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U1 Behavioural Neurological Psychology 211 > lecture 14 > Flashcards

lecture 14 Flashcards

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1
Q

Extinction learning is often dependent on what

A

the neural activity in the prefrontal cortex

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2
Q

what is the Role of the Ventromedial Prefrontal Cortex

A

Region of prefrontal cortex at base of anterior frontal lobes, adjacent to midline; plays an inhibitory role in expression of emotions

Many investigators believe that impulsive violence is consequence of faulty emotional regulation
• For most people, frustrations may elicit urge to respond emotionally, but people usually manage to calm themselves and suppress these urges

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3
Q

what is the case of Phineas Gage

A

The PFC (Prefrontal cortex) has inhibitory connections with the amygdala which are responsible for suppressing emotional responses in social
In the mid 1800’s, Phineas Gage was a victim of a tragic construction accident.
§ An explosion sent a 3 cm thick, 90 cm long tamping rod through his face, skull and brain.
§ Before his injury he was a good natured, kind, responsible, well liked and respectable man.
§ After his injury, he became childish, irresponsible and thoughtless of others. He had severe temper outbursts and used profane language. He was unable to make plans or carry them out. He lost his job and was unable to keep a social network of friends.

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4
Q

what is the Research with Humans with regard to anger, aggression and impulse control

A

Early experiences can certainly foster development of aggressive behavior, but studies demonstrate that heredity plays significant role
• Several studies found that serotonergic neurons play inhibitory role in human aggression
• For example, a depressed rate of serotonin release (indicated by low levels of the serotonin metabolite 5-HIAA in the CSF) are associated with aggression and other forms of antisocial behavior, including assault, arson, murder, and child beating. Drugs that increase the amount of serotonin in the synapse (e.g. Prozac) decreases irritability and aggressiveness

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5
Q

explain RISKY BEHAVIOUR AND IMPULSE CONTROL and monkeys

A

The serotonin metabolite 5-HIAA was measured in the cerebrospinal fluid of young male rhesus monkeys, which were then tracked over 4 years.
The monkeys with the lowest levels of 5-HIAA were risk takers. They took dangerous unprovoked leaps between trees and were highly aggressive towards older, dominant males. They typically died early from attacks by stronger monkeys

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6
Q

Damage to the vmPFC causes what

A

serious and often debilitating impairments of behavioral control and decision-making

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7
Q

Damage to the vmPFC causes serious and often debilitating impairments of behavioral control and decision-making
• These impairments appear to be consequence of what

A

emotional dysregulation, as cognitive abilities are not strongly affected by damage to the vmPFC

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8
Q

what are the PHYSIOLOGICAL REGULATORY MECHANISMS

A 
System variable
set point
correctional mechanism
homeostasis
ingestive behaviour
negative feedback
satiety mechanism
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9
Q

what is Homeostasis

A

Process by which body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level

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10
Q

what is ingestive behaviour

A

Eating or drinking

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11
Q

what is System variable

A

Variable that is controlled by a regulatory mechanism

For example, temperature in a heating system.. if thermostat detects hotness it will stop the electric heater and if it is cold it will start the heater

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12
Q

what is set point

A

Optimal value of the system variable in a regulatory mechanism

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13
Q

what is correctional mechanism

A

In regulatory process, mechanism that is capable of changing value of system variable

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14
Q

what is Negative feedback

A

Process whereby the effect produced by a correctional mechanism serves to diminish or terminate the corrective action
Characteristic of regulatory systems

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15
Q

what is Satiety mechanism

A

Brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water

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16
Q

Thirst occurs when there is either…

A

1) not enough blood circulating in the body (volumetric thirst) or
2) there is too much salt in the blood (osmometric thirst).

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17
Q

what is Volumetric thirst

A

occurs when there is not enough blood circulating in the body, which is called hypovolemia. The heart needs a certain amount of blood to keep beating

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18
Q

Hypovolemia causes what

A

volumetric thirst

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19
Q

Hypovolemia causes volumetric thirst, which is why people feel an intense thirst after they lose lots of what

A

blood

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20
Q

what are the components of volumetric thirst

A

renin
Angiotensin
Subfornical organ

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21
Q

what is renin

A

Hormone secreted by kidneys that causes conversion of angiotensinogen in the blood into angiotensin

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22
Q

what is Angiotensin

A

Peptide hormone that constricts blood vessels, causes retention of sodium and water, and produces thirst and salt appetite

