Final Exam Flashcards
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
2
Q
Lateral hypothalamus
A
the hunger center (neurons that trigger hunger behaviors)
3
Q
ventromedial hypothalamus (VHM) and Paraventricular Nucleus (PVN)
A
satiety centers (tell us when we’re full and change our behaviors accordingly)
4
Q
arcuate nucleus
A
regulates both hunger and satiety
5
Q
The neurotransmitters associated with the satiety pathway
A
melanocyte stimulating hormone activates VMH and RVN neurons and they release the hormones CRH
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
7
Q
What are the different satiety signals
A
Cholecytokinin (CCK)
Glucose
Insulin
Leptin
8
Q
cholectokinin (cck)
A
a peptide released by the stomach when it has food in it
9
Q
glucose
A
blood levels rise during absorption
10
Q
insulin
A
released by pancreas during absorption of tryptophan an amino acid
11
Q
leptin
A
released by fat cells when they are taking up fat
12
Q
What are the different hunger signals
A
Ghrelin
low glucose
endocannabinoids
13
Q
Ghrelin
A
a peptide released by the stomach when its empty
14
Q
endocannabinoids
A
endogenous cannabinoids; their production in the hypothalamus is inhibited by leptin
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
16
Q
What are the factors influencing when we eat
A
work schedules, family routines, culture norms, personal preferences, food availability
17
Q
What are the factors influencing how much we eat
A
exertion, cultural norms, emotion, social setting, “cafeteria effect”, “appetizer effect”
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
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
20
Q
“appetizedr effect”
A
eating a small amount of food often increases hunger
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
22
Q
how does the amygdala influence eating behaviors
A
regulates emotion; provides input the hypothalamus about food references, emotional states stress, etc
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.
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
25
reward centers of the brain
provides input to the hypothalamus about pleasure
26
The pattern of EEG waves of wakefulness
characterized by small and rapid EEG waves
27
The pattern of EEG waves of "slow wave" sleep
characterized by larger slower EEG waves
28
The pattern of EEG waves of "fave wave" sleep
a return to the small and rapid EEG waves wakefulness
29
The EEG, EMG, EOG, of wakefulness
short rapid EEG waves, high EOG activity, high EMG activity
30
The EEG, EMG, EOG, of NREM sleep
larger slower EEG waves, no EOG activity, less EMG activity
31
The EEG, EMG, EOG, of REM sleep
short rapid EEG waves, high EOG activity, No EMG activity
32
EEG
measures electrical activity in the brain
33
EOG
measures the movement of the eyes
34
EMG
measures electrical activity of the muscles, particularly of the neck
35
Characteristics of NREM sleep
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
36
Characteristics of REM sleep
- 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
37
arguments for REM sleep
- 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
38
arguments against REM sleep
- 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
39
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
- 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
40
Know the different proposed function of sleep and the arguments for and against them
- 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
41
the different brain nuclei involved in wakefulness and sleep
Reticular activating system (RAS)
basal forebrain
hypothalamus
42
The reticular activating system's neurotransmitters in reference to to wakefulness and sleep
norepinephrine, histamine, dopamine
43
Basal forebrain neurotransmitters in reference to to wakefulness and sleep
acteylcholine
44
Hypothalamus neurotransmitters in reference to to wakefulness and sleep
wakefulness-acetylcholine, serotonin, histamine, or orexin (all exicatory Nts)
45
Lateral Hypothalamus neurotransmitters in reference to to wakefulness and sleep
orexin
46
VLPO Hypothalamus neurotransmitters in reference to to wakefulness and sleep
GABA
47
Does orexin promote sleep or wakefulness?
wakefulness and arousal
48
Does GABA promote sleep or wakefulness?
sleep
49
Does Acetylcholine promote sleep or wakefulness?
norepinephrine, serotonin, dopamine, histamine, orexin, exicatory neurotransmitters--increased arousal and wakefulness
50
Does Melatonin promote sleep or wakefulness?
sleep
51
Does adenosine promote sleep or wakefulness?
