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Flashcards in Final Deck (242):
1

How do emotions arouse autonomic arousal?

arouses both branches
most situations evoke a combination of both

sympathetic
- stimulates fight or flight, inhibits vegetative activity

parasympathetic
- vice versa

2

What is the James-Lange theory of arousal?

autonomic arousal and skeletal actions come before feeling an emotion

ex. bear attack - run away - fear

3

What is pure autonomic failure?

doesn't react to stressful experiences with changes in arousal

output from autonomic nervous system to body fails

feels emotions much less intensely than before

4

What is a panic attack?

sudden, intense arousal of the sympathetic nervous system

gasp for breath, great anxiety

5

What is Möbius syndrome?

can't move facial muscles to smile

still experience happiness and amusement, shows that facial expressions alter emotions but not necessary

6

What is the limbic system?

forebrain areas surrounding thalamus

critical for emotion

7

What are the main aspects of emotion included by nearly all definitions?

cognition, feeling, action

aspects don't always stick together

8

What is the main support for basic emotions?

existence of facial expressions

happy, sad, fear, anger, disgust, surprise

9

What is the alternative view of emotions?

emotional feelings vary along 2+ continuous dimensions

weak vs. strong, pleasant vs. unpleasant, etc.

10

What is the behavioural activation system? (BAS)

activation of left hemisphere

low-moderate arousal, tendency to approach

characterized by happiness or anger

11

What is the behavioural inhibition system? (BIS)

activation of right hemisphere

increased attention and arousal, inhibits action

characterized by fear or disgust

12

What type of personality does someone typically have when they have greater activity in the left hemisphere?

happier, outgoing

13

What type of personality does someone typically have when they have greater activity in the right hemisphere?

unsatisfied, socially withdrawn

14

What are the functions of emotion?

help us communicate our needs and understands others needs

provide a guide for quick decision making

15

How would damage to the prefrontal cortex affect emotion?

blunts emotions and impairs decision making

16

How would damage to the ventromedial prefrontal cortex affect emotion?

inconsistent preferences (not sure what they want or like)

deficient sense of guilt

17

What happens emotionally after an animal is attacked?

first attack enhances readiness to attack later intruders

activity builds up in amygdala and increases probability of attacking

18

Why does laying down help decrease anger?

it is easier to feel angry when in a position to attack

19

What does embodiment mean?

what you are doing affects how you feel

emotion is embodied

20

Why are the effects of testosterone generally smaller than people imagine?

because cortisol inhibits aggression so aggression depends on ratio of testosterone to cortisol, not just testosterone

serotonin also inhibits violent impulses

21

What is turnover?

the amount of a neurotransmitter that neurons released and replaced

22

What is the impact of low serotonin turnover?

linked to impulsiveness and aggression

measured by concentration of 5-HIAA (serotonin's main metabolite) in the cerebrospinal fluid

23

Why don't genes for low serotonin turnover get eliminated?

2 options

1. evolution selects for intermediate amount of aggression and anxiety
- too much fighting or too much fear leads to problems

2. high-risk, high-payoff strategy
- winning enough fights leads to dominant status within the group

24

What factors in the environment lead to violence?

exposure to lead

abuse

living in violence

hot weather

25

What is MAOa?

enzyme that breaks down excess serotonin/dopamine/norepinephrine to prevent accumulation

low-activity form of this gene increased violent behaviour ONLY in people with troubled childhoods

26

What causes the startle reflex?

sudden loud noise

auditory info goes to cochlear nucleus and then to pons which directs tensing of muscles, especially neck

27

What is the moro reflex?

newborn version of startle reflex

sudden, loud noise causes a newborn to arch back, extend arms and legs, and cry

28

How can the startle reflex vary?

depending on mood or situation

ex. more vigorous reaction if already anxious

29

What makes the amygdala well suited to develop conditioned fears?

many cells get input from pain fibres as well as vision and hearing

30

What is the role of the amygdala in emotion?

controls changes in breathing, avoidance of unsafe places, learning of safe places

31

How does damage to the amygdala affect emotion?

trouble interpreting or understanding stimuli with emotional consequences

ex. show normal startle reflex, but prior signals do not modify the reflex

32

Where does the amygdala send output to in the control of emotion?

hypothalamus
- controls autonomic fear responses
- ex. blood pressure

prefrontal cortex
- controls approach and avoidance responses

33

What is the stria terminalis?