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23
Q

what is Subfornical organ

A

Small organ located at the junction between the lateral ventricles and the 3rd ventricle in the frontal lobe
Contains neurons that detect the presence of angiotensin in blood and excite neural circuits that initiate drinking

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24
Q

what does Tonicity refer to

A

the relative concentration of dissolved molecules (solutes) on either side of a semipermeable membrane. It is used to describe the direction and extent of water diffusion across a (cell) membrane

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25
Q

what are the three stages of Tonicity

A

Isotonic solution:

Hypotonic solution: Hypertonic solution:

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26
Q

what is Isotonic solution

A

similar solute concentrations are present inside and outside the cell. The cell will neither gain nor lose water.

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27
Q

what is Hypotonic solution

A

solute is less concentrated outside the cell than in, so water will enter the cell.

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28
Q

what is Hypertonic solution

A

solute is more concentrated outside the cell than in, so water will leave the cell.

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29
Q

Hypertonic solutions cause what

A

cellular dehydration (water leaves the cell).

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30
Q

what are Osmoreceptors

A

neurons that detect interstitial solute concentration; The membrane potential of osmoreceptors and their release of neurotransmitter relate to their volume (cell size).

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31
Q

Some neurons in the subfornical organ are what

A

osmoreceptors. Other neurons here are sensitive to angiotensin. Some neurons have both qualities

32
Q

Ingestion of hypertonic saline strongly activates what

A

the subfornical organ in humans in an FMRI machine

33
Q

The subfornical organ immediately returns to normal baseline activity upon what

A 
drinking water (before water has
reached the blood), which demonstrates the existence of a rapid feedback mechanism.
34
Q

Cold sensors in the mouth and sensory fibers in the stomach are part of what mechanism

A

the rapid feedback mechanism

35
Q

explain the effects of insulin and glucagon on glucose and glycogen

A

The pancreas detects blood glucose levels. When blood glucose levels are high, the pancreas releases insulin, which causes the body to store glucose as glycogen. When blood glucose levels are low, the pancreas releases glucagon, which causes the body to convert glycogen back into glucose.
• Cells internalize glucose with a glucose transporter. The glucose transporter that neurons have always works. Non-neuronal cells however, have a glucose transporter that only works when insulin is present. They have a insulin-dependent glucose transported.
• The insulin-dependence of the glucose transporter in non-neuronal cells means these cells can also use glucose for fuel when there is an excess of glucose around (signaled by insulin). When insulin is not around, non- neuronal cells have to use fatty acids for energy instead of glucose

36
Q

what is Glycogen

A

Polysaccharide often referred to as animal starch
Stored in liver and muscle
Constitutes the short-term store of nutrients

37
Q

what is insulin

A

Pancreatic hormone that facilitates 1) entry of glucose and amino acids into the cell’s of the body, 2) conversion of glucose into glycogen, and 3) transport of fats into adipose tissue

38
Q

what is Glucagon

A

Pancreatic hormone that promotes conversion of liver glycogen into glucose

39
Q

what is Triglyceride

A

Form of fat storage in adipose cells (fat cells). Constitutes the long-term store of nutrients
Consists of molecule of glycerol joined with three fatty acids

40
Q

what is Glycerol

A

Substance (also called glycerine) derived from breakdown of triglycerides, along with fatty acids
Can be converted by liver into glucose

41
Q

what is Fatty acid

A

Substance derived from breakdown of triglycerides, along with glycerol
Can be metabolized into sugars by most cells of body except for brain

42
Q

what are the parts of metabolism

A 
insulin
Glycogen
Glucagon
Triglyceride
Glycerol
Fatty acid
43
Q

decrease in blood glucose causes the pancreas to do what

A

stop secreting insulin and start secreting glucagon

44
Q

The absence of insulin means what

A

that most of cells of body can no longer use glucose. Thus, all glucose present in blood is reserved for central nervous system.

45
Q

Although many factors influence feelings of hunger (sights and sounds, smells and tastes, time of day and habits, thoughts, etc…), a particularly influential signal comes from what

A

the stomach when it is empty

46
Q

An empty stomach (or, more accurately, an empty duodenum) is communicated to the brain by the stomach’s release of what

A

a peptide hormone called ghrelin

47
Q

Levels of circulating ghrelin increase with hunger and fall with satiation. Exogenous administration of ghrelin does what

A

increases food intake.

aka makes you hungry

48
Q

WHAT STARTS A MEAL?