sleep
52
Circadian rhythms
24 hours rhythms-Daily cycels of physiological, metabolic, biochemical and behavioral processes sleep wake cycles, eating, hormone release temp
53
Zeitgebers
environmental cues about time such as daylight
54
ex. zeitgebers
the level of the hormone melatonin rises in your body during the day
55
How do the SCN regulate sleep-wake cycles
cluster of neurons in the hypothalamus that receives input form eyes which increases action potential firing
56
How does the pineal gland regulate pineal gland sleep wake cycles
receives inhibitory input from SCN releases melatonin, which produces drowsiness and regulates body rhythms
57
what are the functions of the pineal gland with respect to hormone secretion
receives inhibitory input from the SCN, releases melatonin, which produces drowsiness and regulates body rhythms
58
Insomnia
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
59
narcolepsy
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
60
What are the 7 main sites of drug action
```
NT synthesis
NT storage
NT Release
Receptor interaction
inactivation
reuptake
degredation
```
61
What are side effects of a drug action
additional physiological or psychological effects of a drug besides the one intended
62
What causes side effects of a drug action
often arise because NT are used in amy different places throughout the brain and body
63
drugs are metabolized through
often by the liver
64
rugs are eliminated through
by the kidneys or gut
65
drugs are sequestered
in fat or other cells or fluid
66
drugs are degraded
by uptake by neurons or glia
67
Drug addiction
persisten use of a substance despite problems related to use of the substance
68
tolerance
need to increase dosage just to maintain results
69
Dependance
to need to regularly use and or unsuccesful effort to reduce or control use of a drug or substance
70
Withdrawl
a group of physical and psychological symptoms that occurs upon discontinuation or decrease in the intake of a drug
71
What are the 3 types of tolerance
Metabolic or pharmakinetic
cellular or pharmacodynamic
behavioral or psychological
72
metabolic or pharmakinetic tolerance
an increase in the number of enzymes breakin down a drug in the liver, blood or brain
73
Cellular or pharmacodynamic tolerance
response to the drug is decreased at the neuron
74
behavioral or psychological tolerance
adaptations to the effect of a drug
75
what is the most common mechanism of cellular tolerance
decreased post synaptic receptor density
76
The different types of behavioral tolerance
behavioral adaptation
leaned tolerance
environmental
77
behavioral adaptation
ability to act unaltered by high levels of drug because of repeated use and familiarity with the effects of the drug
78
learned tolerance
performing a task when under the influence of a substance improves performance of the task when under the influence of the substance
79
environmental dependent tolerance
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
Definition of stress
stress is a stimulus that challenges the body's homeostasis and triggers arousal
81
Example of acute stress
exams, work deadlines, minor car accident, arguments with significant other, asked to speak in front of a group
82
Example of chronic stress
stressful job, college, bad roommates, high pressure job, being bullied, daily commuting
83
example of chronic stress
close death in the family, sexual or physical abuse, being in a natural disaster
84
The 2 different neuroendocrine pathways associated with the stress response
Sympathetic nervous system
| The hypothalamic/pituitary/ adrenal (HPA) asis
85
The sympathetic nervous system
the "rapid" neural response that increases bodily arousal
86
the hypothalamic/pituitary/adrenal (HPA) axis
more long term hormonal responses (longer term reaction to stress)
87
The main effects of the sympathetic nervous system discussed in class
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
What are the main effects of acute HPA axis activation
- 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
all of the various structure and neurotramsitters involved in inactivating the HPA axis and/or stress response
- 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
What are the main negative health outcomes of chronic stress and are associated with chronic SNS or with HPA activation
- Immune system dysfunction (associated with HPA activation)
- Cardio vascular disorders (associated with SNS)
- GI Issues (associated with both SNS and HPA activation)
91
Immune system dysfunction in association with HPA activation (in reference to stress response)
Chronic HPA activation result in chronically elevated cortisol levels
92
Cardio vascular disorders-- chronically elevated SNS activity (in reference to stress response)
- elevated heart rate and constriction of blood vessels cause high blood pressure and increased risk of stroke
93
Cardio vascular disorders --stress induced disruptions in metabolism due to SNS and cortisol (in reference to stress response)
may also contribute to insulin insensitivity and risk of diabetes, atherosclerosis and risk of heart attack
94
GI Issues--chronically elevate cortisol from the HPA axis
is a contributing factor to the formation of GI ulcers
95
GI Issues-- elevated SNS activity
results in disruptions to GI motility and function causing a wide range of GI issues including nausea, indigestion, constipation
96
What are the 3 different models regarding emotion
common sense theory
James-Lange model
Cannon- bard model
97
Common sense theory of emotion
feeling comes first then physiological reactions
ex: i tremble because I feel afraid
