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Brain and Behaviour > Neural control of motivational behaviour > Flashcards

Neural control of motivational behaviour Flashcards

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The Brain flashcards
1
Q

why are a few areas of the blood brain barrier leaky

A
  • the capillaries are fenestrated in these regions therefore hormones in the blood can move out into the extracellular space of the brain
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2
Q

what are the leaky areas in the brain called

A
  • they are called circumventricular organs
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3
Q

what are the parts of the cricumventricular organs

A 
area postrema
 posterior pituitary
 median eminence
 subfornical organ
 subcommissural organ pineal gland .
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4
Q

why are the circumventricular organs called circumventricalar organs

A
  • this is because they surround the ventricular system
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5
Q

what is the function of the subfornical organ

A
  • this is the area of the brain where it detects the osmolarity of blood
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6
Q

How does the subfornical organ detect the osmolarity of the blood

A
  • it has osmoreceptors
  • for example if our total body water is low, due to inadequate drinking or excess loss in sweat or urine, the osmolarity of the blood increases.
  • therefore the cells shrink and this is translated into action potentials which cause the body to have an urge to drink
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7
Q

where is the subfonrical organ

A
  • it is next to the hypothalamus, and in the wall of the third ventricle
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8
Q

what happens when the subfornical organ is stimulated

A
  • osmoreceptors in the subfornical organ are stimulated by hypertonic blood
  • this activates cells in the medial preoptic nucleus of the hypothalamus
  • this medial preoptic nucleus projects into the limbic system and regulates the sense of thirst
  • when it is act we feel thirsty and seek water
  • the subfornical organ also activates cells in the paraventricular nucleus and supraoptic nucleus
  • these cells project into the posterior pituitary and release ADH this reduces urine flow
  • this reduces the loss of water in urine and prevents blood osmolarity rising even further
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9
Q

What are the 3 effects of ADH

A

1, - causes addition aquaporins in the collecting duct epithelial cells
2, increases the permeability of the collecting duct to urea, this allows increased reabsorption of the urea into the meduallary interstitum which increases the reabsorption of water
3, - ADH stimulates sodium reabsorption in the thick ascending loop of Henle by increasing the activity of the Na+ K+ 2Cl- cotransporter. This increases the osmolarity of the medullary extracellular (interstitial) fluid, and allows even more water to be reabsorbed from the collecting ducts.

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10
Q

Where does ADH act

A

main action is on the collecting ducts, makes the aquaporin proteins insert into the membrane

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11
Q

the greater the activity of the medial preoptic nucleus the…

A

the thirstier we feel

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12
Q

where is the paraventricular nucleus

A

around the 3rd ventricle

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13
Q

where is the supraoptic nucleus

A

above the optic chiasma

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14
Q

what two nucleus project into the posterior pituitary in order to release ADH

A
  • paraventricular nucleus

- supraoptic nucleus

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15
Q

what is more dominant temperature regulation or water regulation

A
  • temperature system is dominant
  • therefore even though you are dehydrated you will still loose water in the form of sweat in order to loose heat
  • this is because if the core temperature goes above 40 the enzymes in the body start to denature
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16
Q

what is feeding behaviour initiated by

A

external and internal cues

  1. External cue – availability of food for example is there food in front of you
    2, internal cue - sense of hunger from inside the body
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17
Q

what makes you stop eating

A

a satiety system

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18
Q

we normally eat due..

A

to a combination of internal or external factors

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19
Q

what controls the body weight

A
  • hypothalamic control of body weight
  • may also be regulated by intestinal absorption - altering the intestinal transit time and therefore altering the absorption of caloric material in the intestine
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20
Q

what controls the amount of fat that we have in the body

A

the adipostat
- there is something that is released from fat cells in the body that gives the sense of saitety if you eat too much and this feedbacks to the hypothalamus

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21
Q

what is the hunger centre nucleus

A
  • lateral hypothalamus
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22
Q

what provides the major storage of energy in mammals

A

adipose tissue

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23
Q

wha is a side effect of a pituitary tumour

A
  • obesity - if the pituitary tumour press upwards on the hypothalamus
  • can also cause anorexia
  • this depends on what part of the hypothalamus that the tumour is pressing on
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24
Q

what happens if you have a lesion of the lateral hypothalamus

A

anorexia

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25
Q

what happens if you have a lesion of the medial hypothalamus

A

obesity

26
Q

what nuclei regulate saitety in the hypothalamus

A
  • arcuate nucleus and periventricular nuclei
27
Q

describe the idea that the medial nucleus of the hypothalamus is the internal cue for satiety

A
  • for example if there is a lesion on the medial hypothalamus you are likely to become obese
  • but researches found that if animals with lesions in the medial hypothalamus were give unpalatable food they became anorexic
  • this led to the idea that the medial structures are not saitety centres but they are where the internal cues for satiety is received - therefore if the food looks bad they will have a feeling of fullness and will not want to eat it
28
Q

what are internal stimuli

A

Internal stimuli are things like contraction of the stomach (hunger pangs), and the levels of various blood chemicals like glucose, insulin, grhelin, cholecytokinin and leptin.