A

Ghrelin

Duodenum

49
Q

what is Ghrelin

A

Peptide hormone released by the empty stomach that increases eating
Also produced by neurons in the brain

50
Q

what is Duodenum

A

First portion of small intestine, attached directly to stomach. The presence or absence of food in the duodenum regulates the release of ghrelin from the stomach

51
Q

WHAT STOPS A MEAL?

A

Gastric Factors

Short-term satiety (fullness) signals are released by the stomach and duodenum immediately after eating, before food is digested .
(Swelling of the stomach causes a bloated feeling, but that is different than feeling full.)
• The most prominent among these are cholecystokinin (CCK) and PYY, which are secreted by the duodenum in response to food ingestion in proportion to the calories ingested. These and other satiety-related peptides correlate with feelings of fullness and inhibit food intake, but the effects are short lived. They mostly influence how long people eat for.
(CCK also regulates gastric motility and causes the gallbladder to release digestive enzymes into the duodenum.)
• The repeated administration of CCK and PYY to healthy individuals does not reliably cause sustained weight loss. It does decrease meal size, but the body will react with an increase in meal frequency.

52
Q

AFTER THE MEAL ENDS what heppens

A

The satiety produced by gastric factors and duodenal factors (CCK & PYY) is anticipatory (i.e. your cells haven’t received the nutrients yet).
• These factors predict that the food in digestive system will, when absorbed, eventually restore system variables that cause hunger
• Not until nutrients are absorbed from intestines can they be used to nourish the cells of body and replenish body’s nutrient reservoirs
• This stage of satiety appears to occur in the liver and pancreas, as they detect when food has been absorbed into the blood and is available to the body.
• The satiety signal released by the pancreas is insulin, which is actively trafficked across the blood brain barrier. There are neurons in the hypothalamus that express insulin receptors and their activity reduces feelings of hunger.
• The liver signals satiety through the vagus nerve

53
Q

In most people, body weight appears to be regulated how

A

over a long-term basis

54
Q

If a healthy animal is force-fed so that it becomes fatter than normal what happens

A

it will reduce its food intake once it is permitted to choose how much to eat

55
Q

what isLeptin

A

a circulating hormone that is secreted by adipocytes (fat cells). Leptin is thought to signal the size of peripheral energy stores in the body

56
Q

As fat cells (energy stores) grow and proliferate what happens to lepin

A

there is a concomitant increase in leptin levels in the blood stream. This leptin provides a negative homeostatic feedback signal that decreases hunger

57
Q

Exogenous administration of leptin does what to meal size

A

decreases meal size in healthy people

58
Q

Humans and animals can be born or become insensitive to leptin. A reduced ability to detect leptin levels increases what

A

hunger and causes obesity.

59
Q

Leptin receptors are located in many areas of the brain.

In the hypothalamus, leptin signaling does what

A

decreases food intake and increases metabolic rate, primarily by inhibiting AGRP/NPY neurons and activating POMC/a-MSH neurons in arcuate nucleus. Leptin also makes these neurons more sensitive to CCK and other satiety peptides

60
Q

Leptin receptors are also located on dopamine neurons that control what

A

the reinforcing value of stimuli, like food. Increases in leptin decrease the likelihood that people will desire (choose) to eat the same food again.

61
Q

what are The hedonic aspects of hunger

A

both the motivational and reinforcing properties of food fluctuate in accordance with hunger and available energy stores. Satiety or fullness reduces both the rewarding and reinforcing value of food. Hunger increases the rewarding and reinforcing value of food.

62
Q

what is Arcuate nucleus of the hypothalamus

A

Nucleus in base of hypothalamus that contains neurons highly sensitive to circulating levels of leptin.
Contains AGRP/NPY neurons and POMC/a-MSH neurons, which are involved in feeding and metabolic rate

63
Q

what is Paraventricular nucleus (PVN)

of the hypothalamus

A

Nucleus of hypothalamus that receives inputs from arcuate nucleus.
Contains oxytocin neurons that signal that body has adequate levels of leptin (fat)

64
Q

explain the Paraventricular Nucleus (PVN) of the Hypothalamus

A

The paraventricular nucleus (PVN) contains oxytocin neurons, whose activity signals that body has enough fat and inhibits hunger.
If PVN neurons have a low firing rate, below some threshold, animals will feel intense hunger.
Excess activity of PVN neurons does not prevent feeding triggered by other parts of the circuitry, so this region is thought to play a large role in low leptin-induced emergency feeding.