set of axons that connect bed nucleus to amygdala

34

What is the bed nucleus of the stria terminalis?

controls long-term, generalized emotional arousal

35

What is Klüver-Bucy syndrome?

effect of amygdala damage in monkeys

tame and placid, impaired at learning what to fear

36

What visual stimuli does the amygdala respond most strongly to?

when a facial expression is a bit ambiguous/difficult to interpret

active when working hard to interpret information

37

What expression does the amygdala react most strongly to?

fear

38

How do genes for reduced serotonin uptake affect anxiety?

show increased responses to threat and increased attention to threatening stimuli

more likely to have anxiety disorders

39

What is reappraisal?

reinterpret stimulus as less threatening

top-down influences from prefrontal cortex inhibit amygdala activity

40

What is Urbach-Wiethe disease?

rare genetic disorder

accumulates calcium is amygdala until it wastes away

becomes impaired at processing emotional info and learning what to fear

41

What happens when the amygdala becomes damaged?

experience the cognitive aspect of emotion but much less the feelings part

often fail to recognize facial expressions, when they do they rate it as less intense

lacks automatic tendency to direct attention towards emotionally significant stimuli

focus vision on mouth and nose, avoid eyes which display fear

42

What is panic disorder?

frequent periods of anxiety and attacks of rapid breathing, increased heart rate, sweating, and trembling

43

What causes panic disorder?

occurs in 15% of people who have joint laxity (double jointed)

genetic predisposition is suggested by twin studies

abnormalities in hypothalmus, decreased GABA activity, increased orexin levels

44

What is PTSD?

distressing flashbacks and nightmares, avoidance of reminders, vigorous reactions to noises and other stimuli

45

What causes an increased susceptibility to PTSD?

a smaller than average hippocampus

46

What are benzodiazepines? How do they work?

most common anti-anxiety drug

bind to GABAa receptor
- twists chloride channel at centre of receptor so GABA can bind more easily

47

What are the side effects of benzodiazepines?

sleepiness, impaired memory, possible addiction

is chemically stable so passes through the body and is excreted into urine/waste, pass through treatment and accumulate in lakes/rivers

48

How does alcohol affect anxiety?

promotes flow of chloride ions through GABAa receptor by binding to special site

49

What is systematic desensitization?

gradual exposure to feared object in hopes of distinction

usually only suppresses original learning
- may reemerge in times of stress
- easiest to extinguish immediately after initial event before it has been consolidated

50

What is reconsolidating?

memory reawakened by a reminder and becomes changeable

followed by a similar experience that strengthens it

51

How does propanol affect reconsolidation?

interferes with protein synthesis at certain synapses in amygdala

blocks reconsolidation, results in much weaker emotional responses

52

What is Hans Selye's definition of stress?

the non-specific response of the body to any demand made upon it

53

What is behavioural medicine?

emphasizes the effects of diet, smoking, exercise, and other behaviour on health

54

What is general adaptation syndrome?

a generalized response to stress activated by any threat to the body

55

What are the 3 stages of general adaptation syndrome?

alarm, resistance, exhaustion

56

What happens in the alarm stage of GAS?

adrenal glands release:
- epinephrine to stimulate sympathetic nervous system, readies body for brief emergency activity
- cortisol which increases blood glucose to provide extra energy
- aldosterone which maintains blood salt and volume

body temporarily suppresses less urgent activities to maintain energy

57

What happens in the resistance stage of GAS?

adrenal glands continue secreting cortisol and other hormones for prolonged alertness

body adapts to prolonged situation in any way it can

58

What happens in the exhaustion stage of GAS?

tired, inactive, vulnerable after prolonged stress

immune systems no longer have energy to sustain responses

59

What is Bruce McEwen's more suitable definition of stress?

events that are interpreted as threatening to an individual and which elicit physiological and behavioural responses

60

What is the HPA axis?

activated by stress

hypothalmus, pituitary gland, and adrenal cortex

dominates responses to prolonged stressors, but reacts more slowly than autonomic nervous system

61

How does the HPA axis work?

hypothalmus is activated and stimulates pituitary gland to secrete adrenocorticotropic hormone (ACTH)

ACTH stimulates adrenal cortex to secrete cortisol

cortisol enhances metabolic activity, elevates blood sugar levels, and increases alertness

62

What are the effects of brief-moderate stress?

improves attention and memory formation

improves performance on simple tasks

63

What are the effects of prolonged stress?

impaired immune activity and memory

64

What is the immune system?

cells that protect body against intruders

like a police force:
- if too weak, "criminals" run wild and create damage
- if too strong, attacks "law-abiding citizens" - the body's own cells

65

What is an autoimmune disease?

when the body attacks it's own cells

66

What is an antigen?

on the surface of the cell
proteins
unique as fingerprints

67

What is an antibody?

