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Final Exam Flashcards

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1
Q

The different hypothalamic nuclei involved in regular hunger and satiety involved in regulating (hunger, satiety, or both)

A

Lateral hypothalamus
ventromedial hypothalamus
arcuate nucleus

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2
Q

Lateral hypothalamus

A

the hunger center (neurons that trigger hunger behaviors)

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3
Q

ventromedial hypothalamus (VHM) and Paraventricular Nucleus (PVN)

A

satiety centers (tell us when we’re full and change our behaviors accordingly)

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4
Q

arcuate nucleus

A

regulates both hunger and satiety

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5
Q

The neurotransmitters associated with the satiety pathway

A

melanocyte stimulating hormone activates VMH and RVN neurons and they release the hormones CRH

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6
Q

The neurotransmitters associated with the hunger pathway

A

neuropeptide y (NPY) activated LH neurons and inhibits VMH and PVN satiety center neurons and the LH hunger neurons release orexin

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7
Q

What are the different satiety signals

A

Cholecytokinin (CCK)
Glucose
Insulin
Leptin

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8
Q

cholectokinin (cck)

A

a peptide released by the stomach when it has food in it

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9
Q

glucose

A

blood levels rise during absorption

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10
Q

insulin

A

released by pancreas during absorption of tryptophan an amino acid

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11
Q

leptin

A

released by fat cells when they are taking up fat

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12
Q

What are the different hunger signals

A

Ghrelin
low glucose
endocannabinoids

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13
Q

Ghrelin

A

a peptide released by the stomach when its empty

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14
Q

endocannabinoids

A

endogenous cannabinoids; their production in the hypothalamus is inhibited by leptin

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15
Q

What are the consequence of defects in leptin signaling and how this is related to human obesity?

A

Defects in leptin signaling usually lead to hyperphagia which leads to obesity
-most human obesity is environmental not genetic, leptin levels are normal even elevated in most obese humans

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16
Q

What are the factors influencing when we eat

A

work schedules, family routines, culture norms, personal preferences, food availability

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17
Q

What are the factors influencing how much we eat

A

exertion, cultural norms, emotion, social setting, “cafeteria effect”, “appetizer effect”

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18
Q

Example of social settings influencing how much we eat

A

you already ate but your friends go out to dinner and you go too

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19
Q

the “cafeteria effect”

A

eating one food decreases the desire for that food but having other foods available will cause you to continue eating because your desire for them has not been reduced as much

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20
Q

“appetizedr effect”

A

eating a small amount of food often increases hunger

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21
Q

the additional brain regions that influence that eating behaviors discussed in class

A

amygdala
hippocampus
inferior frontal lobe
reward centers of the brain

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22
Q

how does the amygdala influence eating behaviors

A

regulates emotion; provides input the hypothalamus about food references, emotional states stress, etc

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23
Q

how does the Hippocampus and medial temporal lobe influence eating behaviors

A

memory storage; provides input to hypothalamus about how recently we ate, how filling it was, how nutricious and good tasting it was and learned craving etc.

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24
Q

how does the inferior frontal lobe influence eating behaviors

A

recieves input from the olfactory bulb about smells and taste provides input the hypothalamus about pleasurable sensory info related to food

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25
Q

reward centers of the brain

A

provides input to the hypothalamus about pleasure

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26
Q

The pattern of EEG waves of wakefulness

A

characterized by small and rapid EEG waves

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27
Q

The pattern of EEG waves of “slow wave” sleep

A

characterized by larger slower EEG waves

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28
Q

The pattern of EEG waves of “fave wave” sleep

A

a return to the small and rapid EEG waves wakefulness

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29
Q

The EEG, EMG, EOG, of wakefulness

A

short rapid EEG waves, high EOG activity, high EMG activity

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30
Q

The EEG, EMG, EOG, of NREM sleep

A

larger slower EEG waves, no EOG activity, less EMG activity

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31
Q

The EEG, EMG, EOG, of REM sleep

A

short rapid EEG waves, high EOG activity, No EMG activity

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32
Q

EEG

A

measures electrical activity in the brain

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33
Q

EOG

A

measures the movement of the eyes

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34
Q

EMG

A

measures electrical activity of the muscles, particularly of the neck

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35
Q

Characteristics of NREM sleep

A

larger, slower EEG waves, Less EMG and no EOG activity

  • accounts most most of sleep in adults (6 or 8 hours)
  • less dreaming, but night terrors in children
  • characterized by the most movement - flailing tossing and turning, sleep walking
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36
Q

