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Brain and Behavior > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

Homeostasis

A

optimal, stable, and balanced internal environment

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2
Q

How does the body respond to deviations from homeostasis?

A

By initiating changes in motivation to restore balance

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3
Q

What are the four main processes of homeostasis?

A

Negative feedback, redundancy, behavioral compensation, and allostasis

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4
Q

Define negative feedback in homeostasis.

A

A process where restoring the set point turns off the response. Example: A thermostat regulating temperature

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5
Q

What is redundancy in homeostasis?

A

Multiple systems performing the same function to ensure fail-safety in vital processes

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6
Q

What is behavioral compensation in homeostasis?

A

Behavioral adjustments to maintain internal stability, such as seeking shade to cool down

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7
Q

Define allostasis.

A

Predictive regulation of bodily processes to maintain stability in response to stressors

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8
Q

What is allostatic load?

A

The wear and tear on the body from chronic stress, potentially causing system breakdown

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9
Q

What is thermoregulation?

A

The process of maintaining a stable internal body temperature

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10
Q

What are the main physiological effectors in thermoregulation?

A

Non-shivering thermogenesis, skin blood flow changes, water evaporation, and shivering thermogenesis

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11
Q

What are behavioral effectors in thermoregulation?

A

Actions like postural changes, temperature choice, and altering the microenvironment (e.g., using air conditioning)

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12
Q

How do endotherms and ectotherms differ in thermoregulation?

A

Endotherms generate heat internally through metabolism, while ectotherms rely on environmental heat sources

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13
Q

What percentage of food energy is used for basal metabolism?

A

About 80%

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14
Q

Why is losing weight difficult according to homeostasis?

A

Allostasis detects starvation and adjusts basal metabolism to conserve energy

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15
Q

What is the role of leptin in hunger regulation?

A

Leptin, produced by fat cells, signals long-term energy stores and decreases hunger

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16
Q

What is the function of ghrelin in hunger?

A

Ghrelin, released by the empty stomach, stimulates hunger by exciting NPY neurons

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17
Q

How do insulin and PYY regulate hunger and satiety?

A

Insulin suppresses hunger in response to high glucose; PYY signals to stop feeding

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18
Q

What is the role of the arcuate nucleus in hunger regulation?

A

It houses neurons that control hunger (NPY neurons) and satiety (POMC neurons)

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19
Q

What happens to leptin-deficient rodents?

A

They overeat, demonstrating leptin’s role in regulating energy storage

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20
Q

How does redundancy support homeostasis?

A

If one system fails, other systems compensate to maintain balance

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21
Q

Why is redundancy vital in thermoregulation?

A

It ensures survival-critical functions even if one neural region is damaged

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22
Q

What does lesioning the ventromedial hypothalamus (VMH) show?

A

VMH lesions lead to higher weight set points but still allow satiety

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23
Q

What does lesioning the lateral hypothalamus (LH) show?

A

LH lesions result in lower weight set points, but hunger is still experienced

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24
Q

How does the hypothalamus regulate hunger and satiety?

A

By integrating signals from gut hormones (e.g., leptin, ghrelin, PYY) to balance energy intake

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25
Q

Homeostasis

A

The maintenance of an optimal, stable, and balanced internal environment

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26
Q

Negative Feedback

A

A mechanism where restoring the set point turns off the response

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27
Q

Redundancy

A

Multiple systems performing the same function to ensure fail-safety for vital processes

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28
Q

Behavioral Compensation

A

Actions taken to maintain stability, such as altering the environment

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29
Q

Allostasis

A

Predictive regulation of bodily processes in response to anticipated stressors

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30
Q

Allostatic Load

A

The wear and tear on the body caused by chronic stress

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31
Q

Basal Metabolism

A

The energy expenditure required to maintain basic bodily functions

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32
Q

Thermoregulation

A

The process of maintaining a stable internal body temperature

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33
Q

Endotherms

A

Animals that generate heat internally through metabolism (e.g., humans)