(see a vicious, feel fear, react by trembling)
98
James-Lange model
physiological reaction, then feeling
ex:i feel afraid because I'm trembling
(see a vicious dog start trembling, feel fear)
99
Cannon-Bard Model
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
What are the different characteristics of facial expressions as they pertain to emotion
- 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
what are the different brain regions involved in emotions
prefrontal cortex
limbic system
hypothalamus
sympathetic nervous system
102
Prefrontal cortex in reference to emotion
important in both the conscious perception and modulation of emotion
103
Limbic system in reference to emotion
set off nuclei that integrate sensory and cortical inputs and determine proper emotional response
104
Hypothalamus in reference to emotion
critical for activating hormonal inputs for physiological arousal responses
105
Sympathetic nervous system in reference to emotion
produces physiological arousal
106
The different components of emotional circuit of the brain
sensory association cortex
prefrontal cortex
cingulate cortex
amygdala
107
sensory association cortex in reference different components of emotional circuit of the brain
provides into about emotionally relevant stimuli
108
prefrontal cortex (PFC) in reference different components of emotional circuit of the brain
receives input from the SAC and helps decide on a plan of action and inhibits inapropriate emotional responses
109
cingulate cortex (CC) in reference different components of emotional circuit of the brain
critical for activating hormonal inputs for physiological arousal responses
110
Amygdala in reference different components of emotional circuit of the brain
sened and receives input from SAC, PFC, CC and determines how much to activate the hypothalamus
111
What are the effects of lesions on the amygdala
results in loss of fear response / electrical stimulation produces produces a fear response
112
The effects of lesions on the prefrontal cortex
can cause increased impulsive aggression
113
the effects of lesions on the septum
also increased aggression
114
What is the role of the amygdala in emotional processes
- important in evaluating emotional salience of situation emotional?
- what level of emotion is appropriate?
- activation of the fear response
115
The relationship between testosterone and the different types of aggression in animals
- 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
The relationship between testosterone and the different types of aggression in humans
more testosterone = more aggression
| in humans, testosterone appears to be associated with social reward which may or may not require aggression
117
What are the different functions or roles of oxytocin
- 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
What are the other "happy molecules" increase positive aspects of brain function and behavior
dopamine
endogenous opiates
endocannbinoids
serotonin
119
Dopamine reference to increasing positive brain function and behavior
involved in mesolimbic antipatory pleasure reward pathway
120
Endogenous opiates reference to increasing positive brain function and behavior
pain suppression (analgesia), euphoria, relaxation
121
Endocannbinoids in reference to increasing positive brain function and behavior
analgesia, euphoria, relaxation, stress reduction
122
serotonin reference to increasing positive brain function and behavior
involved in awakeness / alertness and satiety; low levels of serotonin may be associated with depression
123
Hypothalamus in reference different components of emotional circuit of the brain
activates body's arousal mechanisms through the SNS and HPA axes
124
definition of an antagonist
any drug that decreases neurotransmission
125
Example of Agonists
- black widow spider bite venom--increases release
- nicotine-- activates receptors
- physostigmine-blocks inactivation
126
Example of antagonists
- choline(poor diet)--decreases synthesis
- Botulinium toxin-- inhibits release
- Curare--blocks receptors
127
definition of side effects
additional physiological or psychological effects of a drug beside the one intended
128
definition of antagonist
is any drug that decreases neurotransmission
129
2 components of anxiety
cognitive anxiety
| somatic anxiety
130
cognitive anxiety
psychological thought, within the brain feeling of nervousness, worry or apprehension
131
Somatic anxiety
physical symptoms including increased heart rate
132
example of somatic anxiety
increased heart rate, increased breathing and sweating
133
State anxiety
mood characterized by cognitive and somatic symptoms of anxiety
134
trait anxiety
a predisposition that influences behavior
135
anxiety disorder
a mental disorder that includes chronic feelings of worry and anxiety without any rational cause
136
what are the different brain regions of the emotional circuit are altered in the brains of anxiety disorder patients
cingulate cortex
ventromedial
amygdala
locus ceoruleus
137
Cingulate cortex in reference to anxiety disorder patients
involved in threat and conflict assessment, size is increased in anxiety disorder patients
138
Ventromedial prefrontal cortex in reference to anxiety disorder patients
inhibits negative emotional responses. decreased size in people with anxiety disorders
139
amygdala in reference to anxiety disorder patients
activates stress response. Larger in anxiety patients
140
locus coeruleus in reference to anxiety disorder patients
HPA, SNS activate by the hypothalamus and can be overly active
141
What are the neural basis for anxiety in the amygdala?
