

final prediction of the silent synapse hypothesis

A

if LTP expression is postsynaptic and based on number of AMPA receptors, there should be no change in amplitude of NMDA component of synaptic responses after LTP

conclusion: there is no increase in presynaptic glutamate release by LTP

96
Q

how can we watch new AMPA receptors appear

A

label extraceullar surface of receptor (N terminal) w/ synaptophlourin

synaptophlourin: isn’t fluorescent at acidic vesicle pH (filled w/ AMPAR), fluoresces when vesicles introduced to spine membrane (non-acidic)

97
Q

conclusion about mechanism of induction of LTP in CA1 pyramidal neurons

A

induction is postsynaptic: 2 things needed:

  • sufficient AMPA receptor activation to depolarize cell enough to allow Mg to leave NMDA receptors
  • Calcium influx through NMDA receptors, to bind to calmodulin and the complex activate CaMKII
98
Q

conclusion about mechanism of initial expression of LTP in CA1 pyramidal neurons

A

active CaMKII leads to:

  • enhanced delivery of AMPA receptors to cell surface (transform silent synapses to functional ones)
  • enhancement of responsiveness of individual AMPA receptors
99
Q

morris water maze (hidden platform test)

A

training: opaque liquid w/ invisible platform at fixed location; pictures on wall of room so animal can orient themselves

success in this task depends on intact hippocampus

100
Q

morris water maze: testing:

acquisition, retention, extinction

A

acquisition: how long does it take until the animal climbs onto the hidden platform (normal mice learn quickly)

retention: if well trained animal gets a break of a few hours/days, how well does it perform the task

extinction: if platform moved, how long does it take to stop looking at the old location

101
Q

contextual fear conditioning

A

if given an auditory, visual, or olfactory cue, rodents remember the location where they received a mild shock and act different there (freeze more)

this behavior requires intact hippocampus and amygdala

102
Q

does LTP occur when an animal is learning? experiment to test this

A
  • implant electrodes into CA1 of mice
  • record activity to single stimuli before and after passive avoidance traning
  • some synapses show LTP as mice learn
103
Q

manipulations that impair classical LTP on morris water maze

A
  • NMDA antagonist prevents learning
  • NMDA receptor KO alters learning
  • CaMKII mutation that prevents autophosphorylation alters learning
104
Q

manipulation that increases classical LTP, improves learning on multiple tasks

A

overexpression of one of NMDAR subunits (GluN2) enhances learning

created transgenic mice called Doogie mice

105
Q

how do we know that LTP is different at the mossy fiber synapse onto CA3 neurons

A

NMDA antagonists don’t inhibit LTP

postsynaptic calcium chelators don’t inhibit LTP

106
Q

some synapses on CA3 neurons…

A

express classic NMDA receptor dependent LTP (at associational-commissural synapses on CA3 neurons)

different mechanism at mossy fiber synapses

107
Q

how is LTP different at the mossy fiber synapse onto CA3 neurons

A

presynaptic locus for induction and expression

mossy fiber LTP produces an increase in glutamate release

108
Q

experiment that indicates that glutmate release is increased in mossy fiber LTP

A
  • express receptors at high density in some cell
  • form an outside out patch with many receptors
  • place patch close to the expected source of transmitter release

result show more glutamate after LTP inducing stimulus

109
Q

experiment to determine why more glutamate is released in mossy fiber LTP

A
  • introduce calcium chelator into presynaptic neuron
    • BAPTA: fast calcium chelator, abolishes all NT release
    • EGTA: slow calcium chelator, permits nearly normal amount of release
  • Find that baseline synaptic transmission is unaffected, but LTP not produced
    • presynaptic Ca required to activate mossy fiber LTP
110
Q

what does and does not prevent LTP at mossy fibers

A
  • inhibitor of CaMKII doesn’t prevent LTP
  • inhibitors of PKA prevents LTP
111
Q

common pathway that activates PKA

A
  • calcium activates adenylyl cyclase
  • adenylyl cyclase makes cAMP
  • cAMP activates PKA
112
Q