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34
Q

Ectotherms

A

Animals that rely on environmental heat sources to regulate body temperature

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35
Q

Preoptic Area (POA)

A

A region in the hypothalamus that houses thermosensitive neurons critical for temperature regulation

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36
Q

Arcuate Nucleus

A

A part of the hypothalamus that regulates hunger and satiety through NPY and POMC neurons

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37
Q

NPY Neurons

A

Hunger neurons in the arcuate nucleus excited by ghrelin, promoting feeding

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38
Q

POMC Neurons

A

Satiety neurons in the arcuate nucleus, activated by leptin and GLP to suppress hunger

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39
Q

Lateral Hypothalamus (LH)

A

Brain region involved in hunger regulation; lesions lower weight set points

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40
Q

Ventromedial Hypothalamus (VMH)

A

Brain region associated with satiety; lesions increase weight set points

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41
Q

Hypothalamus

A

The central brain area integrating signals for thermoregulation, hunger, and satiety

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42
Q

Leptin

A

Hormone from fat cells signaling long-term energy storage and decreasing hunger

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43
Q

Ghrelin

A

Hormone from the empty stomach that excites hunger neurons and promotes feeding

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44
Q

Insulin

A

Hormone released with high glucose levels, signaling satiety and suppressing hunger

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45
Q

PYY

A

Gut hormone signaling to stop feeding when food is present in the intestines

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46
Q

GLP (Glucagon-Like Peptide)

A

Intestinal hormone that suppresses hunger and shuts down feeding

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47
Q

Set Point

A

The target value or range maintained by homeostatic processes (e.g., body temperature)

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48
Q

Thermosensitive Neurons

A

Specialized neurons in the POA and hypothalamus that detect temperature changes

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49
Q

Physiological Effectors

A

Mechanisms like shivering, sweating, and vasodilation to regulate internal conditions

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50
Q

Behavioral Effectors

A

Actions such as seeking shade, adjusting posture, or using environmental tools for regulation

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51
Q

Energy Storage

A

Glucose stored with insulin or as fat in adipose tissue; mobilized with glucagon

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52
Q

VMH-Lesion Effects

A

Leads to a new, higher weight set point, but the animal still experiences satiety

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53
Q

Lateral Hypothalamus-Lesion Effects

A

Results in a new, lower weight set point while maintaining hunger sensations

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54
Q

Hormonal Integration

A

Signals like leptin, ghrelin, and insulin work together to regulate energy intake

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55
Q

Thermoregulation is considered a negative feedback sytem because

A

Restoring the desired temperature turns off the response

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56
Q

Which response is not a physiological response of the mammalian thermoregulatory system?

A

Lying in the shade

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57
Q

Which hormone monitors the body’s longer-term energy reservoirs in the form of fat?

A

Leptin

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58
Q

Leptin inhibits the activity of ____ neurons, which work in opposition to POMC neurons.

A

npy

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59
Q

where is the arcuate nucleus?

A

hypothalamus

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60
Q

what are the two neurons in the arcuate nucleus?

A

hunger neuron (NPY neuron) and satiety neuron (POMC)

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61
Q

Leptin

A

A hormone produced by adipose cells that acts as a satiety factor in regulating appetite.; slow single

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62
Q

insulin

A

released when there is a lot of glucose in bloodstream; fast signal to stop feeding (from pancreas)

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63
Q

ghrelin

A

hunger arousing hormone from empty stomach; pretty fast

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64
Q

PYY

A

from intestines; when the levels are high it will slow down or stop feeding; released from digestion

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65
Q

GLP

A

works to shut down feeding; produced by intestines

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66
Q

which hormones cause hunger?

A

Ghrelin

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67
Q

Battle between NPY (hunger) and POMC (satiety)

A

GLP and leptin excite the POMC (decreasing hunger) while inhibiting NPY (decreasing hunger)

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68
Q

Ghrelin excites the NPY neurons (increasing hunger)

A
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69
Q

Which hormones signal satiety?