Characteristics of REM sleep

A
  • short rapid EEG, no EMG, high EOG
  • motor neuron activity is inhibited- muscles occasionally twitch, but large movements are not common
  • much more dreaming and more vivid, narrative dreams
  • accounts for about 2 hours of sleep in adults between bouts of NREM sleep
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37
Q

arguments for REM sleep

A
  • nearly all mammals and many birds REM sleep
  • if deprived of REM sleep, a person experiences, “REM REBOUND”- increased tendency to go into REM sleep and have more REM sleep per sleep session
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38
Q

arguments against REM sleep

A
  • some animals-whales for example have very little REM if any sleep
  • Nearly all anti-depressand medication suppress REM sleep partly or completely and patients who take them go months without REM
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39
Q

The different characteristics of dreaming and it’s hypothesized functions and how activity of specific brain regions is changed in ways consistent with these different functions

A
  • dreams appear to take place in real time
  • dreams often contain conflict or negative emotional states
  • everyone dreams, typically multiple times a night and they last longer as the sleep session progresses
  • sensory info is occasionally incorporated
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40
Q

Know the different proposed function of sleep and the arguments for and against them

A
  • sleep appears to be important in the consolidation of explicit and implicit memory
    • NREM sleep: spatial and explicit memory
    • REM sleep: Implicit mem
  • sleep as a means to solve problems
  • sleep improves mood and blunts emotionally traumatic memories
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41
Q

the different brain nuclei involved in wakefulness and sleep

A

Reticular activating system (RAS)
basal forebrain
hypothalamus

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42
Q

The reticular activating system’s neurotransmitters in reference to to wakefulness and sleep

A

norepinephrine, histamine, dopamine

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43
Q

Basal forebrain neurotransmitters in reference to to wakefulness and sleep

A

acteylcholine

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44
Q

Hypothalamus neurotransmitters in reference to to wakefulness and sleep

A

wakefulness-acetylcholine, serotonin, histamine, or orexin (all exicatory Nts)

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45
Q

Lateral Hypothalamus neurotransmitters in reference to to wakefulness and sleep

A

orexin

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46
Q

VLPO Hypothalamus neurotransmitters in reference to to wakefulness and sleep

A

GABA

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47
Q

Does orexin promote sleep or wakefulness?

A

wakefulness and arousal

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48
Q

Does GABA promote sleep or wakefulness?

A

sleep

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49
Q

Does Acetylcholine promote sleep or wakefulness?

A

norepinephrine, serotonin, dopamine, histamine, orexin, exicatory neurotransmitters–increased arousal and wakefulness

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50
Q

Does Melatonin promote sleep or wakefulness?

A

sleep

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51
Q

Does adenosine promote sleep or wakefulness?

A

sleep

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52
Q

Circadian rhythms

A

24 hours rhythms-Daily cycels of physiological, metabolic, biochemical and behavioral processes sleep wake cycles, eating, hormone release temp

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53
Q

Zeitgebers

A

environmental cues about time such as daylight

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54
Q

ex. zeitgebers

A

the level of the hormone melatonin rises in your body during the day

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55
Q

How do the SCN regulate sleep-wake cycles

A

cluster of neurons in the hypothalamus that receives input form eyes which increases action potential firing

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56
Q

How does the pineal gland regulate pineal gland sleep wake cycles

A

receives inhibitory input from SCN releases melatonin, which produces drowsiness and regulates body rhythms

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57
Q

what are the functions of the pineal gland with respect to hormone secretion

A

receives inhibitory input from the SCN, releases melatonin, which produces drowsiness and regulates body rhythms

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58
Q

Insomnia

A

prolonged inability to sleep, not just fallin asleep but staying asleep and poor sleep quality
-may be caused by defects in LPD activation and GABA release on over activation of the reticular activation system

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59
Q

narcolepsy

A

uncontrollable falling asleep at inapropriate times

  • often accompanied by disturbed nocturnal slee
  • may occur as a result of defects in reticular activating system or lateral hypothesis neuron function
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60
Q

What are the 7 main sites of drug action

A 
NT synthesis
NT storage
NT Release
Receptor interaction 
inactivation 
reuptake
degredation
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61
Q

What are side effects of a drug action

A

additional physiological or psychological effects of a drug besides the one intended