Y-shaped proteins that attach to particular antigens

lock and key

68

What are leukocytes?

white blood cells

most important elements of immune system

69

What are the 3 types of leukocytes?

B-cells, T-cells, natural killer cells

70

What are B-cells?

mature in bone marrow

secrete antibodies to attack unfamiliar antigens

remembers intruders and builds more of the same kind of antibody in case of further encounter

71

What are T-cells?

mature in thymus gland

directly attack intruders

help other T-cells and B-cells multiply

72

What are natural killer cells?

attack tumour cells and cells infected by virus

attack all intruders
- not specific like T-cells and B-cells

73

How do leukocytes combat infection?

leukocytes produce cytokines

cytokines trigger release of prostaglandins

prostaglandins stimulate hypothalmus to produce:
- fever
- sleepiness/lack of energy
- lack of appetite
- etc.

74

How does aspirin/ibuprofen work?

inhibits prostaglandins

75

Why are the symptoms of illness produced?

a part of the body's way of fighting the illness

conserve energy, reduce fuel for intruders

76

What is psychoneuroimmunology?

deals with the way experiences alter the immune system and in turn influence the central nervous system

77

Why does prolonged stress produce depression-like symptoms?

prolonged cortisol increase directs energy to increasing metabolism, detracts from synthesizing proteins of immune system

78

Why does prolonged stress damage the hippocampus?

increased cortisol increases metabolism, when metabolic activity is high in hippocampus its cells become vulnerable

79

What are things that are identified as stress control?

life circumstances
strengthened connections between amygdala and prefrontal cortex
exercise, meditation, social support
successfully coping with previous experiences

80

Why are the symptoms of illness produced?

a part of the body's way of fighting the illness

conserve energy, reduce fuel for intruders

81

What is psychoneuroimmunology?

deals with the way experiences alter the immune system and in turn influence the central nervous system

82

Why does prolonged stress produce depression-like symptoms?

prolonged cortisol increase directs energy to increasing metabolism, detracts from synthesizing proteins of immune system

83

Why does prolonged stress damage the hippocampus?

increased cortisol increases metabolism, when metabolic activity is high in hippocampus its cells become vulnerable

84

What are things that are identified as stress control?

life circumstances
strengthened connections between amygdala and prefrontal cortex
exercise, meditation, social support
successfully coping with previous experiences

85

What is classical conditioning?

pairing 2 stimuli to change response of one

present CS (bell) and UCS (meat) together repeatedly to create new CR and CS (salivation)

86

What is instrumental conditioning?

individual's response leads to a reinforcer or punisher which determines probability of the response occurring again

87

What is a reinforcer?

increases probability of response occurring again

ex. praise

88

What is a punisher?

decreases probability of response occurring again

ex. time out

89

What is an engram?

a physical representation of what has been learned?

90

What is equipotentiality?

the proposed principle that all parts of the cortex contribute equally to complex behaviours and any part of the cortex can substitute for any other

91

What is mass action?

proposed principle that the cortex works as a whole and the more cortex but better

92

What is the lateral interpositus nucleus? (LIP)

nucleus of the cerebellum that is essential for learning

responses increase as learning proceeds

93

What happens when the lateral interpositus nucleus (LIP) is suppressed during training?

the training has not been learned, it has no effect even after suppression wears off

94

What is short-term memory?

events that have just occurred

smaller capacity

depends on rehearsal

once forgotten, is lost

95

What is long-term memory?

events from further back

larger capacity

can be reconstructed once forgotten
- not always 100% accurate

96

What was the initial theory of consolidation? What were the issues with this?

storing something in short-term for a long time allows for the brain to consolidate it with structural changes and become permanent

issues:
- reminders bring old memories into labile state where it can be changed and weakened
- time needed to consolidate varies enormously
(ex. boring facts take longer than gossip_