A

GLP, leptin, insulin, PYY

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70
Q

How does thermo info get to the brain from 1. skin, 2. internal, 3. within brain

A
  1. from the free nerve endings up the spinal cord
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71
Q
  1. from the body core or neck up up the brain stem
A
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72
Q
  1. from the hypothalamus/POA gets the info from within it and from the spinal cord/ brain stem
A
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73
Q

Core features of emotions

A

scalability, valence, persistence, generalization, global coordination, social communication

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74
Q

emotions are _________, _________ states

A

central, causative (there is a relationship between emotional states and behavior)

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75
Q

Scalability

A

Emotions are scalable meaning they exist at different intensities even if the emotion is relatively the same due to different arousal levels and context (annoyance vs. anger. vs. rage)

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76
Q

Valence

A

is it a pleasant or unpleasant emotion (happy vs. sad)

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77
Q

Persistence

A

An emotional response outlasts the stimulus (makes an emotion diff from a reflex; it is longer than the stimulus)

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78
Q

Generalization

A

A conditioned response to one object is exhibited in the presence of similar stimuli (like little albert being scared of rats making him scared of anything fluffy)

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79
Q

Global Coordination

A

Emotional stimuli elicit changes in the brain that are interpreted in a certain way, and that causes changes throughout the body (like changes in hormones, behavior, blood pressure etc)

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80
Q

Social communication

A

We exhibit in our face an expression of the emotional state we are in (so other members of our species can use that info)

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81
Q

What happens during a defensive response?

A

When you see a threat the sensory system sends the raw info to the amygdala. then the amygdala interprets it as threatening so behavior, hormones, and sympathetic response changes

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82
Q

Sham Rage experiments

A

based largely on Phineas Gage; showed that frontal cortex works to inhibit very strong emotions; if they severed connection between frontal cortex and hypothalamus they would get rage response (through more experiments they think anterior hypothalamus is important)

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83
Q

Which part of the hypothalamus was important in rage responses?

A

anterior hypothalamus

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84
Q

The Limbic System

A

Series of interconnected structures that serve emotions (originally defined as subcortical but there is a lot of the cortex that is involved in emotional regulation)

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85
Q

Kluver-Bucy syndrome

A

Lesioned amygdala and hippocampus leads to decreased fear and aggression but also causes diff emotional changes (emotional blunting, weight gain, inappropriate sexual behavior, visual agnosia)

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86
Q

autonomic nervous system and emotion

A

interoceptive feedback means that emotions are somewhat dependent on what is already going on in the body; polygraph tests shows that ANS is involved with emotion

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87
Q

interoceptive feedback

A

the brain is always interpreting what is happening within the body; ex if you give a drug that increases heart rate, people will experience anxiety even without fearful stimuli

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88
Q

Facial expressions in nonhuman animals

A

nonhuman animals have facial expressions; rats have them for pain, tastes (sweet vs bitter), and fear

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89
Q

We know the most about which emotion?

A

Fear bc it is easy to replicate in nonhuman subjects

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90
Q

When does fear happen?

A

When we perceive a threat so we have a defensive response

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91
Q

From which 2 places does sensory info get to the lateral amygdala?

A

From the sensory thalamus (low road) or from the sensory cortex (high road)

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92
Q

Explain the high road

A

sensory info goes through the sensory cortex into the lateral amygdala (this sensory info is more put together than the low road); a memory is formed in the lateral amygdala then the info is sent to the central amygdala; then the central amygdala sends projections to other brain regions to cause the autonomic, physiological, and behavioral changes

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93
Q

Where is the amygdala located?

A

deep in the medial temporal lobe

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94
Q

Explain the low road

A

The sensory thalamus provides fast and coarse info to the lateral amygdala (good for instinctual); a memory is formed in the lateral amygdala then the info is sent to the central amygdala; then the central amygdala sends projections to other brain regions to cause the autonomic, physiological, and behavioral changes

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95
Q

Where does pavlovian fear conditioning happen?

