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Neurobiology > Neural Circuits (CPG, Respiration, Sleep) > Flashcards

Neural Circuits (CPG, Respiration, Sleep) Flashcards

1
Q

central pattern generators

A

neuronal circuits that when activated can produce rhythmic motor patterns such as walking, breathing, flying, and swimming in the absence of sensory or descending inputs that carry specific timing information

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2
Q

why are motor circuits easy to study and measure?

A

motor behaviours are easy to define and measure unlike cognitive

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3
Q

invertebrate examples for CPG models

A

lecture 11 first page

lobster/crab - stomach chewing
crayfish - escape
clione - swimming
tritonia - escape (bend + jump)
leech - muscle activation
locust - complex, flight/kick
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4
Q

advantage of invertebrate models of CPG

disadvantages

A

simple NS (few Ns and small no.types), can record during motor behaviour

may be complex with electrical signals in places where might not see, may not be possible to record close to postsynaptic and integrative sites, techniques not developed for many species, signalling differs for vertebrates so generalisation issue

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5
Q

advantages of vertebrate models of CPG

disadvantages

A

applicable to humans, use molecular genetic techniques, better Abs and pharmacological agents

complexity (tadpole/lamprey better), great redundancy (lots each type), harder to record in situ, anaesthesia in vivo changes activity

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6
Q

vertebrates examples for CPG model

A

cats - locomotion, plot limb movement
lamprey - swim, primitive NS
tadpoles - swim, simple in early development
rat/mice - use gene knockouts

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7
Q

how to study motor pattern generation

A

1) define behaviour - measure
2) neural machinery - record muscles/nerves

see if movement related to neural activity

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8
Q

Leech swimming motor pattern

A

waves of bending and how fast travel along length
measure tension and nerve recordings
left segments activity before right so head to tail bending (delay)

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9
Q

Cat locomotion (phases)

A

swing phase - from PEP to AEP (posterior extreme position to anterior)
stance phase - foot on ground so hip move and other foot move
measure angles and see change in neural activity

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10
Q

Humans walk/run

A

record angles and activation of muscle groups

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11
Q

Reflex Hypothesis

A

rhythmic movements generated through sequence of reflexes (dependent on feedback)

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12
Q

Central Hypothesis

A

central circuits generate without sensory feedback so reflexes not important

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13
Q

which hypothesis is correct? (reflex or central)

A

removing all sensory feedback shows all rhythmic motor behaviour like laughing is controlled by central networks -> CPGs

but movement feedback coordinates behaviour because removing sensory feedback alters motor pattern (but is still generated) so it entrains motor pattern that is centrally generates
e.g. human disease w/o feedback means can still walk but differs

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14
Q

Lamprey (categories, entrain, CC)

A

swim, wiggle spinal cord left right (oscillations in membrane potential match motor nerve recordings)

categories of neurones - 2 motor, CC interneurones, edge cells, dorsal cells, giant interneurones, lateral interneurones, excitatory interneurones

imposing slower movement slows CPG because stretch receptors in spinal cord

killing opposite side of spinal cord disturbs rhythm of other side - CC role

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15
Q

modern view on CPGs (conclusion)

A

central circuit has everything for motor activity
turned on/off by higher command centres (decision)
coordinate sensory input (if in at wrong time)
stretch receptors in muscles fine tune and entrain patterns

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16
Q 
Xenopus embryo (tadpole)
(HRP, classes, origins of drive)
A 
lower vertebrate model of swimming
used HRP (horse radish peroxidase) to see if it would cross the spinal cord from one side to other
categorise types of neurones (lecture 12 first page)

2 classes of C motor neurones - d descending interneurone and c commissural interneurones on opposite sides of spinal cord and form neural circuit for swimming

reciprocal inhibitory interneurones - commissural with crossed axon, important in circuit because glycinergic inhibition (it uses glycine NT) will change speed of swimming/block