65
Q

what is the Prader-Willi Syndrome

A

Prader-Willi syndrome is a rare chromosomal abnormality in which up to 7 genes are deleted from chromosome 15. One of these genes is critical for the development/survival of oxytocin-containing neurons in the PVN.
People with Prader-Willi syndrome are born with very low muscle mass and have little interest in eating. But later, between 2 and 8 years old, these people develop a heightened, permanent and painful sensation of hunger, a feeling of starving to death. Average life expectancy in the United States is 30; most die of obesity-related causes.
People with this disorder have no sensations of satiety to tell them to stop eating or to throw up, so they can accidentally consume enough food in a single binge to fatally rupture their stomach.

66
Q

what are Emergency circuits

A

activated when a specific critical need to eat or not eat overrides energy homeostasis circuitry

67
Q

what are the 2 emergency circuits

A

Glucoprivation

Lipoprivation

68
Q

what is Glucoprivation

A

Dramatic fall in level of glucose available to cells (detected in liver and brain)
Can be caused by a fall in blood level of glucose or by drugs that inhibit glucose metabolism

69
Q

what is Lipoprivation

A

Dramatic fall in level of fatty acids available to cells (detected in liver and brain)
Usually caused by drugs that inhibit fatty acid metabolism

70
Q

what is Hypoglycemia

A

low blood sugar

71
Q

for hypoglycaemia….When the brain senses that it does not have enough glucose (sugar) to support normal brain function (via glucose-sensing neurons in various regions of the brain), it launches an emergency cascade of effects: explain them

A

Suppresses insulin secretion to keep sugar in the blood
• Triggers glucose production in the liver
• Slows energy expenditure (basal metabolic rate) and halts growth and reproduction related systems
• Promotes a potent and sustained feeling of hunger

72
Q

Hypoglycemia-induced feeding overrides energy homeostatic mechanisms, and this does what

A

Hypoglycemia-induced feeding overrides energy homeostatic mechanisms, in that it can stimulate feeding irrespective of body fuel stores (indicated by leptin and insulin levels).
• Excess insulin will also trigger this kind of eating, because insulin causes glucose to leave the blood and enter fat and muscle tissue

73
Q

explain Lipoprivation in its basic terms

A

Not enough fat

74
Q

explain Lipoprivation

A

When the brain senses dangerously low leptin levels, it believes the body has no stored energy (fat) to support the energy homeostasis system. So, it launches an emergency cascade of effects that are almost identical to those observed in response to low blood sugar:
Glucose production is increased, insulin production is decreased, metabolic rate is slowed, and a profound hunger takes hold.
Dangerously low levels of glucose (immediately available fuel) and dangerously low levels of fat (stored fuel via leptin signalling) trigger the same emergency feeding circuits that aim to raise blood glucose levels.
Disruptions in insulin signaling results in high blood sugar (hyperglycemia), because the sugar is not trafficked from the blood and into fat and muscle tissue. Without treatment, this will cause progressive weight loss and a loss of body fat. Without fat cells to release the hormone leptin, leptin levels plunge. Low leptin will initiate a intense hunger (a feeding emergency) even if the person is hyperglycemic (too much sugar in blood).

75
Q

The system in overweight individuals seems to be doing what

A

actively defending elevated levels of body fat. Their bodies have an elevated leptin set point that they are trying to maintain, and they have a blunted response to increases in leptin levels

76
Q

The system in overweight individuals seems to be actively defending elevated levels of body fat. Their bodies have an elevated leptin set point that they are trying to maintain, and they have a blunted response to increases in leptin levels.
…. what is this called

A

This is called leptin resistance

77
Q

In different populations of overweight animals, people have observed:

A

Ø a reduction in leptin’s ability to cross the blood-brain barrier
Ø a reduction in the neuronal response to leptin signalling
Ø a reduction in the downstream consequences of leptin-signalling neurons
After several days of eating a cafeteria-style diet (high fat, high sugar), inflammation has been observed in the hypothalamic arcuate nucleus of rodents.
This results in a decreased sensitivity to leptin. These animals require more leptin in the blood (more fat cells) to maintain their energy homeostatic set point.

U1 Behavioural Neurological Psychology 211 (22 decks)

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