A

lateral amygdala

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96
Q

Urbach-Wiethe Disease (S.M.)

A

A skin calcification disorder that leads to the loss of the amygdala and thus the loss of fear (except a panic response when the amt of CO2 is changed in the air)

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97
Q

What parts of the brain other than the amygdala is involved in fear circuit?

A

Hippocampus, frontal cortex; periaqueductal gray (PAG)

98
Q

What is the periaqueductal gray’s (PAG) function in fear circuitry?

A

It is part of a pain suppression response and is involved in behavior elicited from fearful stimulus

99
Q

If you stimulate the _________ hypothalamus, rage ensues

A

posterior

100
Q

The ________ hypothalamus is important for emotional regulation (as seen in the sham rage experiments)

A

anterior

101
Q

Hypothalamus role in aggression

A

encodes both aggression and mating in rats; deep brain stimulation can help aggression

102
Q

(T/F) All areas involved in emotions involved in other functions as well

A

t

103
Q

Emotions produce _____ brain activity

A

widespread (PAG, amygdala, hypothalamus, etc)

104
Q

Stress Rxn (step-by-step)

A
  1. In response to stress, the hypothalamus activates the sympathetic nervous system to stimulate many physiological systems (like blood pressure, heart rate, etc)
105
Q
  1. The adrenal medulla is activated and releases the hormones epinephrine and norepinephrine
A
106
Q
  1. The hypothalamus also stimulates the anterior pituitary which stimulates the adrenal glands on the kidneys to release steroids like cortisol
A
107
Q

What are the stress hormones

A

Cortisol (released by the adrenal glands), epinephrine, norepinephrine (released by the adrenal medulla)

108
Q

Stress in early life sensitizes people to future stress. This is mediated by:

A

glucocorticoid receptors in hippocampus (so the hippocampus is more susceptible to stress)

109
Q

Retrograde amnesia

A

loss of memory from the point of some injury or trauma backwards, or loss of memory for the past

110
Q

anterograde amnesia

A

inability to form new memories

111
Q

Patient H.M procedure

A

Had a surgery that removed most of the hippocampus from both sides including some of the surrounding cortex (medial temporal lobe)

112
Q

declarative memory

A

the cognitive information retrieved from explicit memory; knowledge that can be declared

113
Q

nondeclarative (procedural) memory

A

shown by performance rather than recollection; like riding a bike

114
Q

HM had trouble with _______ memory, but was OK at _______ memory

A

declarative; nondeclarative (we know bc of the mirror reading)

115
Q

associative learning

A

learning that certain events occur together. The events may be two stimuli (as in classical conditioning) or a response and its consequences (as in operant conditioning). Includes classical conditioning and operant conditioning

116
Q

classical conditioning

A

a learning process that occurs when two stimuli are repeatedly paired; a response that is at first elicited by the second stimulus is eventually elicited by the first stimulus alone. (like ringing a bell before feeding a dog, and then salivation comes from the bell alone)

117
Q

Instrumental (operant) conditioning

A

An association is formed between a behavior and the consequences of that behavior (like a rodent pressing a button to get a food pellet in a skinner box)

118
Q

nonassociative learning

A

responding after repeated exposure to a single stimulus, or event

119
Q

Engram

A

a neuronal encoding that provides a physical location for a memory (a memory trace in the neurons)

120
Q

Sensory memories

A

sensory buffers are fleeting impressions of sensory stimuli (last very short)

121
Q

Iconic memories

A

sensory memories for visual stimuli (fleeting image of a glimpsed scene that vanishes second later)

122
Q

Short-term memories

A

Memory that leaves after around 30 seconds without rehearsal

123
Q

Long-term memories

A

last for days to years (like the address of your childhood home, how to ride a bike, etc)

124
Q

Working memory

A

the ability to actively manipulate info in your short term memory, perhaps retrieving info from long term memory, to solve a problem or otherwise make use of the info

125
Q

What are the three memory stages?