97

Why do emotionally significant memories form faster?

emotional experiences increase secretion of epinephrine and cortisol

small amounts of cortisol activate the amygdala and hippocampus to enhance storage and consolidation

98

What is working memory?

where we store memory while we are working with it

99

What is a delayed response task?

common test of working memory

respond to something you saw/heard a short while ago

prefrontal cortex is used

100

What is amnesia?

memory loss

101

What is retrograde amnesia?

loss of memory for events before brain damage

102

What is anterograde amnesia?

inability to form memories for events after brain damage

103

Where do most patients with amnesia have damage?

hippocampus and surrounding areas in medial temporal lobe

104

What are semantic memories?

factual information

105

What are episodic memories?

single personal events

106

What is explicit memory?

deliberate recall of events that one recognizes as a memory

can state in words

107

What is implicit memory?

influence of experiences on behaviour without recognition

108

What is procedural memory?

a type of implicit memory

development of motor skills and habits

109

What are the effects of amnesia on memory?

working memory
- normal unless distracted

episodic
- difficulty forming, severe loss

procedural
- nearly intact

better implicit than explicit

110

What are the 3 theories on the role of the hippocampus?

1. critical for explicit memory, especially episodic

2. critical for spatial learning
- provides a map of time and place
- responds to particular locations and directions of travel
- grows in response to spatial learning experiences

3. coordinator for reconstructing the context of memory
- parts of memory (ex. sights, sounds) stored in various locations that must be brought together to create full memory

111

What is the delayed matching-to-sample task? What is the delayed nonmatching-to-sample task?

1. see a sample object, later see 2 objects and choose which matches sample

2. see a sample object, later see 2 objects and choose which is different from the sample

112

What is a radial maze?

spatial learning apparatus

rats learn which arms of the maze have food

113

What is the Morris water maze?

spatial learning task

rats learn to swim to platform under the surface

114

What is acute transient global amnesia?

temporary dysfunction of the hippocampus

115

What type of memories depend more on the hippocampus?

recent memories

contain more contextual detail

older, less detailed memories rely more on cerebral cortex

116

What is Korsakoff's Syndrome?

brain damage caused by prolonged thiamine deficiency (vitamin B1)
- needed to metabolize glucose
- leads to shrinkage of brain neurons

117

What happens when someone has Korsakoff's Syndrome?

apathy, confusion, memory loss, poor episodic memory, confabulation

118

Who usually gets Korsakoff's Syndrome?

chronic alcoholics

119

What is confabulation?

fills in memory gaps with guesses

answer was usually true at some point in the past and usually more pleasant than current truth

mostly occurs on questions they would be expected to know the answers to

120

What are the symptoms of Alzheimers disease?

better procedural than explicit memory

memory loss, confusion, hallucinations, depression

121

What chromosome is linked to early-onset Alzheimers disease?

chromosome 21

almost everyone with Down Syndrome gets Alzheimers

122

What is amyloid-B?

protein that accumulates within and outside the neuron causing damage to them

damaged structures cluster into plaques, accumulate and cause areas to waste away

done by genes controlling early-onset Alzheimers

123

What is tau protein?

intracellular support structure of axons

high levels of amyloid-B cause more phosphate groups to attach to tau proteins
- altered tau proteins can't bind to usual targets
- starts spreading throughout cell, adds to attack by amyloid-B
- responsible for tangles

124

What is apolipoprotein E?

helps remove amyloid-B from the brain

125

What is the most common method of treating Alzheimers?

drugs that stimulate acetylcholine receptors or prolong release, increasing arousal

no highly effective treatment

126

What is the role of the basal ganglia in learning?

gradually learning what probably will or will not happen under certain circumstances

when you can't trace inferences to an experience, unaware of cues that helped you decide

127

What is the difference between the basal ganglia and the hippocampus/cerebral cortex in trials it requires to learn?

BG - integrates info over many trials

H/CC - can learn in single trial

128

What is the difference between the basal ganglia and the hippocampus/cerebral cortex in the type of result it produces after learning?

BG - habits

H/CC - flexible responses

129

What is the difference between the basal ganglia and the hippocampus/cerebral cortex in what their learning is based on?

BG - immediate feedback (reward/punishment)

H/CC - connect info over time, can learn from delayed feedback

130

What is the difference between the basal ganglia and the hippocampus/cerebral cortex in type of learning?