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62
Q

What causes side effects of a drug action

A

often arise because NT are used in amy different places throughout the brain and body

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63
Q

drugs are metabolized through

A

often by the liver

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64
Q

rugs are eliminated through

A

by the kidneys or gut

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65
Q

drugs are sequestered

A

in fat or other cells or fluid

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66
Q

drugs are degraded

A

by uptake by neurons or glia

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67
Q

Drug addiction

A

persisten use of a substance despite problems related to use of the substance

68
Q

tolerance

A

need to increase dosage just to maintain results

69
Q

Dependance

A

to need to regularly use and or unsuccesful effort to reduce or control use of a drug or substance

70
Q

Withdrawl

A

a group of physical and psychological symptoms that occurs upon discontinuation or decrease in the intake of a drug

71
Q

What are the 3 types of tolerance

A

Metabolic or pharmakinetic
cellular or pharmacodynamic
behavioral or psychological

72
Q

metabolic or pharmakinetic tolerance

A

an increase in the number of enzymes breakin down a drug in the liver, blood or brain

73
Q

Cellular or pharmacodynamic tolerance

A

response to the drug is decreased at the neuron

74
Q

behavioral or psychological tolerance

A

adaptations to the effect of a drug

75
Q

what is the most common mechanism of cellular tolerance

A

decreased post synaptic receptor density

76
Q

The different types of behavioral tolerance

A

behavioral adaptation
leaned tolerance
environmental

77
Q

behavioral adaptation

A

ability to act unaltered by high levels of drug because of repeated use and familiarity with the effects of the drug

78
Q

learned tolerance

A

performing a task when under the influence of a substance improves performance of the task when under the influence of the substance

79
Q

environmental dependent tolerance

A

the development of tolerance to alcohol’s effects over several drinking session is accelerated if alcohol is always administered in the same environment or is accompanied by the same cues

80
Q

Definition of stress

A

stress is a stimulus that challenges the body’s homeostasis and triggers arousal

81
Q

Example of acute stress

A

exams, work deadlines, minor car accident, arguments with significant other, asked to speak in front of a group

82
Q

Example of chronic stress

A

stressful job, college, bad roommates, high pressure job, being bullied, daily commuting

83
Q

example of chronic stress

A

close death in the family, sexual or physical abuse, being in a natural disaster

84
Q

The 2 different neuroendocrine pathways associated with the stress response

A

Sympathetic nervous system

The hypothalamic/pituitary/ adrenal (HPA) asis

85
Q

The sympathetic nervous system

A

the “rapid” neural response that increases bodily arousal

86
Q

the hypothalamic/pituitary/adrenal (HPA) axis

A

more long term hormonal responses (longer term reaction to stress)

87
Q

The main effects of the sympathetic nervous system discussed in class

A

people with anxiety may either have elevated exicatory input to the amygdala or decreased inhibitory GABA input. Basically it increases the strength of the signal being sent to the HPA and SNS

88
Q

What are the main effects of acute HPA axis activation

A
  • breakdown of muscle protein for amino acids
  • increased uptake of amino acids and gluconeogenesis in the liver
  • breakdown of stored fats in adipose (less fat)
  • suppression of immune system
  • suppression of bone and muscle growth
  • suppression of reproductive function
89
Q

all of the various structure and neurotramsitters involved in inactivating the HPA axis and/or stress response

A
  • cortisol binds to receptors on the hypothalamus and decreases then firing and release CRF
  • cortisol bindos to receptors on the pituitary and decreases its release of ACTH
  • cortisol binds to the hippocampal neurons and increase their inhibitory firing to the hypothalamus it will basically stop them from firing
  • oxytocin– inhibits brain fear and stress pathways by inhibiting amygdala and hypothalamus neurons firing (makes you relax)
  • Endocannabinoid– inhibits chronic stress activation
90
Q

What are the main negative health outcomes of chronic stress and are associated with chronic SNS or with HPA activation

A
  • Immune system dysfunction (associated with HPA activation)
  • Cardio vascular disorders (associated with SNS)
  • GI Issues (associated with both SNS and HPA activation)
91
Q

Immune system dysfunction in association with HPA activation (in reference to stress response)

A

Chronic HPA activation result in chronically elevated cortisol levels

92
Q

Cardio vascular disorders– chronically elevated SNS activity (in reference to stress response)

A
  • elevated heart rate and constriction of blood vessels cause high blood pressure and increased risk of stroke
93
Q

