Unit 11 - Hypothalamus Flashcards
hypothalamic nuclei
part of diencephalon
under corpus callosum
role of hypothalamus
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
thermoregulation
how does our temp change
heat production - heat loss
temp set point
37°C - circadian rhythm 0.5-0.7°C change
how does temp measurement differ in various parts of the body
rectal > head > trunk > hand > feet
exercise increases temp up to 40°C
where are thermoreceptors found
skin
deep tissues
spinal cord
extrahypothalamic regions
hypothalamus (20%)
types of thermoreceptors
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
cold fibres
Aδ
warm fibres
C
peripheral thermoreceptors
anterolateral system to somatosensory cortex - SPINOTHALAMIC TRACT
also projections to thermoregulatory centre in hypothalamus
where are central thermoreceptors located on
GABA neurons
anterolateral system =
spinothalamic tract
increased heat production causes activation of
what does this cause
preoptic area in anterior hypothalamus
promotes heat loss
vasodilation, sweating, increased respiration
anorexia
apathy
lesion of preoptic area in anterior hypothalamus
chronic hypERthermia - inability to lose heat
increased heat loss activates
neurons in posterior hypothalamus
promotes heat generation
shivering, hunger, voluntary activity, vasoconstriction (goose bumps), curling
lesion of posterior hypothalamus
no effects at room temp
in cold, no ability to conserve heat
overview of hypothalamic control of temperature
Under normal circumstances the anterior hypothalamus inhibits posterior hypothalamus
Inhibition prevented with lowering in body temp
thermoregulation
decrease in temp
increase in temp
temp regulation in an infant
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
fever and temp
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
C
factors that stimulate thirst
dryness of pharyngeal mucus membrane
gastric/oropharyngeal signals
psychological and social factors
hyperosmolality
reduced blood volume
hypothalamic mechanisms involved in thirst
organum vasculosum of the lamina terminalis (OVLT)/medial preoptic hypothalamus
plasma osmolality, ECF volume
Medial preoptic nucleus of hypothalamus and OVLT
Close anatomically
Often grouped together
GABAergic and glutaminergic neurons - increases or decreases thirst response
plasma osmolality - receptors
where do they project to
what do they do
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
reduced or absent secretion of ADH
diabetes insipidus
where is ADH produced
supra optic and paraventricular nuclei
what does ADH also act as
NT - emotional response to thirst - prefrontal cortex
thirst and fluid balance (ECF vol) - where and how is pressure monitored
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
RAA system
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
overview of thirst and fluid balance
reduction must be greater than 10%
C
lateral nuclei of hypothalamus =
destruction/stimulation
rate of activity
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
ventromedial nuclei =
function
destruction/stimulation
sense of fullness
inhibits feeding centre (LN of hypo.)
destruction ⇒ obesity due to inability to depress feeding behaviour
stimulation ⇒ reduced appetite, aphagia
apart from VM nuclei and lateral nuclei of hypothalamus, what other nuclei play a part in hunger and feeding
Paraventricular
dorsomedial
arcuate
injection of substances to PV nuclei
leads to selective food intake
NA - CHO e.g. chocolate
Galanin - fat
opiates - protein
NA ⇒
CHO
galanin ⇒
fat
opiates ⇒
protein
overview of hypothalamic control of feeding
short term control of food intake - 4 methods
- GI distension
- GI hormonal factors
- Ghrelin - GI hormone
- Insulin
GI distension
stretch inhibitory receptors activated and inhibit feeding centres + stimulate satiety centre
GI hormonal factors
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
ghrelin
mainly released by stomach, levels rise in fasting and decrease after eating - stimulate feeding behaviour
most GI hormones inhibit feeding centre
overview of influences on hunger/feeding
long term control of food intake
what is produced
what is its effect
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
other effects of leptin
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
leptin deficiency
obesity and hyperphagia - observed in humans with mutations in genes encoding leptin
relative deficiency of leptin may predict future weight gain
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