circadian rhythm Flashcards

1
Q

calendar cells

A

cells responsible for long term time keeping

melatonin target cells

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2
Q

how do calendar cells decode melatonin duration?

A

use a clock-gene based mechanism

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3
Q

melatonin signal generator

A

LD cycle —> photoreceptors in the retina —> pineal glands which release melatonin or SCN circadian cell —> which go to other cell targets

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4
Q

melatonin decoder in the pituitary gland

A
LD= short night = less melatonin signal time 
SD= long night and more melatonin signal time 

this melatonin signal goes to calendar cell —> lactotroph/PRL —> hair papilla, hepatocyte, luteal cell

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5
Q

which receptors of calendar cells pick up melatonin?

A

MTI receptors

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6
Q

long term changes in prolactin secretion in the pelage/moult cycle

A

prolonged SD results in the development of prolactin secretion and the reversion from white to agouti pelage

exposure to prolonged LD results in the initial refractory response that merges into the expression into the expression of circannual cycle; horn growth is suppressed during winter

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7
Q

refractory period

A

insensitive phase to prolactin secretion

calendar cells have inhibition of prolactin secretion which occurs over a long time before it recovers

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8
Q

two models of the photoperiod

A

amplitude model - changes in the amplitude of clock gene expression
phase control- based on relationships between proteins
proteins dimerise, meet in the nucleus and act on gene expression, chance of proteins meeting in the LD is lower, in SD chance of them meeting is higher and get higher gene transcription

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9
Q

symptoms of jetlag

A

constipation- clock is coupled to digestive system
retrieving information- mental performance
retrograde amnesia

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10
Q

zeitgeber

A

time giver- resetting stimulus that functions as a time cue

light

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11
Q

molecular clockworks of circadian rhythms

A

positive elements = CLKC and BMAL
negative elements are PER and CRY

PER and CRY dimerise and inhibit the positive elements in the nucleus

negative elements undergo ubiquitination and phosphorylation to prevent further inhibition

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12
Q

regulation of clockwork genes

A

CLOCK and BMAL dimerise and bind to the promoters of the dock controlled genes and induce the transcription of many genes including PER and CRY

PER and CRY dimerise and interact with CLKOCK and BMAL, initiating their degradation

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13
Q

SCN

A

paired nuclei at the base of the hypothalamus just above the optic chiasm
r

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14
Q

where does SCN receive input from?

A

retinohypothalamic tract

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15
Q

projections from the SCN

A

PVN - relaying information to the periphery, ARC - feeding centres , LHA- behaviour

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16
Q

retinohypothalamic pathway and non-visual photo info

A

cones and rods allow colour vision and shape
retinoganglionic cell- different photoreceptors called melatinopsin and send it to the hypothalamus and reset the clock
non-visual light input pathway, don’t use it to see

17
Q

San lesion

A

get random rhythms of sleep wake, feeding and temperatures

18
Q

disseminating temporal information

A

master clocks in the SCN in the anterior hypothalamus

feeds into PVN

PVN has bilateral communication, receives input and feedback

19
Q

central and peripheral clock coordination

A

light —> SCN —> PVN — IML —> SCG —> pineal gland

from SCN also to peripheral clock systems

20
Q

peripheral clock systems

A

all different hormones occur at different times of the day - sequential, internal master clock determines this to maintain homeostasis of sleep and metabolism

21
Q

body temperature and chronotype

A

not consistent across the day and night- temperature plunges during night time

22
Q

day and night difference in the effects of exercise

A

exercise later at night has a much more efficient glucose removal/uptake

insulin is similar between morning and evening, which needs to be there for glucose uptake

therefore glucose transporters may be regulated by the clock, even if high insulin doesn’t mean there will be glucose uptake if no transporters

23
Q

neurons in SCn

A

GABAergic neurons
= inhibitory
therefore a very strong inhibitory tone from the SCN which inhibits the PVN which usually occurs during the daytime. the inhibition is removed during the nighttime because there is no light coming in to stimulate the SCN

24
Q

connection between SCN and liver- glucose production

A

daytime-

SCN inhibits PVN which inhibits the liver and results in increased glucose during the day

25
Q

SCN and pancreas- feeding induced insulin release

A

SCN strong inhibitory tone during the day which regulates how much PVN can be stimulated but he VMH. At night you take away inhibition to VMH is dominated, which causes the rhythm to occur and stronger pancreatic output

VMH produces glutamate in ultradian pulses so it continuously communicates with PVN during day and nighttime. but the SCN modulates this

26
Q

when does cortisol peak?

A

cortisol peaks immediately prior to the onset of activity –> end of night before we wake

27
Q

cortisol and HPA axis

A

rhythm is generated by the SCN signalling to the pVN, resulting in rhythmic corticotrophin-releasing hormone (CRH) secretion, but the adrenal gland has its own clock

turn on light – adrenal gland sees light —> resetting queue- neuronal

28
Q

melatonin

A

rhythmic signals from the SCN to the pineal gland drive rhythmic melatonin release

melatonin therapy is used for sleep disorders

29
Q

human circadian organisation

A

retina –> SCN —> PVN —> Intermediolateral column of spinal cord —> superior cervical ganglion —> pineal gland

30
Q

nighttime melatonin synthesis

A

have more stimulatory pathways from the SCN. gabaergic neurons are silent