Cardio vascular disorders –stress induced disruptions in metabolism due to SNS and cortisol (in reference to stress response)

A

may also contribute to insulin insensitivity and risk of diabetes, atherosclerosis and risk of heart attack

94
Q

GI Issues–chronically elevate cortisol from the HPA axis

A

is a contributing factor to the formation of GI ulcers

95
Q

GI Issues– elevated SNS activity

A

results in disruptions to GI motility and function causing a wide range of GI issues including nausea, indigestion, constipation

96
Q

What are the 3 different models regarding emotion

A

common sense theory
James-Lange model
Cannon- bard model

97
Q

Common sense theory of emotion

A

feeling comes first then physiological reactions
ex: i tremble because I feel afraid
(see a vicious, feel fear, react by trembling)

98
Q

James-Lange model

A

physiological reaction, then feeling
ex:i feel afraid because I’m trembling
(see a vicious dog start trembling, feel fear)

99
Q

Cannon-Bard Model

A

feeling physiological reaction occur in parallel
ex: the dog makes me tremble and feel afraid
(see dog, react and feel fear at the same time)

100
Q

What are the different characteristics of facial expressions as they pertain to emotion

A
  • Anger, fear, disgust, surprise, happiness, and sadness all have distinct facial expressions (same across cultures)
  • People in different part of the world make and interpret similar facial expression
  • smiling can cause us to feel happier
  • fake smiles can be distinguished from real ones
  • not all emotions are accompanied by facial expressions, so they are’t automatic or necessary part of the emotional response
101
Q

what are the different brain regions involved in emotions

A

prefrontal cortex
limbic system
hypothalamus
sympathetic nervous system

102
Q

Prefrontal cortex in reference to emotion

A

important in both the conscious perception and modulation of emotion

103
Q

Limbic system in reference to emotion

A

set off nuclei that integrate sensory and cortical inputs and determine proper emotional response

104
Q

Hypothalamus in reference to emotion

A

critical for activating hormonal inputs for physiological arousal responses

105
Q

Sympathetic nervous system in reference to emotion

A

produces physiological arousal

106
Q

The different components of emotional circuit of the brain

A

sensory association cortex
prefrontal cortex
cingulate cortex
amygdala

107
Q

sensory association cortex in reference different components of emotional circuit of the brain

A

provides into about emotionally relevant stimuli

108
Q

prefrontal cortex (PFC) in reference different components of emotional circuit of the brain

A

receives input from the SAC and helps decide on a plan of action and inhibits inapropriate emotional responses

109
Q

cingulate cortex (CC) in reference different components of emotional circuit of the brain

A

critical for activating hormonal inputs for physiological arousal responses

110
Q

Amygdala in reference different components of emotional circuit of the brain

A

sened and receives input from SAC, PFC, CC and determines how much to activate the hypothalamus

111
Q

What are the effects of lesions on the amygdala

A

results in loss of fear response / electrical stimulation produces produces a fear response

112
Q

The effects of lesions on the prefrontal cortex

A

can cause increased impulsive aggression

113
Q

the effects of lesions on the septum

A

also increased aggression

114
Q

What is the role of the amygdala in emotional processes

A
  • important in evaluating emotional salience of situation emotional?
  • what level of emotion is appropriate?
  • activation of the fear response
115
Q

The relationship between testosterone and the different types of aggression in animals

A
  • more testosterone = more aggressions
  • animal castration decreases aggression behavior and injecting testosterone brings aggression back
  • in animal, testosterone may be permissive for and exaggerate existing levels of social aggression
116
Q

The relationship between testosterone and the different types of aggression in humans

A

more testosterone = more aggression

in humans, testosterone appears to be associated with social reward which may or may not require aggression

117
Q

What are the different functions or roles of oxytocin

A
  • levels increase during maternal bonding, and after sex in both sexes
  • may foster trust and love
  • inhibits amygdala activation, decreasing the fear, aggression and stress responses
  • can increase suspicion of outsiders
118
Q

What are the other “happy molecules” increase positive aspects of brain function and behavior

A

dopamine
endogenous opiates
endocannbinoids
serotonin

119
Q

Dopamine reference to increasing positive brain function and behavior

A

involved in mesolimbic antipatory pleasure reward pathway

120
Q

Endogenous opiates reference to increasing positive brain function and behavior

A

pain suppression (analgesia), euphoria, relaxation

121
Q

Endocannbinoids in reference to increasing positive brain function and behavior

A

analgesia, euphoria, relaxation, stress reduction

122
Q

serotonin reference to increasing positive brain function and behavior

A

involved in awakeness / alertness and satiety; low levels of serotonin may be associated with depression

