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CNS > Unit 11 - Hypothalamus > Flashcards

Unit 11 - Hypothalamus Flashcards

1
Q

hypothalamic nuclei

A

part of diencephalon

under corpus callosum

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2
Q

role of hypothalamus

A

integrates autonomic responses and endocrine function with behaviour

  • controls BP and electrolyte composition - drinking, salt, appetite, blood osmolality, vasomotor tone
  • regulates temp - metabolic thermogenesis, behaviour
  • controls energy/metabolism - feeding, digestion, metabolic rate
  • behavioural expression - reproduction, emotional expression, circadian rhythm
  • controls stress response - vasomotor tone, secretion of stress hormones

compares sensory info with biological set points

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3
Q

thermoregulation

how does our temp change

A

heat production - heat loss

temp set point

37°C - circadian rhythm 0.5-0.7°C change

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4
Q

how does temp measurement differ in various parts of the body

A

rectal > head > trunk > hand > feet

exercise increases temp up to 40°C

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5
Q

where are thermoreceptors found

A

skin

deep tissues

spinal cord

extrahypothalamic regions

hypothalamus (20%)

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6
Q

types of thermoreceptors

A

Aδ and C fibres

separate warm and cold receptors (TPRV, Transient Potential voltage, receptors)

cold (Aδ) > warm (C)

activated at temperatures that are not necessarily painful

>42°C or <17°C is painful

lower threshold

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7
Q

cold fibres

A

Aδ

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8
Q

warm fibres

A

C

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9
Q

peripheral thermoreceptors

A

anterolateral system to somatosensory cortex - SPINOTHALAMIC TRACT

also projections to thermoregulatory centre in hypothalamus

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10
Q

where are central thermoreceptors located on

A

GABA neurons

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11
Q

anterolateral system =

A

spinothalamic tract

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12
Q

increased heat production causes activation of

what does this cause

A

preoptic area in anterior hypothalamus

promotes heat loss

vasodilation, sweating, increased respiration

anorexia

apathy

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13
Q

lesion of preoptic area in anterior hypothalamus

A

chronic hypERthermia - inability to lose heat

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14
Q

increased heat loss activates

A

neurons in posterior hypothalamus

promotes heat generation

shivering, hunger, voluntary activity, vasoconstriction (goose bumps), curling

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15
Q

lesion of posterior hypothalamus

A

no effects at room temp

in cold, no ability to conserve heat

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16
Q

overview of hypothalamic control of temperature

A

Under normal circumstances the anterior hypothalamus inhibits posterior hypothalamus

Inhibition prevented with lowering in body temp

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17
Q

thermoregulation

A
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18
Q

decrease in temp

A
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19
Q

increase in temp

A
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20
Q

temp regulation in an infant

A

neonate has very narrow temp zone

very little capacity for heat conservation

brown fat has a high rate of metabolism, thermogenic function - High thermogenic value so produces a lot of heat but can also get used up

BY 3 MONTHS

metabolic rate increases

rise in ratio of mass to SA

increase in body fat

maturation of shiver response

3 month old has less capacity to dissipate heat than neonate

head - 40% of heat production, 85% of heat loss

if head is covered or overwrapped, CNS temp can increase dangerously

resp affected - SIDS

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21
Q

fever and temp

A

pyrogens/toxins → cytokines → OVLT → preoptic area

IL-1B, IL-6, IFNβ, IFNγ, TNFα: receptors in OVLT

causes local release of PGs in preoptic area which alter set point

heat production mechanisms ⇒ fever

beneficial in certain instances e.g. leprosy, viral infections

antipyretic effect of COX2 inhibitors (COX makes PGs) e.g. aspirin

22
Q
A

C

23
Q

factors that stimulate thirst

A

dryness of pharyngeal mucus membrane

gastric/oropharyngeal signals

psychological and social factors

hyperosmolality

reduced blood volume

24
Q

hypothalamic mechanisms involved in thirst

A

organum vasculosum of the lamina terminalis (OVLT)/medial preoptic hypothalamus

plasma osmolality, ECF volume

25
Q

Medial preoptic nucleus of hypothalamus and OVLT

A

Close anatomically

Often grouped together

GABAergic and glutaminergic neurons - increases or decreases thirst response

26
Q

plasma osmolality - receptors

where do they project to

what do they do

A

osmoreceptors in OVLT

detect change <1% Na2+ conc (monitoring blood flow over them)

projections to supra-optic and paraventricular nuclei to produce ADH

released by pituitary

increases thirst response and promotes fluid intake

also, increases water permeability in DCT of kidney - AQP-2, which allow water to be reabsorbed ⇒ reduction in osmolality