BG - implicit

H/CC - explicit

131

What is the difference between the basal ganglia and the hippocampus/cerebral cortex in the effects of damage?

BG - loss of motor patterns, impaired at learning skills/habits

H/CC - poor explicit memory, especially episodic

132

What kind of memories is the amygdala responsible for?

fear memories

133

What is the role of the parietal lobe in memory?

associates one detail with another to form complete thoughts

134

What is sensitization?

increase in response to mild stimuli as a result of exposure to more intense stimuli

strong stimulation excites facilitating interneuron that releases serotonin onto presynaptic terminals of sensory neuron

serotonin blocks potassium channels in membranes, takes longer to repolarize after action potentials

presynaptic neuron releases neurotransmitter for longer than usual

135

What is the role of the prefrontal cortex in memory?

inhibits inappropriate responses and shifts to other behaviours

learns about reward/punishment and makes decisions based off them

responds flexibly and alters responses when rules change

136

What is a Hebbian synapse?

synapse that increases in effectiveness become of simultaneous activity in presynaptic and postsynaptic neuron

ex. A excites B, C excites B more, effects of A and C lead to action potential, increases future effect of A on B

137

What is an aplysia and why are they studied?

marine invertebrate related to the slug

fewer, larger neurons that are virtually identical between individuals

138

What is habituation?

decrease in response to a stimulus that is presented repeatedly

depends on change in synapse between sensory and motor neuron

139

What is sensitization?

increase in response to mild stimuli as a result of exposure to more intense stimuli

140

What is long-term potentiation (LTP)?

one or more axons connected to a dendrite bombard it with stimuli, burst leaves some of the synapses more responsive for a period of time

dependant on glutamate

141

What are the 3 properties of LTP that make it relevant for learning?

specificity
- only highly active synapses are strengthened

cooperativity
- nearly simultaneous stimulation by multiple axons produce LTP more strongly than repeated stimulation by one axon

associativity
- pairing a weak input with a strong input enhances later response to weak input

142

What is long-term depression (LTD)?

opposite of LTP

dependant on glutamate

prolonged decrease in response at a synapse for axons that are less active than others

143

What type of process is LTP + LTD?

compensatory process

allows strengthened synapses to flourish without requiring the brain to need more fuel

144

What is an AMPA receptor?

ionotropic

responds to glutamate

opens sodium channels

145

What happens at an NDMA receptor?

response to glutamate depends on polarization across the membrane

when at resting potential, magnesium ions are blocking ion channel
- attracted to inside but don't fit

when depolarized, magnesium detaches and allows sodium and calcium to enter NDMA ion channels

146

How do presynaptic changes sometimes play a role in LTP?

retrograde transmitter (often nitric oxide) released from excessive stimulation
- travels back to presynaptic cell and modifies it

many roles there

147

What is the role of CaMKII?

activated when calcium enters NMDA channel

sets in motion a series of reactions leading to release of CREB (protein)

148

What is the role of CREB?

goes to nucleus and regulates expression of several genes (epigenetics)

key to maintaining LTP and for types of learning

149

What is the role of BDNF in learning?

neurotrophin that magnifies effects of CaMKII and CREB

when action potentials back propagate into dendrites, BDNF is released

150

What is the overall outcome of depolarization of membrane with AMPA/NDMA receptors?

changes potentiate dendrite's future responsiveness to glutamate at AMPA receptors
- once LTP established, stay potentiated regardless of NMDA activity

NMDA receptors revert to original condition

151

How do presynaptic changes sometimes play a role in LTP?

retrograde transmitter released from excessive stimulation

152

How can memory be improved?

moderate doses of stimulants before or shortly after time of learning
- by increasing arousal

emotional experiences
- by activating amygdala

cortisol shortly before testing
- helps access memories

153

What is an antagonist?

drug that blocks a neurotransmitter

154

What is an agonist?

drug that mimics/increases effects of a neurotransmitter

155

What is a mixed antagonist-agonist?

agonist for some effects/doses of a neurotransmitter, antagonist for other effects/doses

156

What is affinity?

likelihood of a drug binding to a receptor

varies from strong to weak

157

What is efficacy?

tendency to activate the receptor

158

Why are plant-based drugs the most commonly abused?

