Hypothalamus Flashcards
what are the functions of the hypothalamus?
regulates and integrates autonomic and endocrine functions with behavior that are primarily concerned with homeostasis
does this by regulating:
- BP and electrolyte balance (drinking, salt appetite)
- body temp (behavior, ANS- shivering, endocrine)
- energy metabolism (feeding, digestion, metabolic rate)
- reproduction (hormone- mating, pregnancy and lactation)
- emergency responses (BF to ms, secretion of adrenal stress hormones)
- mediation of emotional responses
- controls the release of 8 major hormones by the hypophysis (pituitary)
what are the 3 mechanisms that the hypothalamus uses?
1- receives sensory signals from all parts of the body
2- compares these sensory signals with biological set points
3- if a deviation is detected- homeostasis is restored by:
- adjusts in the ANS
- endocrine system
- behavior
what are the 2 lobes? of the hypophysis (pituitary)?
adenohypophyseal system
neurohypophyseal system
what is the adenohypophyseal system?
endocrine
regulates what you need (thyroxine for metabolism)
hypothalamus neurons produce releasing factors or inhibiting factors into the portal system
–>adenohypophysis (anterior pituitary lobe) produces and stores other releasing factors
–> peripheral glands- produces hormones and release them into systemic circulation
what is the neurohypophyseal system?
hypothalamus produces hormones
axoplasmic flow to neurohypophypophsis where hormones are stored (posterior lobe of pituitary)
to release hormones, these cells fire off APs in hypothalamus and fire off cells in post pituitary to release ADH and oxytocin into systemic blood supply
hypohypophseal tract –> neurohypophsis (releases stored hormone into the systemic circulation)
what is the biggest function of oxytocin?
lactation, suppress hypothalamic function
what do vasopressins do?
regulate blood volume and salt concentration
coronal anatomy:
nuclear masses: -medial -lateral -periventricular names from columns of fornix surrounding 3rd ventricle
how does the hypothalamus control hormonal and hypothalamic regulation of body fat?
body fat and foot consumption:
- lipostatic hypothesis
- Leptin
- Leptin depletion– incites adaptive responses to fight starvation
what is leptin?
the hormone responsible for regulating body mass
decreases appetite
increases energy expenditure
a lesion of the lateral hypothalamus would make an animal:
lose weight
feeding centers are in the lateral hypothalamus
a lesion of the medial hypothalamus would make an animal:
gain weight
satiety centers are in the medial hypothalamus
what are the effects of elevated leptin levels on the hypothalamus?
a rise in leptin levels in the blood is detected by neurons in the arcuate nucleus that contain the peptides aMSH and CART. (located at the base of the 3rd ventricle)
these neurons project axons to:
- the lower BS and SC
- the paraventricular nuclei of the hypothalamus
- the lateral hypothalamic area
each of these connections contributes to the coordinated humoral, visceromotor and somatic motor responses
what are the effects of decreased leptin levels on the hypothalamus?
activation of arcuate neurons that release NPY and AgRP
effects on energy balance: opposite to the effects of aMSG and CART
orexigenic peptides- increase appetite
-NPY and AgRP inhibit secretion of TSH and ACTH
activate parasympathetic division of ANS
-stimulate feeding behavior
how can you control feeding by the lateral hypothalamic peptides?
lateral hypothalamus: motivation to eat
-electrical stimulation: triggers feeding behavior in satiated animals
neurons intrinsic to lateral hypothalamus; axons passin through the lateral hypothalamus
MCH: peptide neurotransmitter
- informs cortex about leptin levels
- motivates the search for food
what does the motivation to eat depend on?
time and quantity of last meal
are the 3 phases of appetite, eating, digestion and satiety?
1-cephalic
2-gastric
3-substrate
increases blood insulin levels
what is the short term regulation of feeding behavior?
appetite
eating (cephalic)
digestion
satiety
- gastric distension
- cholecystokinin (CKK)- hunger suppressant
- increases insulin
CCK–> gastric distension–> vagus nerve–> nucleus of solitary tract –> SATIETY
why do we eat?
reinforcement and reward (reward hormones are released when eating (dopamine and serotonin)– why depressed ppl are overweight - food activates reward systems
dopamine motivates to eat, serotonin spikes when you eat . no serotonin-don’t want to eat
liking-hedonic
wanting- drive reduction
electrical self stimulation- experiments to identify sites of reinforcement
effective sites for self stimulation- trajectory of dopaminergic axons in the ventral segmental area projecting to the forebrain
drugs that block dopamine receptors: reduce self stimulation
what is the role of dopamine in motivation?
old belief: dopamine projection served hedonic reward
new understanding:
- dopamine-depleted animals “like” food but “do not want” food
- lack motivation to seek food, but enjoy it when available
stimulation of the dopamine axons
-craving for food without increasing the hedonic impact
how does serotonin affect food and mood?
serotonin as a neuromodulator
serotonin levels:
- low- postabsoptive period
- rise: in anticipation of food
- spike: during meals
mood elevation: rise in blood tryptophan and brain serotonin
drugs that elevate serotonin levels: dexfenfluramine (redux)
what are disorders and treatment concerning serotonin?
disorders:
-anorexia nervosa
-bulimia nervosa
both often accompanied by depression
treatment:
- antidepressant drugs- elevate brain serotonin levels
what is another motivating factor besides dopamine?
drinking
1-hypovolemia (decrease in blood volume)
2- hypertonicity (increase in the concentration of dissolved substances in the blood)
no water- kidney regulates- releases angiotensin II to blood supply. heart is affected, goes up vagus nerve to solitary to hypothalamus. hypovolemia goes to subfornix which regulates water
salt content- too much–>need more water - produces ADH, too little salt= inhibit ADH
what is volumetric thirst?
thirst triggered by hypovolemia