Flashcards in neural control of motivational behaviour Deck (55):
what are circumventricular organs?
structures where the BBB is leaky at some points bc of fenestrated capillaries
where are circumventricular organs found?
surround the ventricular system
name some circumventricular organs
what can cause blood osmolarity to increase?
o if total body water is low bc of sweating/lack of drinking t
what senses blood osmolarity?
sensed by osmoreceptor cells in the subfornical organ – a circumventricular organ
explain the pathway of detecting high blood osmolarity and how this is kept under control?
- subfornical organ detects
high blood osmolarity
- activates cells in medial preoptic nucleus of hypothalamus
- nucleus projects into limbic system --> regulates thirst
- cells of the paraventricular and supraoptic nucleus are also activated
- their axons project to the posterior pituitary --> release ADH --> reduce urine -> reduce water loss in urine -> prevents blood osmolarity rising even further
which nucleus makes us feel thirst?
medial preoptic nucleus
where is the paraventricular nucleus found?
around the 3rd ventricle
where is the supraoptic nucleus found?
above the optic chiasm
what are the 3 effects of ADH to decrease loss of water?
- aquaporins: more move into the collecting duct epithelial membranes. water moves into renal medulla - less urine, higher conc
- increases collecting duct permeability to urea
- stimulates Na+ reabsorption in the ascending loop of Henle through the Na+ K+ 2CL- cotransporter. Increases osmolarity of medullary extracellular fluid -> more water reabsorbed from collecting ducts
what does the body do when water is lost by sweat during heat stress?
we drink more water to compensate
Body also increases aldosterone secretion and decreases atrial natriuretic peptide secretion -> decreases sodium loss in urine -> compensates for sodium loss in the sweat and prevents hyponatraemia
which 2 factors initiate feeding behaviour?
o External cue – immediate availability of food
o Internal cue – sense of hunger from inside your body
what is the major store of energy in mammals?
what is weight maintained by?
o Adipostatic model – factors released by fat target the hypothalamus to control feeding and maintain weight
o Intestinal absorption - altering intestinal transit time --> altering absorption of caloric material in the intestine
describe the early evidence for the role of the hypothalamus in appetite?
o Patients with pituitary tumours pressing up on the hypothalamus demonstrated voracious appetite, morbid obesity and hypogonadism – known as adiposogenital syndrome
what do lesions in the lateral hypothalamus cause?
what do lesions in the medial hypothalamus cause?
what does the ventromedial satiety centre do?
inhibited feeding when stimulated
what stimuli does the hypothalamus respond to to regulate food intake?
o Internal stimuli – contraction of the stomach, the levels of various blood chemicals e.g. glucose, insulin, ghrelin, cholecystokinin and leptin
o External stimuli – sight and smell of food
what does whether we eat food or not depend on?
the balance between external stimuli (how attractive the food is) and internal stimuli (how hungry we feel)
what does the arcuate nucleus detect?
internal cues e.g. levels of blood hormones
what do arcuate lesions do?
destroy the animal’s ability to detect internal signals
o If presented with palatable food, it will eat until it can physically eat no more
o If presented with unpalatable food, it will starve to death as it has no ability to detect internal hunger signals
what are the main cell types in the arcuate and periventricular nuclei?
o ‘Agouti-related peptide*’ (AGRP) & ‘Neuropeptide Y’ neurones (NPY) neurones
o ‘Cocaine & amphetamine related transcript’ neurones (CART) & ‘Pro-opiomelanocortin (POMC)’ neurones
what is ghrelin?
protein hormone produced by special ghrelinergic cells
where are ghrelinergic cells found?
found mainly in the fundus, but also in other parts of gut e.g. duodenum and ileum (to a lesser extent) and epsilon cells of the pancreas
what detects stomach contractions and where does this signal?
signals to the hypothalamus and the brainstem
when is ghrelin released?
when the stomach contracts
when blood glucose is low
what does ghrelin do?