A

encoding, consolidation, retrieval

126
Q

encoding

A

involves the encoding of raw info rom sensory channels into short term memory

127
Q

Consolidation

A

consolidating STM into LTM (some STM are not consolidated and are lost)

128
Q

Retrieval

A

A memory can be retrieved from LTM into the STM or working memory when needed

129
Q

Hebb’s postulate

A

neurons that fire together wire together; theory that explains how neurons adapt during learning (basically the certain pathways get stronger)

130
Q

Which lobe is important for memory?

A

the medial temporal lobes including the hippocampus, the adjacent areas of cortex, and the amygdala

131
Q

long-term potentiation (LTP)

A

A stable and long-lasting enhancement of synaptic transmission; certain communication of neurons becomes easier after a learning event

132
Q

What proved Hebb’s postulate?

A

LTP

133
Q

LTP induction steps

A
  1. Cortical (presynaptic) neuron releases glutamate into the synaptic cleft
134
Q
  1. Receptors activate on the hippocampal (post-synaptic) neuron; Glutamate binds to AMPA receptors, opening to let NA+ ions flow into the post synaptic neuron; When the postsynaptic neuron is depolarized glutamate can bind to NMDA receptors, allwoing Ca2+ ions to enter the postsynaptic neuron
A
135
Q
  1. Calcium influx triggers synaptic strengthening bc they activate key enzymes (2nd messengers) including CaMkII and PKC
A
136
Q
  1. The synapse strengthens due to increase in AMPA receptors and structural growth
A
137
Q

AMPA receptors in LTP

A

Glutamate binds to AMPA receptors on the hippocampal neuron allowing Na+ ions to flow in. This depolarizes the neuron and allows the NMDA receptors to become unblcoked

138
Q

NMDA receptors

A

at rest, NMDA receptors are blocked by Mg2+ ions (like a plug); when the postsynaptic (hippocampal) neuron is depolarized, the Mg2+ block is ejects (this can happen if the learning event is important enough to remember); then glutamate can bind to them, allowing Ca2+ ions to enter the hippocampal neuron

139
Q

What are the two 2nd messengers (enzymes) that are activating by calcium during LTP?

A

CaMKII (calcium/calmodulin-dependent protein kinase II): strengthens synapses by modifying receptors; PKC (protein kinase C): helps with long-term synaptic changes

140
Q

What does CaMKII do?

A

It phosphorylates (chemically modifies) AMPA receptors, making them more effective at conducting NA+ ions; More AMPA receptors are also added to the postsynaptic membrane, increasing the response to glutamate

141
Q

What does PKC do?

A

helps with long-term synaptic changes

142
Q

What structural growth helps strengthen the synapse after LTP?

A

the dendritic spine grows longer and stronger; repeated stimulation can also lead to the formation of new synaptic connections, further increasing synaptic strength

143
Q

Blocking LTP _____ learning

A

stops

144
Q

What kind of drugs could prevent LTP and learning?

A

drugs that block NMDA receptors or interfere with calcium signaling

145
Q

Properties of LTP

A

input specific, coincidence (timing), requires NMDA receptor, Ca2+ dependent, Requires 2nd messengers (CaMKII and PKC)

146
Q

What does input specific mean in relation to LTP?

A

That LTP strengthens only the synapses that are actively involved in the learning process (so neuron specificity)

147
Q

What does coincidence (timing) mean in relation to LTP?

A

LTP relies on timing between presynaptic and postsynaptic activity;

148
Q

Glutamate must be released by the presynaptic neuron at the same time that the postsynaptic neuron is sufficiently depolarized

A
149
Q

LTP causes:

A

more AMPA receptors, better ion conductance, but also weakens ineffective or meaningless connections (the brain only spends energy on shit that matters)

150
Q

LTP changes:

A

both presynaptic and postsynaptic neurons; increases number and size of synapses, dendritic spines, and number of AMPA receptors

151
Q

What does learning can occlude LTP mean?