target of active PKA

A

RIM1α and Rab3a are known targets

both proteins play role in mobilizing vesicles

KOs of both are deficient in LTP at mossy fibers

113
Q

example of chemogenetics with fruit flies

A

fruit flies have no receptors for ATP, but mammals do

  • P2X receptors are non-selective cation channels that excite cells, respond to ATP
  • Make UAS-P2X2 transgenic flies, cross w/ line that has promoter that drives GAL4
  • only cells w/ promoter of interest will be activated when ATP is applied
114
Q

chemogenetics example with DREADDS (designer receptors exclusively activated by designer drugs)

A
  • making minor mutations to muscaranic ACh receptors (metabotropic) can make them sensitive to a drug
    • excitatory DREADD: modified human M3 receptor (hM3Di)
    • inhibitory DREADD: modified human M4 receptor (hM4Di)
  • transgenic animals w/ floxed allele crossed w/ cre line to express designer receptor
  • feed drug to animal to chronically excite or inhibit neurons of interest
    • first agonist was CNO (can be metabolized to clozapine, acts on serotonin and DA receptors
115
Q

birth of optogenetics: flies

A

a lab introduced drosophila rhodopsin and its downstream molecules into mammalian neurons to trigger activity

116
Q

green algae has two opsins that are ion channels:

experiment

A

ChR1: proton selective

ChR2: channel rhodopsin that is nonselective cation channel (jackpot)

express fusion protein of ChR2-EYFP (fluorescent protein) in hippocampal neurons in culture, goes to plasma membrane of neurons

can excite ChR2 w/ blue light, which depolarizes cells

117
Q

what maintains LTP? CaMKII hypothesis + experiment

A

ongoing expression of high CaMKII activity in the absence of elevated calcium (self-sustaining autophosphorylation)

add caged glutamate, shine UV light to release glutamate, measure CaMKII activity

CaMKII activation at first, but returns to baseline soon after

118
Q

what is the actual way that learning is maintaied for weeks+?

A

CA1 long term LTP requires new mRNA and protein synthesis (aplysia long term sensitization requires this)

-new proteins cause permanent changes in synaptic structure: spines grow larger quickly w/ LTP

119
Q

homeostatic scaling

A

global upward or downward adjustments across all synapses (strengthen or weaken)

120
Q

long term depression

A

synapse specific decrease in synaptic strength

121
Q

how does homeostatic scaling work

A
  • neurons have set point for spike activity
  • if spiking deviates significantly for a sustained time period, global changes in synaptic strength occur
122
Q

long term depression experiment

A

at slow enough stimulus frequency, synapses show long term depression

all synapses that are capable of LTP are capable of LTD

123
Q

metaplasticity

A

the stimulus frequency at which there is no long-term change varies w/ previous history of the synapses

124
Q

what is cellular mechanism of induction of LTD at schaffer collateral-CA1 synapses

A

similar to LTP:

  • requires NMDA postsynaptic receptor activation
  • requires rise in postsynaptic intracellular calcium, but not enough to effectively activate CaMKII

low calcium activates calcium dependent phosphatases (causes fewer AMPA receptors)

125
Q

potential paradox of how LTP works

A

after large calcium influx that produces LTP, there is a period of time that calcium remains elevated at a level that would produce LTD

LTP isn’t cancelled out though because high intracellular calcium that triggers LTP also activates pathway that prevents LTD

126
Q

O’Keefe, Moser, and Moser

A

made recordings from hippocampus and entorhinal cortex of free moving rodents

Mosers discovered entorhinal cortex grid cells

O’keefe discovered hippocampal place neurons

127
Q

Tonegawa experiment overview

A

developed method to erase memories or create false memories in mice:

