Lecture 5- How do Clock Cells Talk Flashcards

1
Q

What indicates that the SCN depends on intracellular communication

A

The fact that the SCN contains synchronised high amplitude rhythms and desynchronised low amplitude rhythms

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2
Q

AVP (vasopressin)
location of receptor expression

location of AVP neurons within the SCN

A

V1a and V1b are expressed in the SCN, with AVP neurons being more prevalent along the medial aspect of the SCN (in shell)

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3
Q

What kind of receptors are neuropeptide receptors?

A

GPCRs

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4
Q

Mice lacking in V1a and V1b receptors are

A

resistant to jet lag; can re-entrain much better than WT; rapidly phase shift w changes in LD; do not show transient re-entrainment

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5
Q

IN AVP receptor KO mice, PER gene expression

A

is reset ~half the time of WT

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6
Q

Clock gene expression in both liver and SCN of V1a/b KOs mice

A

phase shift rapidly with LD changes i

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7
Q

AVP receptor mice KO considerations

A

could be because these mice have developed without these key receptors, however pharmacological blockade mimics AVP KO effects making this unlikely

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8
Q

AVP signalling (via V1a and V1b receptors) on the circadian system

A

ordinarily act as an intrinsic brake on the circadian system to control the rate of re-entrainment, interneural signalling between cells of the SCN normally acts to resist external perturbation on the clock

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9
Q

Jet lag

A

recovery is about 1 hour per day, harder for the clock to go phase advance than it is delay

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10
Q

VIP (expression)

A

is abundant in the SCN near OX

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11
Q

VPAC2

A

also heavily expressed in the SCN

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12
Q

VIP-VPAC2 signalling

A

has been implicated in the photic entrainment of the SCN via RHT

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13
Q

VIPR2 KO mice

A

have significantly disrupted wheel running behaviours and almost completely non-existent phasic firing w zeitgeber time, and have a disorganised molecular clock

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14
Q

Pharmacological blockade of VIPR2

A

prevents peaking in firing rate rhythm (but rhythms are rescued as antagonist washes out)

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15
Q

In the absence of VIP-VPR2 signalling

A

both amplitude and synchrony are impaired in SCN neurons

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16
Q

VIP and VIPR2 KO mice

A

are behaviourally arrhythmic, or express accelerated behavioural rhythms

17
Q

In vitro, VIPR2 KO neurons

A

show dampened firing and appear arrhythmic

18
Q

VIPR2 SCN cannot

A

gate the actions of light on the P-ERK pathway

19
Q

Insect correlate of VIP

A

PDF

20
Q

PDF is analogous to

A

PDH, but lacks a chromatophore

21
Q

PDF is found in

A

SLNvs and LLNvs

22
Q

PDF signalling takes place via

A

the PDFR receptor, a B1 class GPCR, +vely coupled to adenylate cyclase

23
Q

PDF KO flies

A

show disrupted circadian rhythms, lacking morning anticipation and advancement in evening anticipation

24
Q

PDF and PDFR mutants also show

A

a marked decrease in rhythm amplitude in DD or may even be arryhthmic

25
Q

PDF has complex actions that may differ between clock cells

A

may lengthen or shorten the period of a clock cell

26
Q

PDF has mixed function in neurons

A

in some PDF signal is needed to synchronise the clock, in others it is needed for clock cycling

27
Q

number of VIP neurons in humans

A

decrease with age

28
Q

In PD

A

the number of VIP and AVP neurons are greatly reduced

29
Q

Genetic mutations in the VIPR2 gene

A

is linked to increase risk of developing schizophrenia

30
Q

Scheduled exercise

A

can restore rhythms in VIPR2 KO mice