Systems Exam - Motivation Flashcards
What is the humoral response of the body to return to homeostasis?
regulating the release of hormones from the pituatry gland into the blood stream - stimulating or inhibiting the release of pituatary hormones
What is the visceromotor response for the body to return to homeostasis?
adjusting the balance of sympathetic and parasympthetic
what is the somatic motor response of the body to return to homeostasis?
responding to sensory signals by inciting the appropriate somatic motor behavioural response
the body’s energy stores are replenished following consumation of a meal, when this happens the blood is filled with nutrients. This is called the _____ state
prandial
energy is stored in what two forms
glycogen and triglycerides
where is glycogen found
liver and skeletal muscle
where is triglycerides found
in fat tissue (adipose tissue)
can glycogen and triglycerides be continually made forever?
glycogen has a finite number that can be stored, but triglycerides can virtually infinite
the stage during the assembly of macromolecules glycogen and triglycerides from simple precursors
anabolism
the stage where complex macromolecules are broken down into their constituants
catabolism
the fasting period between meals; when glycogen and triglycerides undergo catabolism to feed cells - cellular metabolism
postabsorptive state
what does glycogen break down into? what does it then feed?
glucose. then glucose feeds neurons and all cells
what does truglycerides break down into? what does it then feed?
glucose, fatty acids, ketones…… the glucose feeds neurons and all cells, and the fatty acids and ketons feed all cells
explain the lipostatic hypothesis
brain monitors amound of body fat and works to keep it at the same amount - at the optimal level
what is the ob gene
the gene hypothesized to carry protein that tells brain that fat reserves are normal
explain the ob/ob mice explain
ob/ob mice lack the ob gene, mice brains were told the mice fat reserves were too low, when in reality they were fine –> lead to overeating and obesity
- then fused two mice together (parabosis, blood fusal as well) one ob/ob and one normal and then ob/ob craving for food was greatly reduced and they lost some weight
humans lacking ______ crave food, this lack also slows metabolism and the humans become morbidly obese
leptin
how to treat leptin deficient humans?
Potential Problems?
injections of leptin
problem: when its not the amount of leptin circulating but a problem with the penetration of leptin through the blood brain barrier, reduced expresseion of leptin receptors in periventricular hypothaamus or altered CNS responses to change hypothalamic activity –> untreatable
___(Bilateral or ipislateral) ___ lesions of the___ results in anorexia
bilateral lesions of the lateral hypothalammus caused anorexia
___(Bilateral or ipislateral) ___ lesions of the___ results in obesity
bilateral lesions of the ventomedial hypothalamus caused animals to overeat and become obese
what is lateral hypothalamic syndrome
anorexia caused by damage to the lateral hypothalamus
ventromedial hypothalamic syndrome
overeating and obesity caused by lesions to the ventromedial hypothalamus
the beginnig of the respons to elevated leptin, starting with its release
- fat cells release leptin into the bloodstream, which activates leptin receptors on the arculate nucleus of the hypothalamus
- aplha MSH (alpha-melanocyte-stimulating hormone) and CART (cocaine- and amphetamine-regulated transcript) neurons within the arculate nucleus then activate the paraventricular nuclei, and start down the connections with the cells in lateral hypothalamus
what does alpha-MSH stand for
alpha-melanocyte-stimulating hormone
what does CART stand for
cocaine- and amphetamine- regulated transcript
explain the humoral, visceral, and somatic repsonse of the body to elevated leptin
humoral response:
when alpha MSH and CART neurons are stimulated and activate the paraventricular nuclei stimulatoing the release of hypophysiotropic hormones which stimulates the anterior pituatary secretion of ACTH and TSH which acts on the thyroid and adrenal glands to increase cell metabolic rate
visceral response:
alphaMSH and CART neurons of arculate nucleus activate paraventricular nucli which activate brain stem and preganglionic neurosn conrtrolling the sympthatic divisions, which increases cell metabolic rate, partly by raising the body temperature
Somatic response: alpha MSH and CART neurons of the arculate nucleus have connections with cells in the lateral hypothalamus which inhibit feeding behaviour
explain the humoral, visceral, and somatic response of the body to decreased leptin
humoral response:
NPY and AgRP neurons of the arcuate nucleus inhibit the paraventricular nuclei which means noh hydrophysiotropic hormones are released. This inhibits the secretion of TSH and ACTH from the anterior pituitary
visceral response:
NPY and AgRP neurons of the arculate nucleys are stimulated which activate the parasympathetic divisions of the NS
somatic response: NPY and AgrP neurons of the arculate nucleus have connectiosn with the laterla hypothalamus which results in stimulated feeding behaviour
what neurons of the arculate nuclues respond to elevated leptin? decreased leptin?