123
Q

Hypothalamus in reference different components of emotional circuit of the brain

A

activates body’s arousal mechanisms through the SNS and HPA axes

124
Q

definition of an antagonist

A

any drug that decreases neurotransmission

125
Q

Example of Agonists

A
  • black widow spider bite venom–increases release
  • nicotine– activates receptors
  • physostigmine-blocks inactivation
126
Q

Example of antagonists

A
  • choline(poor diet)–decreases synthesis
  • Botulinium toxin– inhibits release
  • Curare–blocks receptors
127
Q

definition of side effects

A

additional physiological or psychological effects of a drug beside the one intended

128
Q

definition of antagonist

A

is any drug that decreases neurotransmission

129
Q

2 components of anxiety

A

cognitive anxiety

somatic anxiety

130
Q

cognitive anxiety

A

psychological thought, within the brain feeling of nervousness, worry or apprehension

131
Q

Somatic anxiety

A

physical symptoms including increased heart rate

132
Q

example of somatic anxiety

A

increased heart rate, increased breathing and sweating

133
Q

State anxiety

A

mood characterized by cognitive and somatic symptoms of anxiety

134
Q

trait anxiety

A

a predisposition that influences behavior

135
Q

anxiety disorder

A

a mental disorder that includes chronic feelings of worry and anxiety without any rational cause

136
Q

what are the different brain regions of the emotional circuit are altered in the brains of anxiety disorder patients

A

cingulate cortex
ventromedial
amygdala
locus ceoruleus

137
Q

Cingulate cortex in reference to anxiety disorder patients

A

involved in threat and conflict assessment, size is increased in anxiety disorder patients

138
Q

Ventromedial prefrontal cortex in reference to anxiety disorder patients

A

inhibits negative emotional responses. decreased size in people with anxiety disorders

139
Q

amygdala in reference to anxiety disorder patients

A

activates stress response. Larger in anxiety patients

140
Q

locus coeruleus in reference to anxiety disorder patients

A

HPA, SNS activate by the hypothalamus and can be overly active

141
Q

What are the neural basis for anxiety in the amygdala?

A
  • The amygdala is involved with transmitting fear signals to the hypothalamus and activating the SNS and the HPA axis
  • PPL with anxiety disorder may have either elevated or exicatory input to the amygdala or decreased inhibitory GABAergic input
  • amygdala neurons can also increase in dendritic branching in anxiety suffers
  • anxiolytic drugs like benzodiazapines increase GABA signaling and reduce anygdala activation of the hypothalamus
142
Q

What are the neurotransmitters assiociated with the monoamine hypothesis of depression

A

serotonin
dopamine
norepinephrine

143
Q

serotonin in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with

A

involved in sleep, eating, mood and depressed patients have mood problems as well as vegetative symptoms of sleep and eating disruptions

144
Q

Dopamine in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with

A

involved in pleasure and reward and depressed patients have anhedonia or lack of pleasure

145
Q

Norepinephrine in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with

A

involved in arousal and depressed patients have psychomotor retardation or lethargy and decreased arousal

146
Q

what are the arguments against the monoamine hypothesis of depression

A
  • anti-depressant medications are only effective for about 25%-50 of depressed patients and are completely inaffetive for about 20% of depressed patients
  • monoamine depletion does not worsen symptoms in depressed patients not taking medication, nor does it cause depression in healthy volunteers with no depressive illness
  • the effects of many anti depressant medications take weeks to improve depression even though monoamine levels increase almost immediately
147
Q

What is the role of BDNF and neurogenesis in depression and the evidence supporting these roles in depression

A
  • neurotrotrophins such as BDNF promote long term potentiation, dendritic branching and hippocampal neurogensis and neuronal survival
  • BNDF levels are decreased by stress and in depressed patients
  • Neurogenesis and dentritic branching are impaired are impaired and hippocampal size is decreased in depressed patients
  • monoamine synaptic transmission increase BDNF release
  • anti-depression increase BDNF levels and increase dendritic branching and neurogenesis is in hippocampus and blocking BDNF inhibits the beneficial effects of anti depressants
148
Q