27
Q

reduced or absent secretion of ADH

A

diabetes insipidus

28
Q

where is ADH produced

A

supra optic and paraventricular nuclei

29
Q

what does ADH also act as

A

NT - emotional response to thirst - prefrontal cortex

30
Q

thirst and fluid balance (ECF vol) - where and how is pressure monitored

A

BARORECEPTORS

aortic arch and carotid sinus

decrease ECF vol (>10%) → low BP

ADH release

Mechanoreceptor - sense stretch depending on EC fluid vol - if we lose fluid, we decrease stretch and neural signal sent to hypothalamus - goes to OVLT and PV nucleus to produce ADH

31
Q

RAA system

A

Renin produced in response to decrease in EC fluid vol

angiotensin II receptors in subfornical (SFO) organ and OVLT

signal sent to preoptic, supra-optic and PV nuclei

ADH release

32
Q

overview of thirst and fluid balance

A

reduction must be greater than 10%

33
Q
A

C

34
Q

lateral nuclei of hypothalamus =

destruction/stimulation

rate of activity

A

feeding centre

chronically active - if there is not inhibitory control, we would never be hungry

destruction ⇒ lack of desire for food, emaciation

stimulation ⇒ increased appetite

35
Q

ventromedial nuclei =

function

destruction/stimulation

A

sense of fullness

inhibits feeding centre (LN of hypo.)

destruction ⇒ obesity due to inability to depress feeding behaviour

stimulation ⇒ reduced appetite, aphagia

36
Q

apart from VM nuclei and lateral nuclei of hypothalamus, what other nuclei play a part in hunger and feeding

A

Paraventricular

dorsomedial

arcuate

37
Q

injection of substances to PV nuclei

A

leads to selective food intake

NA - CHO e.g. chocolate

Galanin - fat

opiates - protein

38
Q

NA ⇒

A

CHO

39
Q

galanin ⇒

A

fat

40
Q

opiates ⇒

A

protein

41
Q

overview of hypothalamic control of feeding

A
42
Q

short term control of food intake - 4 methods

A
  1. GI distension
  2. GI hormonal factors
  3. Ghrelin - GI hormone
  4. Insulin
43
Q

GI distension

A

stretch inhibitory receptors activated and inhibit feeding centres + stimulate satiety centre

44
Q

GI hormonal factors

A

CCK - release due to fat entering duodenum and inhibits feeding centre - travel In blood - directly inhibit feeding centre and activate satiety centre

Peptide YY - released by G tract 1-2hrs post feeding, inhibits feeding centre - longer effect - not hungry straight after a meal

Glucagon Like Peptide and Insulin - appetite suppressant

45
Q

ghrelin

A

mainly released by stomach, levels rise in fasting and decrease after eating - stimulate feeding behaviour

most GI hormones inhibit feeding centre

46
Q

overview of influences on hunger/feeding

A
47
Q

long term control of food intake

what is produced

what is its effect

A

adipose tissue produces leptin - decreases food intake, increases energy use

SUPPRESSES APPETITE

release appetite-suppressing neuropeptides

α-melanocyte stimulating hormone (α-MSH)

cocaine and amphetamine related transcript (CART)

INHIBITS STIMULATION OF FOOD INTAKE

inhibits release of appetite-stimulating neuropeptides

neuropeptide Y

Agouti-related peptide

48
Q

other effects of leptin

A

increased CRH (decreases food intake)

increases SNS (neural projections from hypothalamus to vasomotor areas - increase in metabolic rate and energy expenditure)

decreased insulin secretion by pancreatic β cells, which decreases energy stores

overall acts to signal that enough energy stored and intake of food is no longer required

49
Q

leptin deficiency

A

obesity and hyperphagia - observed in humans with mutations in genes encoding leptin

relative deficiency of leptin may predict future weight gain

50
Q
A

D

CNS (36 decks)

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