  • introduce mice to two boxes w/ different attributes, figure out which cells respond to Box A but not Box B (potential engram cells)
  • Shock in Box B while activating Box A engram cells
  • if animal freezes in Box A and B, not C, have created false memory
128
Q

engram

A

physical location or set of locations at which a memory is stored

129
Q

marking and controlling engram cells: trangenic mice portion

A
  • intersectional genetics: transgenic and viral expression approach, using tet-off strategy
  • recently active neurons make c-fos mRNA
  • make transgenic mice that have c-fos promoter driving tTA (only make tTA if neurons recently active)
    • if DOX present, tTA can’t bind to TRE and expression of target gene is off
    • if DOX taken away, tTA drives downstream target gene
130
Q

making and controlling engram cells: virus expression portion

A
  • AAV (virus) infects all neurons, replace most of viral genes w/ sequence of interest
  • trangenic mice receive virus w/ TRE driving fusion of ChR2 (channelrhodopsin) and mCherry sequences
    • ChR2 causes depolarization when excited by blue light
    • mCherry fluoresces red to green light
  • sequences that were inserted in the virus are only expressed when tTA is present and DOX is absent
131
Q

experimental design of creating false memories

A
  • feed transgenic cfos-tTA animals DOX
  • inject virus into dentate gyrus, implant optic fibers to deliver blue light
  • remove DOX when ready to test behavior
132
Q

pupil + lens + macula definiton

A

pupil limits amount of light that gets to retina

lens focuses light onto retina

macula part of retina that is specialized for fine form vision (includes fovea_

133
Q

experimental conclusion of photon experiment

A

abosroption of a single photon can lead to visual sensation

134
Q

range fractionation

A

multiple receptors respond to different amplitude levels, eg rods highly sensitive, cones less sensitive

135
Q

Hartline

A

used limulus eye to characterize mechanisms of visual encoding and contrast detection (lateral inhibition)

136
Q

Wald

A

characterized the biochemistry of light absorption

137
Q

limulus horseshoe crab eye structure

A

each facet (ommatidium) has a single large neuron (eccentric cell) with an axon projecting to the CNS

eccentric cell depolarizes and fires AP in response to light

138
Q

rate coding of light intensity in the limulus eye

A

shine light on one ommatidium and record from its axon extraceullarly:

the more intense the light, the higher the spike frequency, but takes 100x increase in intensity to get 2x increase in firing rate

139
Q

Weber-Fechner law

A

one’s ability to detect a change in stimulus is related to a constant fraction of the stimulus, not the absolute amount of change

relationship b/w actual intensity and perceived intensity is logarithmic (larger stimuli require bigger changes to detect difference)

140
Q

relationship b/w amplitude of stimulus and AP frequency is:

A

logarithmic

141
Q

adaptation

A

the range a cell responds to changes

change sensitivity of receptors

142
Q

lateral inhibition in limulus

A

shining light on one ommatidium, then shine on nearby ones (frequency goes down)

lateral inhibition is reciprocal (every ommatidium inhibits its neighbors), and graded (more intense surround stimulus, stronger the inhibition), and logarithmic

143
Q

eccentric cell center surround organization

A

on center, off surround

144
Q

what is the point of lateral inhibition

A

enhances edges/contrast

145
Q

photoreceptors in arthropods vs vertebrates

A

arthropods: photoreceptors depolarize to light
vertebrate: rod and cones hyperpolarize to light

146
Q

melanopsin positive retinal ganglion cells

A

directly respond to light as well as receiving synaptic input indirectly from rods and cones

important for circadian regulation and pupil reflexes

147
Q

retinal and light

A

11-cis-retinal –light–> all-trans-retinal

retinal is bound to an opsin protein to form either rhodopsin or cone opsin

148
Q

retinal pigment epithelium cells (RPE)

