Mkgrady8 Neuro 3 Hypothalamus

Front 1

hypothalamus: receives info from internal environment from where

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internal hypothalamis sensories for: plasma levels of glucose, peptides, and hormones, plasma osmolality, core temp; peripheral visceral sensory input about: arterial pressure, skin and spinal cord temp, GI function, biorhythms

Front 2

what does it do with this info

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integrates it (negative feedback control); coordinates outputs designs to: CORRECT unwanted changes in internal environment, PROTECT internal environment form external, ADJUST internal to meet new demands

Front 3

functions influenced by the hypothalamus

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feeding, energy balance, fluid balance, emotional state, sleep state, temp regulation, cardiovascular, endocrine

Front 4

symptoms observed with abnormal function of the hypothalamus: food intake, fluid intake, emotional state

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hyperphagia (lack of satiety), anorexia; polydpsia, hypodypsia, inappropriate ADH secretion (excess) leading to hypo-osmolality and hypo-natremia; depression, irritability, rage, confusion, hallucinations, memory loss

Front 5

symptoms observed with abnormal function of the hypothalamus: sleep state, temp regulation, cardiovascular, endocrine

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drawsiness, sleep cycle reversal; poikilothermia, hyperthemia, hypothermia; labile blood pressure (can't control), cardiac arrhythmias; isolated pit deficiency, panhypopituitarism, Kallman's syndrome= hypogonadotropic hypogonadism, hyperpituitarism

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hypothalamus: causes of dysfunction

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congenital= developmental malformation (midline brain defects, hydrocephalus), developmental failure (cell migration=kallman's), absence of secretory product; vascular= hemorrhage, thrombotic event; blunt trauma= increased intracranial pressure, direct damage; presence of tumor= intrahypothalamic, extrahypothalamic; infectious agents (bacterial and viral)= encephalitis, meningitis; inflammatory process= response to infection, sarcoidosis

Front 7

4 different regions in the hypothalamus moving from anterior to posterior

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anterior, anterior tuberal, posterior tuberal, and posterior

Front 8

the nuclei of the hypothalamus from anterior to posterior

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anterior region (and at the level of the optic chiasm (below it) and anterior commissure (above it)= third ventricles divides it down the middle (in a superior to inferior manner) so lateral to medial it goes lateral preoptic nulecus, medial preoptic nucleus, 3rd ventricle, medial preoptic nucleus, lateral preoptic nucleus, and there are 2 suprachiasmatic nuclei between the optic chiasm and these other nuclei; anterior tuberal region (at the level of the optic chiasm (below it) and the 3rd ventricle going through the center (sup to inf))= lateral to medial it goes supraoptic nucleus, lateral nucleus, anterior nucleus, paraventricular nucleus, periventricular nuc, 3rd vent, periventricular nuc, paraventricular nucleus, anterior nucleus, lateral nucleus, supraoptic nucleus; posterior tuberal region (at the level of the optic tracts on either side of it and the 3rd ventricle in the middle)= lateral to medial it goes supraoptic nucleus, lateral nucleus, ventromedial nucleus and dorsomedial nucleus and dorsal nucleus (inf to sup), 3rd vent, ventromedial nuc and dorsomedial nuc and dorsal nuc (inf to sup), lateral nuc, superaoptic nuc; posterior region (at the level with the optic tracts on either side and the mammilary bodies inferior)= lateral to medial lateral nuc, posterior nucleus, posterior nuc, lateral nuc

Front 9

the functions of the various nuclei

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more than one nuc can influence a specific function and each nucleus can influence more than one function so it's hard to tie them all down

Front 10

hypothalamus: neural inputs

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visceral efferents to nucleus tractus solitarius (NTS); NTS to hypothalamus; NTS to other brain centers and to centers that in turn send efferents to the hypothalamus

Front 11

hypothalamus: connections with other brain centers: forebrain, medulla, anterior and posterior pit

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forebrain= connects to the limbic system (behavior, mood), limbic system to hypothalamus reciprocal with central nucleus of amygdala and hippocampus; medulla= visceral efferents to NTS to hypothalamus, hypothalamus to NTS, to rostral ventrolateral medulla (sympathetic NS), to nucleus ambiguus/dorsal motor nucleus X (parasympathetic); anterior and posterior pit= hypothalamo-hypophyseal tract (NEURAL CONNECTION) to posterior pit, hypothalamo-hypophyseal portal system (VASCULAR CONNECTION) to anterior pit

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hypothalamus: neural pathways

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cerebral cortex to hypo to autonomic centers in brainstem tegmentum to amygdala or thalamus or preganlgionic neurons in brainstem and spinal cord to end organs (smooth and cardiac muscle and glands); end organs to nucleus solitary tract to autonomic centers in brainstem tegmentum to amygdala or thalamus or hypo to cerebral cortex

