Functional Systems Of Hypothalamus

Front 1

What is the main function of the hypothalamus?

Back 1

to compare inputs to the SET POINT
--sensory input and input from higher centers

Front 2

What molecule is major signaling element in long-term control of feeding?

Back 2

LEPTIN: hormone produced and released by adipose cells at levels directly related to amount of stored lipid

--increased leptin, decreases feeding and increases E consumption

--decreased leptin increases feeding and decreases E consumption

Front 3

what nucleus of the hypothalamus is the hypothalamic sensor of leptin molecules?

Back 3

arcuate nucleus

Front 4

what two molecules are stimulated by rise in leptin levels?

and what do those molecules do?

Back 4

alpha-MSH and CART --their activation suppresses appetite and increases E utilization (anorexigenic)

Front 5

what two molecules are active at low levels of leptin?

what is their function?

Back 5

NPY and AgRP are active at reduced leptin; their activation increases appetite and decreases energy utilization (orexigenic)

Front 6

the arcuate nucleus also projects to the ______
--paraventricular nucleus which does what?

Back 6

the paraventricular nucleus activates ENDOcrine and AUTOnomic responses associated with INCREASED E use.

--some cells in paraventricular contain releasing factors for ant pit. hormones (TSH) (ACTH) and also sympathetic neurons that increase metabolism

increased leptin = + energy balance

Front 7

the arcuate nucleus also projects to the lateral hypothalamic nucleus

Back 7

stimulates feeding behaviors (therefore activates when low leptin)

--cells containing MCH project thru brain to activate feeding behaviors

Front 8

Short-term regulation of feeding
--feeding behavior promoted by ? (hormone)

Back 8

ghrelin; a hormone prod by stomach at beginn of expected meal
-strongly stimulates AgRP and NPY in arcuate nucleus

Front 9

what are satiety signals?

Back 9

insulin --acts direcly on cells of arcuate nucleus

CCK - cholecytokinin increases to digest fat

gastric distension

Front 10

TEMP REGULATION
--neurons in ___________receive inputs from temp-sensing neurons in ____ hypothalmaus, and from thermal receptors in ____ and mucous membranes

Back 10

medial preoptic area

ant hypo

skin

Front 11

how is the thermostatic set point increased as in fever?

Back 11

pyrogens reach endothelial cells of hypothalamic capillary beds, stimulate COX-2 which induces PG E2 which increases set point.

Front 12

where are osmoreceptor neurons located?

Back 12

OVLT (vascular organ of lamina terminalis) or adj areas of ant hypothal. --LACK BB BARRIER

Front 13

where do OVLT neurons project to? and what does this cause?

Back 13

OVLT projects to paraventricular nucleus (PVN) and supraoptic nucleus (SON) which are MAGNOCELLULAR neurons which project to post pit so it will release ADH hormone.

-ADH makes kidney reabsorb water

OVLT also project elsewhere- thirst. MODULATE BEHAVIOR

Front 14

What are the two signals for decreased fluid volume?

Back 14

stretch receptors of R atrium and carotid/aortic arches --project via vagus to nucleus of solitary tract (NST)
-dec blood flow to kidney --ANG II -- acts on subfornical organ and activates

--neurons of both NST and SFO project to magnocellular nerons of SON and PVN --inc release of ADH
-may also project to dorsomedial nucleus for thirst.

Front 15

disorders in OVLT or SFO affect?
--water retention and or thirst mech

Back 15

both.

Front 16

disorders in magnocellular neurons affect
--water rentention and or thirst mech

Back 16

only water retention