A

take up all-trans-retinal from photoreceptors and reform 11-cis-retinal

149
Q

resting potential in retinal cells

A

resting potential in many retinal cell types is not as negative as other neurons

photoreceptors hyperpolarize to light

150
Q

what produces hyperpolarization in response to light in rods and cones

A

non-selective cation channels are open in dark, close in response to light, causing decrease in conductance

when these channels close, membrane potential is closer to Ek

151
Q

second messenger in rods

A

non-selective cation channels are in plasma membrane, rhodopsin is in intracellular disks

second message b/w these two is cGMP

152
Q

metabolism of cGMP: enzymes

A

guanylate cyclase: GTP → cGMP

phosphodiesterase (PDE): cGMP → GMP

153
Q

dark and light: cGMP and enzyme levels

A

dark: low PDE activity, high cGMP concentration

light: high PDE activity, low cGMP concentration

154
Q

evidence that second messenger in photoreceptors is cGMP: what did they use

A

inside out patches used to test whether cGMP activates channels in plasma membrane of photoreceptors from intracellular side

155
Q

cascade for activation of PDE

A
  • rhodopsin absorbs light
  • G protein binds GTP, releases α subunit
  • α subunit interacts with PDE
  • PDE catalyzes cGMP → GMP
156
Q

phosphodiesterase is activated by

A

transducins

157
Q

cGMP gated channels

A
  • do not select well b/w Na, K, Ca
  • not voltage dependent
  • have extra C terminal region that binds cGMP, which causes opening of channel
158
Q

in the dark, what is happening

A
  • cGMP concentration high
  • cGMP-gated channels are open
  • glutamate released continuously
159
Q

in light, what is happening

A
  • PDE activated
  • cGMP destroyed
  • cGMP channels close
  • cell hyperpolarizes, voltage gated Ca channels close
  • glutamate release stops
160
Q

mechanisms of rod adaptation in constant light

A

rod responses begin to decline after 1 second:

  • in darkness, Ca entry through cGMP-gated channels inhibits guanylate cyclase by binding to GCAP
  • in light, low calcium increases guanylate cyclase activity, increasing cGMP, rod response decreases
161
Q

GCAP KO mice

A

have larger light response

show less adapatation

GCAP is important for rod adaptation

162
Q

mechanism of recovery after rod adaptation

A

RGS9 is a GAP, which accelerates GTP hydrolysis

arrestin phosphorylates rhodopsin, making it inactive

163
Q

compared to rods, cone responses are:

A

faster and more transient

require more photons

depend on wavelength: S blue, M green, L red

164
Q

in humans, mutations in which cones are common

A

red and green cone opsins

165
Q

receptive fields of retinal ganglion cells

A

most have center surround antagonism

some on-center/off surround, some off-center/on-surround

166
Q

properties of bipolar cells

A

don’t fire action potentials

have center-surround organization (50% off-center, 50% on-center)

167
Q

how do photoreceptors communicate w/ bipolar cells

A

photoreceptors release glutamate, change membrane potential in postsynaptic bipolar cells

rod bipolar cells receive information from rods, cone bipolar cells from cones

168
Q

glutmate receptors of bipolar cells

A

off center: have AMPA receptors w/ GluA2 + another AMPA subunit (light hyperpolarizes these)

on center: have metabotropic glutamate receptors (light depolarizes these) that close TRP-M channels when active

169
Q

how do bipolar cells communicate w/ ganglion cells

A
  • bipolar cells don’t spike, release glutamate when depolarized
  • ganglion cells spike: have ionotropic glutamate receptors that depolarize the cell when active
  • on-center bipolar cells connect to on-center ganglion cells and vice versa
170
Q

horizontal cells characteristics

A
  • build the surround
  • do not fire APs
  • express AMPA receptors (glutamate released by photoreceptors depolarizes)
  • receive input from many more photoreceptors than do bipolar cells
    • have larger receptive fields than bipolar cells
171
Q

presynaptic terminals of horizontal cells communicate w/

A

photoreceptor presynaptic terminals, not bipolar cell postsynaptic dendrite

when horizontal cells are depolarized, they release signal that makes photoreceptor transmitter release mechanism less effective

172
Q

what creates antagonistic surround for bipolar cells

A

lateral inhibition from horizontal cells:

Light → Center photoreceptor hyperpolarization → Horizontal cell hyperpolarization → Surround photoreceptor depolarization

173
Q

proton hypothesis for horizontal cell signaling

A

dark: resting horizontal cells release protons, making calcium channels of photoreceptors less effective, less glutamate released

light: hyperpolarization of horizontal cells, less proton release, calcium channels open easier, more glutamate