Front 13

hypothalamus: humoral input

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blood born substances reaching the areas where BBB is incomplete (circumventricular organs) can enter the brain and activate receptors; these chemicals would include hormones, drugs, toxins (chemotaxic centers), and substances that can act as transmitters and bind to receptors in the brain; important for feedback control

Front 14

the circumventricular organs: what are the 2 main ones, what are these regions

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the organs with an imperfect BBB permitting passage of substances from blood; SUBFORNICAL ORGAN (SFO) AND ORGANUM VASCULOSUM OF LAMINA TERMINALIS (OVTL)

Front 15

ok so sensory input from the visceral organs goes in where and what eventually comes out

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sensory input to the nucleus tractus solitarius and then the hypothalamus that then activates the limbic system that then activates endocrine system to have a hormonal output of activates the premotor neurons to cause an neuronal autonomic output

Front 16

hypothalamus: anterior pit regulation

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hypothalamic releasing hormones secreted from neurons in hypothalamus and transported by portal system to ant pit to stimulate or inhibit hormone secretion by ant pit; control of secretion regulated by innervation from other neural centers and feedback regulation by hormones (entering the brain at area of circumventricular organs); secretion from VENTROMEDIAL/ARCUATE NUCLEUS of GnRH, GHRH, and dopamine, PARAVENTRICULAR NUCLEUS of somatostatin, CRH, and TRH, and each nucleus may secrete more than one

Front 17

hypothalamus: posterior pit regulation

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hormones vasopressin (AVP/ADH) and oxytocin made in neurons and axonally transported to posterior pit for release; oxytocin stimulates milk let down from breast, ADH decreases free water clearance by kidney; secretory stimuli= neural afferents activated by suckling (oxytocin), osmoreceptors (in hypothalamus), renin angiotensin system, volume receptors (low pressure receptors in atria), and baroreceptor reflex (all ADH/vasopressin)

Front 18

location of ADH and oxytocin secretion cells (what nuclei?)

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paraventricular nucleus and supraoptic nucleus of the hypothalamus (both produce both)

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hypothalamus dysfunction leading to endocrine pathology: congenital

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deficiency in secretory mechanisms at cellular level; ex is Kallman's syndrome in which LHRH (GnRH) secreting cells fail to migrate from medial olfactory pit resulting in hypogonadotropism; LHRH is the only releasing hormone not secreted; anosmia (failure to smell) is also present

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hypothalamus dysfunction leading to endocrine pathology: acquired

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space occupying lesion; secreting tumor; damage to secretory region; damage to tract or portal system; neural damage irreversible; portal damage may lead to irreversible damage in which a small post partem hemorrhage can lead to spasm of portal vessels and death and atrophy of cells in anterior pit (Sheehan's syndrome)

Front 21

hypothalamus: regulation of water balance

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sensors: osmoreceptors and angiotensin II receptors in median preoptic nucleus and in circumventricular organs (OVLT and SFO), monitors of effective blood volume, osmolality, and arterial pressure; afferent pathways= increased plasma angiotensin binds to hypothalamic receptors, central renin angiotensin system involved with afferent pathways in the hypothalamus, pathways for conscious response to thirst unknown; hypothalamic actions in responses to dehydration= decreased water loss in urine resulting from increase in ADH secretion, increased water intake (thirst) with activation of osmoreceptors and hypothalamic and peripheral angiotensin II

Front 22

hypothalamus water balance pathology: diabetes, SIADH, renal failure

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diabetes insipidus= neurogenic (failure to secrete ADH) and nephrogenic (failure to respond to ADH) leading to increased plasma osmolality; SIADH (syndrome of inappropriate ADH)= increased ADH with normal or low osmolality leads to hypo osmolality and hypo natremia; renal failure; no access to water

Front 23

hypothalamus: cardiovascular function influences

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major influences exerted via autonomics; reciprocal connections wIth NTS= input from baro and volume receptors, input from higher center, OUTPUT CAN OVERRIDE BAROREFLEX (EXERCISE (need higher BP for oxygen delivery)); cardio inhibitory area (preoptic); cardio excitatory area (posterior); sham range (defense reaction)= input from limbic, can be conditioned, mostly involves PVN, increases SNS and decreases PNS

Front 24

hypothalamus: regulation of body temp

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preoptic, anterior, and septal regions= contain cells sensing core temp, receive input from peripheral thermoreceptors, match with 'set point' and coordinate outputs; fever= increased set point involving prostaglandins, increase opposed by Motrin, blocked by indomethacin (blocks prostaglandin synthesis); anterior mediates responses to increased temp (heat)= vasodilation --> increased heat loss, inhibition of heat production; posterior mediates responses to decreased temp (cold)= vasoconstriction, increased heat production (shivering and non shivering thermogenesis); behavioral i.e. increasing or decreasing layers of clothing

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hypothalamus: regulation of food intake

