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Cellular and Systems Neuroscience > Neural Circuitry in the cerebral cortex > Flashcards

Neural Circuitry in the cerebral cortex Flashcards

1
Q

2 cell types in the cerebral cortex

A

pyramidal cells - excitatory (glutamate), connections with cortical/subcortical areas, 80%
interneurons - inhibitory (GABA), local, 20%

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2
Q

how do cortical circuits emerge

A

progenitors
post-mitotic (birth)
axons finding targets
dendrites merge
synapse formation
modification of synaptic connections

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3
Q

layers of the cerebral cortex

A

neocortex - 6 layers - 90% cerebral hemisphere, sensory/motor
mesocortex - 3-6 layers - majority of the limbic lobe
allocortex - 6 layers - hippocampal formation (archicortex)/primary olfactory areas (paleocortex)

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4
Q

allocortex circuitry

A

DG is an accumulation of granule cells
DG -> CA3 (mossy fibres)
CA3->CA1 (schaffer collaterals)
entorhinal cortex -> hippocampus (perforant pathway)

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5
Q

what do rodent somatosensory cortex contain

A

barrels
(whiskers)

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6
Q

inputs of the neocortex

A

thalamic inputs terminate in layer IV (primary input layer)
layer IV contains special code (ephrins) about axon guidance - tells axons to stay in layer IV

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7
Q

outputs of the neocortex

A

commissural (cross to other hemisphere) - callosal projections (II, V, VI)
associative (neurons communicate in the same hemisphere) mainly in LII-V
corticofugal (different regions not the cortex): corticothalamic (VI) subcerebral (V): corticotectal, corticobulbar, corticospinal

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8
Q

neuronal diversity

A

layer II/III - larger pyramidal neurons compared to layer V
interneurons have larger diversity in terms of morphology

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9
Q

neuron types in the cerebral cortex

A

somatostatin SST (type of martinotti cell) - regular spiking, low threshold spiking
VIP - regular adapting spiking
basket cells (PV+) local , need to buffer Ca2+ (increase metabolic rate/mitochondria) - fast spiking
chandelier cells (PV+/-) contain many terminals for precise control - fast spiking

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10
Q

how do genes make neurons different

A

different interneurons have different glutamate receptor expression
use RNA seq/single cell seq
transcripts do not always code for a protein

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11
Q

how can we used multimodal data collected from patch clamping interneurons

A

understand: morphology, electrophysiology, transcriptome MET type 1/2

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12
Q

limitation of MET

A

not all transcripts express proteins
different axon/soma/dendrites distribution

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13
Q

what are the different cell states

A

V1
S1

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14
Q

list reasons why 20000 genes specify 10^14 connections

A
  1. many proteins from a single gene (splicing isoforms) e.g. neurexins
  2. many levels from single gene
  3. multiple proteins from a single protein
  4. same protein used multiple times
  5. combinatorial use of proteins
  6. use of experience/spontaneous neuronal activity via transcription/translation
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15
Q

role of neurexins

A

pre-synaptic
cell adhesion
slm2 - RNA binding protein (modifies RNA to form different isoforms) WT - 2NRXNB isoform Slm2 KO- longer isoform

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16
Q

what occurs in GluN1 KO

A

less neural activity
no barrels

17
Q

CC vs CT pathway

A

CC pathway - main input from V1-broad selectivity to stimulus orientation
CT pathway - pyramidal neurons tuned to orientation and direction

18
Q

describe the connectivity of interneurons in the hippocampus

A

deep layer has more PV interneurons than the superficial layer
gephyrin is the scaffolding for inhibitory synapses
Pyramidal cells with more inhibition project to the amygdala
Pyramidal cells with less inhibition project to the medial entorhinal cortex

19
Q

what is cell targeting specificity

A

interneurons connect to dendrites and axons by using Lgi2 in PV interneurons
use syt2 (synaptotagmin) marker - fast spiking

20
Q

unbalanced excitation/inhibition

A

hyperexcitation/acute decrease in inhibition - epileptiform
acute decrease in excitation/silent - comatose

cortical inhibition does not prevent epileptiform activity
ratio of e/i is highly dynamic via homeostatic plasticity

21
Q

feedback inhibition

A

individual interneurons inhibit >50% principal cells within 100um and receive excitatory inputs from a large portion of them

22
Q

feedforward inhibition

A

pyramidal cells and interneurons receive divergent excitatory inputs from different subcortical/cortical regions and layers

23
Q

failure between excitation and inhibition

A

neurodegenerative disorders:
ASD
schizophrenia
epilepsy

24
Q

how do interneurons shape activity of the pyramidal cells

A

sharpens tuning
if you conduct the pharmacological block of GABAa receptors - this reduces stimulus selectivity in neurons

25
Q

rodents in darkness vs visual stimuli

A

GCAMP - ca2+ sensory and is cre dependent
VIP - more activity in darkness
SST/PV - more activity in visual stimuli

26
Q

different behaviours within the same interneuron

A

Rat turning L - chocolate Rat turning R - cherry
PV1 - goal run - PV very active
PV2 - goal run - PV not active (more VIP interneurons)

27
Q

what is the local field potential (LFP)

A

electrical activity (rhythms/oscillations) close to electrodes used to measure synchronisation
fast oscillations are spontaneous, respond to sensory stimuli, transmission of information

28
Q

oscillation types

A

gamma (30-100Hz)
theta (4-8Hz)

multiple gamma oscillations form theta oscillations

29
Q

optogenetics

A

channelrhodopsin (cation channel) - membrane depolarisation
halorhodopsin (chloride channel) - membrane hyperpolarisation

30
Q

how do we know if PV is needed for gamma oscillations

A

activate PV (express ChR) increase in gamma power at 40x
Sohal et al., 2009 PV silenced - decrease in gamma power

31
Q

gamma band in humans

A

adults (18-21) gamma oscillations in facial activity
late adolescents - DA and 5HT still arriving at PFC

32
Q

high vs low gamma

A

high gamma = 65-140 Hz
low gamma = 25-50 Hz

33
Q

what is needed for high gamma oscillations

Yamamoto et al., 2014

A

if block synaptic transmission using toxin MT between entorhinal cortex and hippocampus - worsen mice performance in free run vs forced turn
optogenetic inhibition of high frequency gamma decreases success rate (use halorhodopsin)

34
Q

ErbB4 disruption

A

schizophrenia (altered gamma oscillations)
impaired cognitive function (shown in T maze experiment)
less CCK interneurons - stable gamma oscillations but reduced theta oscillations

control - place cells know coordinates
ErbB4 mutants - no refinement in MWM task

Cellular and Systems Neuroscience (21 decks)

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