29
Q

what are external stimuli

A

External stimuli are the sight and smell of food

30
Q

if internal stimuli is strong…

A

you will eat anything whereas if it is weak you will not eat it unless it looks attractive and is tasty

31
Q

what detects internal cues such as the level of blood hormones

A

the arcuate nucleus

32
Q

what happens when the arcuate nucleus is damaged

A
  • it destroys the animals ability to detect internal signals
  • therefore if it is presented with nice food it will eat until it cannot eat anymore
  • has no ability to detect internal satiety signals
  • if it is presented with bad food it will starve to death as it has no ability to detect internal hunger signal
33
Q

what are the main neurones that are in the arcuate and perventircular nuclei

A

1, Agouti-related peptide*’ (AGRP) & ‘Neuropeptide Y’ neurones (NPY) neurones (arcuate nucleus)
2. ‘Cocaine & amphetamine related transcript’ neurones (CART) & ‘Pro-opiomelanocortin (POMC)’ neurones (paraventricular nucleus)

34
Q

what is the key hormone that is released from the gut when you are hungry

A

Ghrelin

35
Q

where is ghrelin produced

A

Produced in stomach, duodenum, ileum and epsilon cells of pancreas

36
Q

what produces ghrelin

A

ghrelinergic cells

37
Q

what stimulates the production of Ghrelin

A
  • the stomach contracts when it is empty
  • the vagus nerve detects these contractions and this signals the brainstem and hypothalamus
  • Ghrelin is released when the stomach contractions and when blood glucose is low
  • it generates a sense of hunger by action on neuropeptide Y and agouti-related peptide cells in the arcuate nucleus
  • inhibits satiety signalling in the arcuate nucleus and paraventricular nucleus neurones
38
Q

when is ghrelin released

A
  • when the stomach contractions

- when blood glucose is low

39
Q

what type of receptor is ghrelin receptor

A

G protein receptor

40
Q

describe how ghrelin links to anorexia

A
  • it stimulates the dopamine pathway in the brain that is responsible for the pleasurable aspect of eating
  • in anorexics this pathway may be disconnected
41
Q

what hormones inhibit eating

A
  • CCK

- Glucagon like peptide 1

42
Q

describe how CCK inhibits eating (satiety signal)

A
  • synthesised by the mucosal epithelium in the small intestine and secreted in the duodenum
  • causes release of digestive enzymes from the pancreas and bile from the gallballder
  • travels in the blood to the hypothalamus
  • acts on the arcuate nucleus
  • produces satiety signal
43
Q

how does glucagon like peptide 1 inhibit eating ( Satiety signal)

A
  • it is released as a consequence of food in the gut
  • acts on the arcuate cells inducing a satiety signal
  • it inhibits gastric emptying therefore produces a feeling of fullness and stimulates insulin secretion and decreases glucagon which together lowers the blood glucose
44
Q

there is a mutate inhibition between..

A

between the ‘hunger’ neurons and the ‘satiety’ neurons. This kind of feedback makes feeding an ‘all-or-none behavior; once you start you don’t stop until you are sated.

45
Q

what neurones do CCK and glucagon like peptide 1 stimulate

A

CCK, GLP-1 and other peptides inhibiting feeding stimulate neurones in the arcuate nucleus that contain POMC & CART. These neurones stimulate a sense of satiety & stop feeding behaviour

46
Q

what is pancreatic peptide YY

A
  • this is a large peptide hormone that is synthesised within the GI tract in specialised enteroendorcine cells named L cells
47
Q

what does pancreatic peptide YY do

A
  • it increases ill absorption
  • slows gastric emptying
  • delays gallbladder and pancreatic secretion
48
Q

what is leptin

A
  • Leptin is a protein hormone that is produced by adipose tissue
49
Q

the total amount of leptin reflects…

A
  • The amount of circulating leptin appears to reflect the total amount of adipose tissue in the body
50
Q

what is the long term regulator of apetite

A
  • leptin

- if there is an increased amount of leptin then you have a chronically reduced apeittie

51
Q

what does leptin give the brain

A
  • the circulating leptin levels give the brain a reading of total energy storage
  • it tells the brain whether the body is above its set point or below it
52
Q

how does leptin effect obese people

A

Leptin insensitivity causing chronic overeating

- some leptin receptors in the hypothalamus may have been deleted

53
Q

How does leptin affect fertility

A

A woman ceases to menstruate and ovulate if circulating leptin decreases below a certain level; the low level of leptin prevents gonadotrophic hormones from being released.

54
Q

describe the inputs into the arcuate and paraventricular nucleus

A

Arcuate nucleus
ventrolateral nucleus
- Ghrelin inputs into the ventrolateral arcuate nucleus
- this stimulates the neurones NPY and AGRP

dorsolateral nucleus

  • CCK, GPY1 PYY oxytocmodulin projects into the dorsalalteral arcuate nucleus
  • this stimulates the neurones POMC
  • the ventrolateral arcuate nucleus then projects into feeding centre in the paraventricular nucleus
  • the dorsolateral nucleus then projects into the satiety centre in the paraventricular nucleus
55
Q

what does damage to both the arcuate and paraventricular nuclei lead to

A
  • Damage to the arcuate and paraventricular nuclei leads to a loss of the ability to detect hormones released from the gut.
  • This leads to overeating and obesity when food is readily available.
56
Q

why are reward pathways important

A
  • drinking is connected to the reward system as we drink wheterh we are dehydrated or not, as well a chewing
  • if we did not we would die as it would not be rewarding
57
Q

how does the reward system link to feeling

A
  • chewing is rewarding
  • actions of the orafacial muscles during drinking or feeding activate dopamine neurons in the ventral tegmental area of the brainstem.
  • These project to and activate neurons in the nucleus accumbens
  • It seems that activation of the accumbens neurons is the neuronal correlate of feelings of pleasure or reward.
58
Q

what is anorexia nervosa

A

this is an eating disorder characterized by low weight, fear of gaining weight, and a strong desire to be thin, resulting in voluntary food restriction

59
Q

what are the complications for anorexia nervosa

A

osteoporosis, infertility, and heart damage, women will stop having menstrual periods

60
Q

what is the severity of anorexia nervosa based on

A
  • body mass index (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.
61
Q

what happens in anorexia nervosa

A
  • food and drink is no longer pleasurable to them

Brain and Behaviour (34 decks)

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