- 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
What are the neurotransmitters assiociated with the monoamine hypothesis of depression
serotonin
dopamine
norepinephrine
143
serotonin in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with
involved in sleep, eating, mood and depressed patients have mood problems as well as vegetative symptoms of sleep and eating disruptions
144
Dopamine in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with
involved in pleasure and reward and depressed patients have anhedonia or lack of pleasure
145
Norepinephrine in reference to the monoamine hypothesis of depression and the symptoms of depression they are associated with
involved in arousal and depressed patients have psychomotor retardation or lethargy and decreased arousal
146
what are the arguments against the monoamine hypothesis of depression
- 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
What is the role of BDNF and neurogenesis in depression and the evidence supporting these roles in depression
- 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
What are the 7 classes of drugs
- Anti-anxiety agents and sedatives
- antipsychotic agents
- antidepressants
- mood stabilizers
- opioid analgesics
- psychomotor stimulants
- psychadelics and hallucinogens
149
What are the conditions for anti-anxiety agents and sedatives for which this drug might be prescribed or used
low doses: they reduce anxiety; at medium doses they sedate at
high doses: they anethesize
150
What are the conditions for antipsychotic agents for which this drug might be prescribed or used
reduce motor activity, wild moods, and disconnected thoughts in schizophrenics
151
What are the conditions for anti-depressants for which this drug might be prescribed or used
treating clinical depression
152
What are the conditions for mood stabilizers for which this drug might be prescribed or used
important in treating bipolar disorder (manic depressive illness)
153
What are the conditions for opiod analgesics for which this drug might be prescribed or used
narcotics and pain relievers or producing feeling of euphoria or intense calm pleasure
154
What are the conditions for psychomotor stimulants for which this drug might be prescribed or used
increase motor and alertness and elevate mood
155
What are the conditions for psychadelics and hallucinogens for which this drug might be prescribed or used
cancer patients going through chemo
156
What are the actions of anti-anxiety drugs with respect to their action on the GABA receptor/ion channel
enhance binding of GABA to CL- channel/receptor
157
What are the actions of sedatives with respect to their action on the GABA receptor/ion channel
open GABA and CL- channel
158
What are the actions of both sedatives and anti anxiety drugs with respect to their action on the GABA receptor/ion channel
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
How do anti depressants influence dopamine
- reduce dopamine levels
| - MAO inhibitors inhibit breakdown of serotonin, dopamine, norepinephrine
160
how do psychomotor stimulants influence dopamine levels
-stimulates dopaminergic neurons to release dopamine by binding to acetylcholine receptors on dopaminergic neruons and activating them
161
How do opiod analgeiscs stimulants influence dopamine levels
inhibit reuptake of dopamine
| more dopamine bind to its receptor on the post synaptic cell
162
How does THC influence synaptic transmission
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
what are the cellular mechanisms involved in tolerance with respect to the reward systems of the brain
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
what are the cellular mechanisms involved in withdrawal with respect to the reward systems of the brain
May represent the greatly reduced signaling through this pathway when drug use is discontinued
165
What is the role of the mesolimbic pathway in eating behaviors?
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
How is the role of the mesolimbic pathway defective in obesity?
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