• Generates hunger by action on (NPY) and (AGRP) cells in arcuate nucleus
- stimulates dopamine pathway in brain --> responsible for hedonic aspect of eating
what type of receptors are ghrelin receptors?
G protein-coupled receptors
how does ghrelin generate a sense of hunger?
stimulate action on NPY and AGRP cells in the arcuate nucleus
these neurons stimulate neurons in the limbic system that mediate hunger sensation and inhibit ‘satiety’ (POMC & CART) neurons
what is cholecystokinin?
a peptide synthesised by cells in the mucosal epithelium of the small intestine and secreted into the duodenum when food moves from stomach --> duodenum
what does CCK do?
• Causes release of digestive enzyme from pancreas and bile from gallbladder
• Released into the blood and travels to the hypothalamus
• CCK acts on cells in arcuate nucleus to produce satiety --> a satiety signal
what is glucagon like peptide 1?
• Hormone released as a result of food in the gut
what does GLP-1 do?
• Produces rapid satiety by an action on the arcuate cells
• Inhibits gastric emptying --> produces a feeling of fullness
• Stimulates insulin secretion and decreases glucagon --> lowers blood glucose
what do CCK, GLP-1 and other peptides do?
stimulate feeding stimulate neurones in the arcuate nucleus that contain POMC & CART
These neurons stimulate sense of satiety + stop feeding behavior
what is PPY?
• Pancreatic peptide YY – large peptide hormone synthesised within gastrointestinal tract in L cells
what are L cells?
specialised enteroendocrine cells
what does PPY do?
increases ileal absorption, slows gastric emptying and delays gallbladder and pancreatic secretion
what is leptin?
protein hormone produced by adipose tissue
what does the amount of circulating leptin reflect?
reflects total amount of adipose tissue in the body and therefore gives brain a reading of total energy storage
o Tells hypothalamus whether the body is above its set point weight or below it
what does deletion of leptin receptors in the hypothalamus cause?
induces chronic obesity
why is leptin a long term regulator of appetite?
• Leptin levels don’t rise rapidly after a meal --> cannot be a fast acting ‘satiety signal’ to stop eating
modulates response to fast acting satiety signals
how can leptin affect fertility?
Woman ceases to menstruate and ovulate if circulating leptin decreases below a certain level bc it prevents gonadotrophic hormones from being released.
what does arcuate+ adjacent hypothalamic nuclei damage cause?
reduces ability to sense internal cues
feeding behaviour therefore controlled by external cues alone
what does a ventromedial lesion cause?
will cause a person to overeat if given palatable food but starve if given unpalatable food --> people become picky with their diet
what do lesions in the lateral hypothalamus cause?
why are lesions in the lateral hypothalamus difficult to interpret?
these lesions may interrupt several neuronal pathways e.g. dopamine pathways which destroy pleasure of eating
what are reward pathways in the brain?
brain systems that are active when you feel happy
why are reward pathways important in babies?
act of suckling activates this pathway
if it didn’t activate this pathwy then the baby would not feed and die
how is the act of chewing rewarding?
o Actions of the orofacial muscles during drinking or feeding activate dopamine neurons in the ventral tegmental area of the brainstem project to and activate neurons in the nucleus accumbens (found deep in the frontal lobe)
o Activation of the accumbens neurons is the neuronal correlate of feelings of pleasure/reward
what is anorexia nervosa?
• An eating disorder characterised by low weight, fear of gaining weight and a strong desire to be thin, resulting in voluntary food restriction
what are complications of anorexia?
osteoporosis, infertility, and heart damage. Women will stop having menstrual periods.
how is the severity of anorexia classified?
based on BMI
Mild disease is a BMI of 17-18
moderate a BMI of 16-17,
severe a BMI of 15-16
extreme a BMI less than 15.
how is anorexia partly a psychological perceptual problem?
view themselves as overweight when they aren’t, usually deny having a problem with low weight, weigh themselves frequently, only eat small amounts etc