A

A learning event can use up the mechanisms needed for LTP, making it harder to induce further LTP at the same synapses immediately after firing

152
Q

cellular consolidation

A

memory consolidation as a consequence of synaptic biochemical events initiated by the original experience (time frame of hours); more about neurobiology; THINK LTP

153
Q

systems consolidation

A

a consolidation process that involves the gradual reorganization of circuits within brain regions and takes place on a long time scale, lasting weeks, months, or even years; consequence of an interaction between the hippocampus and cortex; think HM (he couldn’t do LTP, but could remember stuff from childhood)

154
Q

spatial memory and hippocampus

A

memory for the physical environment; place cells can help encode space and time to tell you where you are; the hippocampus essentially maps the whole environment by firing diff neurons together

155
Q

What part of the brain has to do with spatial memory?

A

hippocampus

156
Q

What parts of the brain have to do with procedural (nondeclarative) memories

A

stratum, cerebellum, motor cortex

157
Q

what parts of the brain have to do with classical conditioning?

A

amygdala and cerebellum

158
Q

What parts of the brain have to do with short term memory?

A

The cortex in the medial temporal lobes

159
Q

Sleep cycles differ by

A

sex, age, different chronotypes (late risers vs. early risers), and factors we don’t know

160
Q

EEG (electroencephalogram)

A

Measures brain activity outside your head

161
Q

EOG (electrooculogram)

A

this measures eye movements

162
Q

EMG (electromyography)

A

a measurement technique that records the electrical activity of a muscle or group of muscles. Helpful for REM sleep

163
Q

How do we study sleep?

A

EEG, EOG, EMG

164
Q

Brain oscillations

A

waves of electrical activity from the brain (can be measured with a EEG); includes beta waves and alpha waves

165
Q

Beta waves (and activity)

A

present when we are awake and alert; the waves are fast and desynchronized (a mix of diff frequencies/kind of random)

166
Q

Alpha waves (and activity)

A

appear as we get drowsy, marking the transition from wakefulness to light sleep

167
Q

Stage 1 sleep

A

Light sleep; transition from wakefulness to sleep; characterized by switching from beta to alpha waves; muscles start to relax, heart rate slows, eyes may roll under closed eyelids

168
Q

Stage 2 sleep

A

Brain oscillations switch again; defined by unique brain activity called sleep spindles and k-complexes

169
Q

Stage 3 sleep

A

slow-wave/deep sleep; characterized by delta waves; most restorative sleep stage

170
Q

delta waves

A

large, slow oscillations present during slow-wave sleep

171
Q

REM sleep

A

Brain waves resemble the beta waves seen when awake; muscles are paralyzed to prevent acting out dreams, but eyes move rapidly under eyelids; also known as paradoxical sleep due to brain activity resembling wakefulness

172
Q

Typical sleep cycle

A

cycle through the stages multiple times; first half of the night has more stage 3 sleep while second half has more REM sleep; people wake up multiple times during the night

173
Q

The first half of the night is characterized by _______ sleep, while the second half is by _______

A

stage 3, REM

174
Q

REM cycles get _____ as you get closer to waking up

A

longer

175
Q

Infant sleep patterns

A

irregular bc their circadian rhythms dont develop until 4 months; a lot of REM sleep

176
Q

As you age you get less _____ and _____ sleep

A

stage 3 (slow wave) and REM

177
Q

Functions of sleep

A

necessary for life, energy conservation, niche adaptation, body and brain restoration, memory consolidation

178
Q

Niche adaptation example for hamsters

A

they sleep during the day so they do not get eaten

179
Q

During _______ sleep we see brain activity that is correlated with memory

A

slow-wave (stage 3)

180
Q

What are the 4 systems that regulate diff aspects of sleep?