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17
Q

immunocytochemistry to identify neurones

A

stain with glycine Ab so show neurones that use glycine as NT

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18
Q

criteria to determine if neurone contributes to CPG

lecture 12 bottom first page and top second page

A

is it active during motor behaviour? (some copy rhythm not generate) - necessary but not sufficient
is it used to reset rhythm? - sufficient but not necessary
if inactivate/destroy/block activity does the generation stop?

need to demonstrate all 3

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19
Q

tonic and phasic

A

slow and fast

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20
Q

V2a in Zebrafish

A

excitatory interneurones, removing cells affects ability to produce swimming and NMDA which usually excites neurones and swimming has a weaker effect

activation of these cells sufficient for swimming (blue light experiment - have light sensitive ion channels

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21
Q

the wiring diagram

A

lecture 12 page 3

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22
Q

post-inhibitory rebound

A

inject -ve current so hyperpolarises, then fires AP when recovers (rebound) so circuit carries on

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23
Q

pacemaker neurones in Clione

A

carry on generating rhythm without input (endogenously)

carries on if drag cell out ganglion so endogenous pacemaker

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24
Q

mid-cycle inhibition

A

between APs

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25
lamprey spinal neurones pacemaker properties
some cells still oscilate w/o AP (NMDA and TTX to stop AP) | injecting current changes speed/freq of oscillations
26
computational and mathematical models of neural circuits | uses?
want simple model to understand complex combine models of body and movement to neurones understand roles of cells and components make predictions on function extract general principles of circuit behaviour
27
breathing disorders
``` Joubert syndrome (rapid breath) Rett syndrome (difficult while awake) Ondine's curse (while asleep) Sleep apnoea (obstructive) Sudden Infant Death Syndrome (don't know cause) ```
28
phases of respiratory pattern
inspiratory (phrenic nerve innervates diaphragm) expiratory (post-inspiratory) then active expiration (induced by exercise, cough, sneeze, force air out)
29
The pre-Bötzinger complex (preBötC)
a central pattern generator in brain stem in medulla oblongata that is important for the generation of respiratory rhythm with long columns of cells going from cVRG (caudal ventral respiratory group) to rVRG (rostral) and a few nuclei in pons
30
NTS
sensory control of breathing
31
damage to medulla
severely compromise breathing
32
experiment in rodent neonates showing breathing CPG
record from nerves equivalent to phrenic, shows rhythmic bursts of respiration without pons the brainstem can generate rhythm but speeds a bit
33
weak evidence that preBotC involved in breathing good evidence (Jack Feldman)
neurones fire before breathing axonal projections restricted to medulla activation GABA receptors cause apnoea (maybe leaked and affected others) isolate medulla and chop bits off and record hardly any rhythm w/o region 8 and none w/o region 9 so critical area with preBotC
34
experiment showing NK1 receptor
substance P on preBotC speeds and enhances respiratory rhythm so have receptor for P (NK1) toxin with P ligand internalised and kills neurones
35
saporin toxin (from flower)
ribosome inhibitor - so protein production SP-saporin, SP-SAP (substance p with saporin) injected to brainstem and NK1R neurones killed and severe breathing perturbations
36
why is the genetic approach better?
better than killing neurones because genetic is reversible
37
genetic approach to preBotC
insect allatostatin receptor in preBotC expressed in mammal brain, nothing happens till inject allatostatin ligand which is inhibitory and rapid inactivation of neurones (reversible) breathing weaker and apnea
38
chemosensory control of breathing
PO2 falls, PCO2 increases --> breathing increases
39
where is O2 sensed?
in periphery, chemosensory cells in carotid bodies in bifurcation (branches) of carotid artery external branch to head, internal branch to brain (supplies blood to brain)