174
Q

amacrine cells

A

fire APs

release GABA or glycine and cause inhibition of ganglion and/or bipolar cells

175
Q

major types of retinal ganglion cells

A

P-type: small RF, high resolution analysis of object shape, sustained response to light

M type: large RF, low spatial resolution, transient response, sensitive to movement

176
Q

receptive fields of every retinal ganglion cells type ______ toward the periphery of the retina

A

RFs get progressively bigger

177
Q

outside fovea and very dim environemnt

A

outside fovea: low acuity and poor color vision

dim environment: no color vision, blind spot at central fovea

178
Q

color senstiive (P-type) bipolar and ganglion cells are:

A

color opponent

blue yellow: blue on center, yellow no response

red-green

179
Q

blue-On bipolar cells

A

receive photoreceptor input from only S cones

have m-GluRs that result in hyperpolarization when active

180
Q

midget bipolar cells

A

in the fovea, each red/green cone contacts a single midget bipolar cell

there are on and off midget bipolars

this circuity creates red-green color opponent receptive fields in the fovea

181
Q

Sperry

A

discovered funcational specialization of cerebral hemispheres

182
Q

Hubel

A

discoveries concerning information processing in the visual system

characterized V1

183
Q

Wiesel

A

discoveries concerning information processing in the visual system

characterized V1

184
Q

optic chiasm

A

axons from nasal retina cross, axons from temporal retina do not cross

185
Q

LGN layer inputs

A

6 layers:

  • Layers 1, 2: input from M-type RGCs
  • Layers 3, 4, 5, 6: input from P-type RBCs
186
Q

LGN layer eye inputs

A

Layers 1, 4, 6: info from contralateral eye

Layers 2, 3, 5: info from ipsilateral eye

187
Q

cerebral cortex: LGN terminals end in:

A

layer 4

188
Q

V1 layers input

A

in cortex:

Layer 4a: from parvocellular layers

Layer 4c-α: from magnocellular layers

Layer 4c-β: from parvocellar layers

189
Q

simple cells found in what layers in V1

A

layers 1-3, 4b, 5-6

190
Q

simple cells respond to what

A

respond to bars or edges

motion sensitive

orientation of bar matters

191
Q

mechanism that helps for simple cell receptive fields

A

LGN neurons receptive fields (center surround) combine to form the receptive field of a single simple cell

192
Q

complex cells of V1

A

respond to bars or edges, but bar can be at multiple locations and still activate

motion sensitive

orientation matters

193
Q

binocular vision

A

cortex uses small differences in where singal hits the retina in two eyes to create a 3D image

194
Q

monocular vs binocular cells

A

LGN cells monocular

V1 layer 4a and 4c monocular

most cells in other layers of V1 are binocular

195
Q

monocular deprivation

A

if one eye is kept closed past critical period that end w/in months of birth, animal behaves as if blind in that eye

disuse leads to atrophy

196
Q

binocular deprivation

A

animals can still see and use both eyes

197
Q

monocular deprivation experiment

A
  • inject radioactive AA into eye
    • some are taken up into ganglion cells, transported to LGN
    • at LGN, some of these proteins are broken down, made into new proteins, transported to V1
  • injection into non deprived eye labels all of layer 4 in V1
  • injection into deprived eye, only tiny area of layer 4 is labelled
  • conclusion: patterno f terminations from the LGN is altered
198
Q

what mechanism produces change in termination patterns during critical period for monocular deprivation

A

termination patterns start out mixed, then some pull back terminal branches, causing input elimination

199
Q

ocular dominance column

A

cells with similar ocular dominance (cells in cortex driven by open eye), tend to be grouped together

200
Q

strabismus

A

eyes don’t converge to a common point

humans with this have no stereo vision (get 3D image from 2D input)

shows that tightly synchronized activity from two eyes is required to maintain binocularity

Bio 222 Cell/Molec Neuroscience (7 decks)

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