A

Basal forebrain, Brain stem (reticular formation), Hypothalamus (orexin neurons), Medulla (in the hindbrain)

181
Q

Basal forebrain sleep function

A

promotes slow-wave sleep; stimulation of this area can induce sleep, while lesions can cause insomnia

182
Q

Brain stem (reticular formation) sleep function

A

responsible for arousal and wakefulness by sending activating signals throughout the brain

183
Q

Orexin Nuerons

A

neurons in the hypothalamus that coordinate sleep; control sleep-wake transitions and help integrate signals across sleep centers; a loss of orexin neurons is linked to narcolepsy

184
Q

Medulla function in sleep

A

Regulates muscle paralysis during REM sleep to prevent acting out dreams; sleep walking is when this doesnt work

185
Q

Memory function of sleep

A

brain basically replays memories during slow-wave sleep so the memories solidify

186
Q

Circadian rhythms

A

the body’s internal clock (24 hours) that regulates physical, mental, and behavioral changes

187
Q

diurnal animals

A

most active during the day; body temp/cortisol is higher during day then drops at night; melatonin is higher at night

188
Q

The ______ was the dominant model for circadian rhythms

A

hamster wheel (measured how many rotations on the wheel)

189
Q

phase shift

A

a shift in the activity of a biological rhythm, typically provided by a synchronizing environmental stimulus (essentially jet lag)

190
Q

When you have jet lag the light information is used to ____ the internal ________

A

entrain; endogenous clock

191
Q

Entrainment

A

the process of synchronizing a biological rhythm to an environmental stimulus (like light or food)

192
Q

endogenous clock

A

internal clock that generates circadian rhythms

193
Q

Zeitgeber

A

the cue (stimulus) that is used to synchronize during entrainment (so light would be the zeitgeber during jet lag)

194
Q

What anatomy is important for circadian rhythms?

A

The suprachiasmatic nucleus (SCN) in the hypothalamus. The SCN houses the endogenous clock

195
Q

Hamsters with SCN lesions

A

showed no circadian rhythm, but could still entrain to zeitgabers

196
Q

Role of the eye and light cues (step-by-step)

A
  1. light enters the eye and specialized retinal cones detect blue light (which is abundant in daylight)
197
Q
  1. The detected light is sent to the SCN thru a specific pathway called the retino-hypothalamic tract (does not go thru thalamus like other visual cues, goes straight to SCN)
A
198
Q
  1. SCN uses the light info to entrain and synchronize the endogenous clock to align with the external light-dark cycle
A
199
Q

suprachiasmatic nucleus (SCN)

A

area of the hypothalamus in which the body’s biological clock is located

200
Q

retino-hypothalamic tract

A

sends light info from specialized cones in the retina straight to the SCN

201
Q

Role of melatonin

A

melatonin is produced by the pineal gland in response to darkness (darkness excites the pineal gland); so light inhibits melatonin production

202
Q

Step-by-step of the clock

A
  1. 2 proteins (clock and cycle) form a dimer
203
Q
  1. the clock/cycle dimer enters the nucleus of the SCN neuron where they interact with DNA which leads to an increase of the production of the proteins period (Per) and cryptochrome (Cry) which also form a dimer
A
204
Q
  1. The Per-Cry dimer moves back into the nucleus to inhibit the activity of the clock-cycle dimer, basically stopping further production of per and cry (creating a negative feedback loop)
A
205
Q
  1. When you go to sleep the proteins degrade overnight, and you start the cycle again
A
206
Q
  1. Light info from the retino-hypothalamic tract signals the SCN, causing it to release glutamate (a NT that promotes wakefulness) this allows the clock to be 24-hours instead of the natural 25
A
207
Q

The longer you are awake the ____ per-cry you will have

A

more

208
Q

glutamate promotes ____

A

wakefulness

209
Q

What percentage of people overall with aserious mental illness in the US?

A

6%; 10% young adults

210
Q

A combination of what two things leads to mental illness?

A

Stress and genetics

211
Q

When were lobotomies used?