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intrahypothalamic senosry detect= plasma glucose (glucostat), plasma leptin (lipostat), plasma ghrelin (increases intake); extrahypothalamic input= oropharyngeal monitors, GI tract stretch receptors, GI hormones, transmitters such as peptide YY released from the GI tract, mostly ileum and colon, inhibit hunger; satiety (anorexigenic) center= lesions in ventromedial nucleus (hyperphagia), LEPTIN, neuromedin U and peptide YY signal satiety; feeding (orexigenic) venter= lesions in lateral hypothalamus (anorexia), hunger signaled by ghrelin

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hypothalamus: putative peptides for regulating appetite

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various peptides such as leptin and ghrelin are transported to the hypothalamus from other sites to affect appetite and exert other metabolic effects; these also may be secreted within the hypothalamus; receptors are located in many sites in the hypothalamus; usually stimulate one arm while inhibiting the other; major peptides INHIBITING appetite include leptin (from adipocytes), peptide YY (from the colon), insulin (from the pancreas), neuromedin (GI tract, hypothalamus) acts independently of leptin pathway, a-MSH, CRH, propriomelanocortin (POMC) stimulated by leptin; major peptides STIMULATING appetite include ghrelin (from the stomach)

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hypothalamus: anorexigenic effects of leptin

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protein hormone expressed by adipocytes containing high level of triglycerides; amount of secretion increases as fat content in adiopocytes increases; regulates body weight by inhibiting feeding center (VMH, arcuate nucleus) and increasing metabolic rate; works through stimulation of the POMC (pro opiomelanocortin) pathway which is catabolic; in humans serum leptin levels elevated in obesity; suggests that leptin production normal but response not present; transport across BBB may be impaired perhaps by circulating triglycerides; insulin may affect rate of leptin secretion; also simulates GnRH secretion

Front 28

hypothalamus: leptin secretion and actions

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leptin secreted from adipocytes; acts to suppress food intake and increase metabolic rate; insulin (secretion stimulated by elevated glucose) may act to stimulate leptin secretion and suppress appetite; leptin may feed back to inhibit insulin secretion from islet cells

Front 29

leptin: metabolic effects

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genetically altered mice unable to produce leptin are obese and have reduced oxygen consumption and body temp; treatment with leptin increases both and causes loss of body weight; ineffective in mice without leptin receptor; suggests that this genetic lesion does not explain obesity in humans

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hypothalamus: could leptin be used to treat obesity?

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replacement therapy in those who do not make leptin works but just therapy in obese people does NOT work (they don't respond to the exogenous leptin); may reflect decreased sensitivity to leptin in obesity or presence of factors preventing entry into the brain

Front 31

hypothalamus: does leptin influence reproduction?

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basal level of leptin required for stimulation of GnRH; lack of cycling and delayed onset of puberty in very thin individuals may be due to very low levels of leptin; leptin treatment can restore cycling in hypothalamic amenorrhea; excess leptin inhibits steroidogenesis, decreasing negative feedback inhibition; levels in obese males may be sufficient to inhibit testosterone production

Front 32

hypothalamus: ghrelin secretion and actions

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ghrelin is a peptide most of which comes from the stomach; plasma levels increase with fasting; acts on the hypothalamus to STIMULATE FOOD APPETITE; INHIBITS INSULIN SECRETION from islet cells leading to elevated glucose levels; STIMULATES GROWTH HORMONE (GH) secretion; note that there are other peptides found in the hypothalamus that stimulate appetite when infused directly into the hypothalamus

Front 33

hypothalamus: orexogenic effects of ghrelin

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ghrelin increases food appetite; levels lowest after eating a meal; they are highest just prior to next meal; levels correlate inveresly with leptin levels and the actions on satiety are directly opposite

Front 34

hypothalamus: food intake with ghrelin absent

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correlation of plasma ghrelin levels with feeding in normal controls, obese subjects who lost weight by dieting and obese subjects with weight loss occurring in some after gastric bypass surgery

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hypothalamus: ghrelin: effects on sleep and GH secretion

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ghrelin promotes sleep; a major GH secretory pulse occurs during sleep; intravenous ghrelin STIMULATES GH SECRETION; low glucose levels when ghrelin levels are high stimulate GH secretion providing an alternate metabolic substrate

Front 36

other effects of ghrelin

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binds to receptors on islet cells and inhibits glucose induced insulin secretion; insulin levels increase with low ghrelin levels; increases plasma glucose levels; intravenous ghrelin stimulates GH secretion and a major GH secretory pulse occurs during sleep; promotes sleep; when ghrelin levels are high low glucose levels stimulate GH secretion; opposes the cachexia occurring in pts with advanced cancer

Front 37

hypothalamus: influences on emotions/behavior

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limbic system input activates hypothalamus= limbic system output modulated by neocortex, association cortex via cingulate gyrus to hippocampus to hypothalamus; medial (PVN) initiates 'affective' aggression (defense reaction); lateral initiates 'predatory' aggression; central nucleus of amygdala activates medial and inhibits lateral; major output via autonomics