40
what are the effect of changing O2?
phrenic nerve more powerful and breathing stronger in hypoxia type 1 glomus cells release ATP which activates P2X 2/3 receptors on sinus nerve which acts as NT so firing of sinus nerve
41
what happens when cut carotid sinus nerve?
this goes from the carotid body to the NS, there is no response but weaker phrenic nerve so important in detection
42
plasticity of hypoxia
periodic hypoxia caused short term enhancements of breathing but then long term facilitation minutes after last hypoxia
43
Congenital Central Hypoventilation Syndrome
Ondine's curse - breathing stops when asleep lack chemosensitive reflexes need ventilation when young, fine when adult (only in sleep)
44
where is PCO2 detected?
ventral surface of medulla oblongata rostral and caudal area detected as CO2 or pH (bigger response if pH too)
45
Cx26
connexin 26 gap junction protein receptor opens when CO2 binds CO2 binds lysine residue (amine of lysin) which salt bridge to arginine of neighbour subunits conformational change traps channel in open state so allow ATP to leave cell and excite respiratory neurones so breathe stronger knockout Cx26 from glial cells causes no change in CO2 dependent respiratory rate (carotid body affect it) but tidal volume reduced by 1/2 so 1/2 reponse mediated by CO2 sensing
46
Keratitis Ichthyosis Deafness (KID) syndrome
mis-sense mutation Cx26 skin abnormalities, visual impairement, deafness central apnea
47
patterns of sleep
slow wave sleep (non-REM) REM sleep occur in organised fashion with diff characteristics
48
slow wave sleep (non-REM)
deepest slow Delta waves in EEG brain relatively inactive - energy expenditure low muscles relaxed but capable at moving - adjust every 20 mins some dreaming but less vivid
49
REM sleep
rapid eye movement paradoxical short periods throughout night get longer till wake might wake during night brain as active as consciousness (energy expenditure high) vivid dreams body paralysed so don't act out dreams
50
underwater mammals
dolphins have to come to surface to breathe | sleep with 1/2 brain at a time or microsleep (short) add up to enough throughout day
51
evolution of sleep
can't record EEG and have no SW/REM of fish/amphibia so look at behavioural sleep birds/mammals/placentals (humans) have behavioural and REM/SW invertebrates have behavioural sleep
52
behavioural sleep
sleeping posture, sleeping site, quiescent, elevated arousal threshold (hard to wake)
53
purpose of sleep
``` out of trouble (maybe) rest/repair brain coding development learning/memory resistance to illness brain flushing ```
54
illness and sleep experiment
given rhinovirus | < 7 hours sleep meant 3x more likely to get cold than >8 hrs
55
brain temperature and sleep
rats - sleep in light so less metabolic activity and brain cooler dolphins - temp drops in 1/2 sleeping humans - raised temp increases SW
56
development and sleep
``` 10 weeks premature - 80% REM 2-4 weeks premature - 60-65% REM born - 50% REM age 2 - 30-35% REM adult - 25% REM ```
57
brain flushing of waste in sleep | experiments
CSF tracer diffuses further in brain during sleep inject TMA ion - less current in sleep, extracellular space bigger so more parts for TMA to escape and assists removal of waste toxic AB peptide - beta amyloid link to Alzheimer's, come out quicker during sleep
58
memory and sleep
unrelated words not remembered if 12 hrs awake, unrelated when 12 hrs sleep remembered as well as related words when awake performance increases as sleep increases (if both components of sleep) benefits with motor skills, visual, word association rats replayed brain activity during maze during sleep but quicker
59
areas of brain controlling sleep
VLPO (ventral lateral preoptic area) controls SW (slow wave) basal forebrain TMN (tuberomammillary nucleus) in wakefulness LDT + PPT REM on nuclei Raphe + LC REM off nuclei lateral hypothalamus many more
60
basal forebrain
Stimulating the basal forebrain gives rise to acetylcholine release, which induces wakefulness and REM sleep, whereas inhibition of acetylcholine release in the basal forebrain by adenosine causes slow wave sleep preoptic areas, cholinergic neurones, projections to cortex so awake and inhibition sends to sleep neurones active during SW not REM/awake some state dependent activity so active in SW or awake/REM or don't care lesion in basal forebrain causes insomnia