A

1935-1970s

212
Q

Frontal lobotomy

A

procedure that destroys part of the frontal cortex; used on ppl with severe psychosis and other disorders; makes people sedated and easier to deal with

213
Q

electroconvulsive therapy (ECT)

A

a biomedical therapy for severely depressed patients in which a brief electric current is sent through the brain of an anesthetized patient. still used today

214
Q

Vast majority of drugs for mental illness were discovered by ___ and then reverse engineer

A

accident

215
Q

The first antipsychotic drugs worked to antagonize ____ receptors

A

dopamine

216
Q

Schizophrenia positive symptoms

A

hallucinations, delusions, disorganized thought and speech; bizarre behaviors

217
Q

Schizophrenia negative symptoms

A

emotional dysregulation (lack of emotional expression; flat affect; anhedonia/ inability to xp pleasure in everyday activities)

218
Q

Impaired motivation (reduced convos, social withdrawal)

A
219
Q

Cognitive symptoms (memory problems, poor attention, difficulty planning, abnormal movement patterns, etc)

A
220
Q

Heritability of schizophrenia

A

50% from twin studies

221
Q

Living in cities ______ the risk of schizophrenia

A

increases (likely due to chronic stress)

222
Q

In genetically susceptible people, stress in developmental periods like _______ and ______ can lead to schizophrenia

A

in utero and adolescence

223
Q

Brain features in schizophrenia include

A

accelerated loss of gray matter and ventricular enlargement in schizophrenia

224
Q

gray matter

A

Brain and spinal cord tissue that appears gray with the naked eye; consists mainly of neuronal cell bodies (nuclei) and lacks myelinated axons.

225
Q

ventricles of the brain

A

canals in the brain that contain cerebrospinal fluid

226
Q

Typical Antipsychotics

A

A class of older drugs to treat schizophrenia and related psychotic disorders primarily by antagonizing dopamine (but they also affect other monoamines)

227
Q

The greater the antagonism of dopamine, the (more/less) powerful a typical antipsychotic is for treating psychosis

A

more (so the better antagonists need lower doses)

228
Q

Atypical antipsychotics

A

Newer antipsychotics that work on other neurotransmitters (specifically serotonin) more than dopamine

229
Q

Depression symptoms

A

Feelings of despair, hypoactivity, sleep problems, withdrawal, lack of appetite, inability to care for oneself

230
Q

heritability of depression

A

30-40%

231
Q

How does sleep differ in depressed people?

A

they get much less/no stage 3 (slow wave/deep sleep); REM sleep is distributed differently (more frequent but shorter periods); they have a harder time staying asleep

232
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

First kind of antidepressant; Inhibit the enzyme monoamine oxidase, which breaks down serotonin, norepinephrine, and dopamine; agonize (increase) monoamines (like serotonin, etc.); have severe side effects

233
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

Block the reuptake of serotonin leading to more being available in the synapse; has little effect on other monoamines

234
Q

How does monoamine reuptake inhibition work (like with SSRIs)?

A

The drug blocks the reuptake sites on the presynaptic neuron so that more of the monoamine stays in the synapse and is eventually received by the postsynaptic neuron

235
Q

Why do we think ketamine is effective for treating depression?

A

It regulates parts of the brain that signal negative valence (the bad emotions)

236
Q

Brain activity in depression

A

Increased activity in the prefrontal cortex (involved with emotional regulation) and the amygdala (involved with assigning emotional value)

237
Q

transcranial magnetic stimulation (TMS)

A

the use of strong magnets to briefly interrupt normal brain activity as a way to treat depression

238
Q

Deep brain stimulation

A

Implantation of bilateral anterior cingulate ( in prefrontal cortex) electrodes and a stimulator for chronic deep brain stimulation; for severe/treatment resistant depression

239
Q

cognitive-behavioral therapy (CBT)

A

depression therapy break the cycle (negative thoughts -> low mood -> reduced behavior) of negative thoughts through directed changes in behavior, thought exercises, and changes in physical

240
Q

The ultimate goal in treating depression is to increase ________

A

neuroplasticity

Brain and Behavior (3 decks)

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