What are the 7 classes of drugs

A
  • Anti-anxiety agents and sedatives
  • antipsychotic agents
  • antidepressants
  • mood stabilizers
  • opioid analgesics
  • psychomotor stimulants
  • psychadelics and hallucinogens
149
Q

What are the conditions for anti-anxiety agents and sedatives for which this drug might be prescribed or used

A

low doses: they reduce anxiety; at medium doses they sedate at
high doses: they anethesize

150
Q

What are the conditions for antipsychotic agents for which this drug might be prescribed or used

A

reduce motor activity, wild moods, and disconnected thoughts in schizophrenics

151
Q

What are the conditions for anti-depressants for which this drug might be prescribed or used

A

treating clinical depression

152
Q

What are the conditions for mood stabilizers for which this drug might be prescribed or used

A

important in treating bipolar disorder (manic depressive illness)

153
Q

What are the conditions for opiod analgesics for which this drug might be prescribed or used

A

narcotics and pain relievers or producing feeling of euphoria or intense calm pleasure

154
Q

What are the conditions for psychomotor stimulants for which this drug might be prescribed or used

A

increase motor and alertness and elevate mood

155
Q

What are the conditions for psychadelics and hallucinogens for which this drug might be prescribed or used

A

cancer patients going through chemo

156
Q

What are the actions of anti-anxiety drugs with respect to their action on the GABA receptor/ion channel

A

enhance binding of GABA to CL- channel/receptor

157
Q

What are the actions of sedatives with respect to their action on the GABA receptor/ion channel

A

open GABA and CL- channel

158
Q

What are the actions of both sedatives and anti anxiety drugs with respect to their action on the GABA receptor/ion channel

A

increase the flow of CL- into post synaptic neurons, FLow of CL- into post synaptic neuron hyperpolarizes it . Hyper polarized neuron is less likely to fire an action potential. Both globally decrease neuronal firing in CNS. Which decreases arousal
MAIN EFFECTS of overdose include drowsiness, decreased arousal, coma and death

159
Q

How do anti depressants influence dopamine

A
  • reduce dopamine levels

- MAO inhibitors inhibit breakdown of serotonin, dopamine, norepinephrine

160
Q

how do psychomotor stimulants influence dopamine levels

A

-stimulates dopaminergic neurons to release dopamine by binding to acetylcholine receptors on dopaminergic neruons and activating them

161
Q

How do opiod analgeiscs stimulants influence dopamine levels

A

inhibit reuptake of dopamine

more dopamine bind to its receptor on the post synaptic cell

162
Q

How does THC influence synaptic transmission

A

THC binds to endogenous cannabinoid receptors CB1 and CB2 on presynaptic neuron and closes the voltage gated Ca2+ channel
Closing of Ca2+ channel decreases influx of Ca2+ into presynaptic cell, which results in less neurotransmitter release
-By inhibiting neuronal firing in the basal ganglia and cerebellum, THC decreases motor behavior
-By inhibiting neuronal firing/LTP in the hippocampus, THC decreases memory
-By inhibiting neuronal firing of pain sensory neurons, THC inhibits pain sensation
-By inhibiting neuronal firing in the cortex, THC slows cognition
-By inhibiting GABAergic neurons synapsing on hunger neurons in the lateral hypothalamus, THC increases appetite

163
Q

what are the cellular mechanisms involved in tolerance with respect to the reward systems of the brain

A

May occur because of adaptations in the dopaminergic pathways that decrease dopamine synthesis, release, receptor binding, etc. so that greater amounts of drug are needed to achieve the same dopamine release

164
Q

what are the cellular mechanisms involved in withdrawal with respect to the reward systems of the brain

A

May represent the greatly reduced signaling through this pathway when drug use is discontinued

165
Q

What is the role of the mesolimbic pathway in eating behaviors?

A

neurons in the ventral tegmental area release dopamine onto neurons in the hippocampus, nucleus accumbens and the frontal cortex. Dopamine stimulation int the nucleus accumbens increases the anticipation of the stimulus (food). Dopamine is invoved in teh want of the pleasure and reward.

166
Q

How is the role of the mesolimbic pathway defective in obesity?

A

In some obese patients, dopamine receptor levels decreased in the nucleus accumbens which may cause them to over eat to compensate for low levels of pressure.
-in obese patients who binge eat dopamine is being released in response to cues and recieve a higher level of want than normal

Bio Psychology (11 decks)

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