61
areas controlling REM
LDT/PPT cholinergic switch REM on LC/DRN switch REM off (noradrenaline&5-HT) ascending arousal system - nuclei using 5-HT or histamine or noradrenaline project up to cortex and tweak circuit so awake TMN uses histamine for wakefulness neurones fire before REM, others during REM to turn off
62
REM/SW coordinated by...?
VLPO area | part in REM, other in SW
63
orexin (hypocretin) | mRNA, peptides, narcolepsy, neurones in LH
mRNA in hypothalamus peptide stimulate orphan G-coupled R and increase foot uptake 2 peptides and 2 receptors - orexin A activates both Rs, orexin B only Ox2R narcolepsy - suddenly fall asleep, lack orexin neurones in hypothalamus orexinergic neurones in lateral hypothalamus (LH) project to other nuclei that control sleep , prevent rapid switching from sleep to wakefulness if lose neurones
64
orphan G-coupled receptor
without ligand
65
learning and plasticity changes....
microstructure of brain
66
brain stops developing around age..? | but can...
20 | still change in adults like taxi drivers learn roads
67
spatial knowledge in..? | so taxi drivers have..?
hippocampus | bigger posterior hippocampus because more neurones activated and anterior slightly smaller
68
simple model of learning
aplysia lives in the sea gill withdrawal reflex inhibits plasticity when prod - learn that it's meaningless so withdraw less each time but if shock tail gill withdrawal increases then decrease again
69
types of synaptic plasticity
homosynaptic heterosynaaptic
70
homosynaptic plasticity
activity-dependent only require pre and post synaptic cell enhancement(facilitation) or depression depends on activity in pre
71
heterosynaptic
modulatory input-dependent | 3rd player - modulator neurones change strength of synapse
72
changes in synaptic transmission (aplysia e.g.)
increase NT with more vesicles per AP or increase receptor sensitivity with more of them Aplysia - more vesicles, AP broadens with 5-HT because inhibits K in repolarisation so takes longer so more Ca (5-HT act on GPCR activates cAMP activates PKA phosphorylates S type K channel so prevent opening) long term changes - some PKA to nucleus activate CREB activates genes, alter expression, new synapses
73
human hippocampus pathway
``` input to Dentate gyrus synapse to CA3 to CA1 AP cause EPSP in CA1 (glutamate release from pre) activate AMPA receptor (glutamate R) synapse highly plastic (homosynaptic) ```
74
Morris water maze
hidden platform, mouse tries to find it | can't remember where with hippocampal lesion
75
LTP (definition, experiment, requirement)
long term potentiation persistent strengthening of synapses based on recent patterns of activity - so learning and memory activate Schaffer colateral axons CA3 to 1 and measure amplitude - tetanus increases synaptic strength and repeated tetanus means increase lasts a few hours requirements for LTP - post synaptic cell (CA1) depolarisation and calcium influx and activation of NMDARs
76
NMDA receptor features
1) EPSP slower lasts longer so window for coincidence detection (if another neurone is stimulated) and summations of EPSP during tetanus 2) voltage dependent Mg blockage of NMDA channel, detect coincidence, depolarise to draw Mg out 3) Ca permeability, so influx into post critical to triggering consequence of coincidence and results in synapse strengthening
77
coicidence
neurone encodes info by detecting temporally close but spatially distributed input signals
78
LTP process
high f firing of presynaptic causes EPSP by AMPA AMPA potentials summate and depolarisation causes NMDA unblock so Ca influx Ca activates calmodulin which activates calmodulin kinase 2 (CaMKII) and phosphorylates AMPA and vesicles with AMPA fuse so more receptors in membrane and enhanced synapse
79
Hebbian plasticity
if activation of synapse results in postsynaptic firing AP then synapse strengthens (depolarise enough to unlock NMDA)
80
aplysia vs hippocampal LTP
heterosynaptic and homosynaptic while hippocampal is homo change down to presynaptic NT increase while hippoc. down to change in receptor number and kinetics 5HT triggers cAMP as 2nd messenger while hippoc. Ca influx through NMDA activates CaMKII

Neurobiology (4 decks)

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