elevated: alpha MSH and CART
decreased: NPY and AgRP
alphaMSH and AgRP are anatagnoistic because_____
they both bind to the MC4 recepto on the postsmphathetic neurosn of the hypothalamus but alphaMSH activated MC4 to inhibit feeding and
AgRP inhibits MC4 to activate feeding
the area that is involved with motivation to eat
lateral hypothalamus and axons passing through the lateral hypothalamus
the two populations of neurons in the lateral hypothalamus and what they do
Population 1) MCH: melanin-concentrating hormone
- widespread connections in the brain to inform cortex of leptin levels in the blood
- injection = stimulation of feeding behaviour
Population 2) orexin
- widespread cortical connections, direct input from arculate nucleus
- role in wakefulness
Orexin and MCH are complemetary
- both MCH and orexin increase when leptin levels fall
- orexin promotes meal initiation
- MCH prolongs meal consumption
what do orexigenic signals do
increase in response to period of fasting; drives you to eat
what do satiety signals do
inhibit drive to eat; occur when we eat and then begin digestion process - teminate meal - inhibit feeding for some time after meal
The three stages of eating with descriptions
- cephalic phase:
sight/smell of food triggers physiological response –> parasympathetic and enteric divisions of ANS are activated: secretion of salivia, and digestive juices - gastric phase: responses become more intense are you start eating
- substrate phase: as stomach fills and food begins moving into intestines nutrients being to absorb into bloodstream
Overview of ghrelin
- highly concentrated in stomach and is released into bloodstream when stomach is empty
- growling stomach releases shrelin
- activates NPY/AgRP containing arculate nucleus
neurons
overview of gastric distention
- stomach wall is stretchy and contains/ is innervated by mechanosesnory axons that mostly ascenf to brain via vagus nerve (whose axons activate nucleys of solitary trract in medulla)
- inhibits feeding behaviour
overview cholecystokinin (CCK)
- present in some intestin lining cells and some enteric NS neurons
- released in response to certain types of food in intestine (especially fatty ones)
- CCK action exerted on vagal sensory axons
- inhibits feeding behaviour
Overview of Insulin
released into bloodstream by beta cells of pancreas
- Glucose transport into other cells requires insulin
- insertion of glucose transporters into the membrane occurs when insulin binds to cell surface insluine receptors - glucose needed for anabolic metabolism (storing energy)
- level of glucose in blood highly regulated by levels fo insulin
when blood glucose levels increase, insulin
levels decrease
when blood glucose levels decrease, insulin levels increase
relatinship between glucose and insulin
when blood glucose levels increase, insulin
levels decrease
when blood glucose levels decrease, insulin levels increase
insulin is released by pancreas when
1) cephalic phase: parasympathetic innervation of pancreas stimulates the beta cells to release insulin when anticipating food
2) gastric phase: when food enters stomach insulin secretion is stimulated further by gastrointestinal hormones liek CCK
3) substrate phase: food finally absorbed –> max insulin level
During what ohase is insulin at its max
substrate phase when food is finally absorbed
when reduces hedonic repsonses to food even tho the animal has stopped eating the food infront of them
destruction of dopamine acons passing through lateral hypothalamus fails to reduce the aniamls enjoyment of food but it does stop them from eating the food even when it is right infront of them
reward prediction - what happens to dopamine neuron signals if events are:
better than expected
worse than expected
as expected
better than expected: dopamine neurons come to life
worse than expected: dopamine neurons are inhibited
as expected: no change in firing of dopamine neurons
what behaviours are repeated
behaviours that are as expected or better than expected
what do highly addictive drugs act on in the brain
dopamine synapses in the brain
Link between serotonin and food: low, rising, and spiking serotonin
low - postabsorptive state
rising - anticipation of food (cephalic state)
spiking - during a meal - especially if eating carbs