nearly all neurotransmitters/hormones are the same in humans as in others

if a plant evolves a chemical to affect something, will likely affect humans too

159

What are cravings?

insistent search for an activity

distinguishing feature of any addiction

a strong WANT, not a strong like
- may cause more distress than pleasure, but still can't stop

160

What is the nucleus accumbens?

addictive drugs strongly activate this area by releasing dopamine or norepinephrine

161

How do stimulants work?

block reuptake or reverse transporter of dopamine to release it instead of reuptake

162

How do opiates work?

inhibit neurons that release GABA
- NT that inhibits firing of dopamine neurons
- inhibiting an inhibitor = increased dopamine release

163

What types of other things release dopamine in the nucleus accumbens?

sexual excitement
music
sugar

164

What are cravings?

insistent search for an activity

distinguishing

165

How does the gene that controls variations in dopamine type 4 receptors affect addiction?

2 common forms - long and short

long form is less sensitive, people report stronger cravings for more after 1 drink

166

What happens to the prefrontal cortex after repeated exposure to an addictive substance?

disrupts areas for restraining impulses

fails to overrule reward-seeking areas

167

What is tolerance?

effects decrease as addiction develops

must raise amount and frequency continuously

to a large extent is learned
- can be weakened through extinction procedures

168

What is withdrawl?

strong reaction when the drug is absent after the body comes to expect it

169

What are the 2 theories of addiction?

1. behaviours are an attempt to avoid withdrawl

2. someone with addiction learns to use addiction to cope with stress

170

How does the gene that controls COMT affect addiction?

more active form of COMT breaks down more dopamine tends to decrease reinforcement

tends to lead to more impulsivity

171

What is COMT?

enzyme that breaks down dopamine after its release

172

How does the childhood environment affect addiction?

people with less sensitive form of gene that controls GABA receptors has difficulty inhibiting impulses

careful parental supervision decreases chances of developing these impulse issues

173

How does the adult environment affect addiction?

important for late-onset

depends more on stressful circumstances

174

What is acetaldehyde dehydrogenase?

enzyme that converts acetaldehyde (from alcohol) into acetic acid for energy for the body

175

What are the 2 types of alcoholism?

Type I/A
- gradual onset
- usually after age 25

Type II/B
- rapid onset
- usually before age 25
- mostly in men with a family history of alcoholism

176

What are some behavioural predictors of alcoholism?

impulsive, easily bored, risk-taker, outgoing

less intoxication after drinking a moderate amount

alcohol decreases stress to a higher degree

177

What are the 3 most common types of treatment for alcoholism?

self recovery

therapy

medication

178

What is acetaldehyde dehydrogenase?

enzyme that converts acetaldehyde (from alcohol)

179

What happens to a person who has a gene to produce less than average acetaldehyde dehydrogenase?

metabolizes acetaldehyde slower after drinking

accumulates, causes bad symptoms

180

What is antabuse?

antagonizes effects of acetaldehyde dehydrogenase by binding to its copper ion

causes the person to not be able to drink without sickness

reaffirms decision that already exists to stop drinking

181

How can you create an aversion to alcohol?

drink and then take nausea-producing pill, forms a learned aversion to the taste

182

What does Naloxone/Naltrexone do?

blocks opiate receptors

decreases pleasure from alcohol

183

What is methadone?

similar effects as heroin and morphine

can be taken orally
- not broken down by stomach acid
- effects rise gradually avoiding "rush" experience that disrupts behaviour
- withdrawl symptoms also gradual

184

What is buprenorphine and levomethadyl aceteate?

similar to methadone

produces long lasting effects
- clinic 3 times a week instead of daily

185

What is major depression?

absence of happiness more than increased sadness

trouble sleeping, low concentration, contemplate suicide

changes in synapses to nucleus accumbens make it less responsive to reward

usually episodes of depression seperated by periods of normal mood

186

How does the first depressive episode differ from the preceding ones?

longer

triggered by high stress

187

Who is depression most common in?

more common in adults, but more likely to persist when in children

more common in females after age 14

188

Why is it difficult to find one particular gene responsible for depression?

may be combining separate syndromes

early-onset similar to many things

late-onset similar to circulatory issues

189

What are serotonin transporter genes and how do they affect depression?

protein that regulates the ability of axons to reabsorb serotonin after its release

short form of gene magnifies reaction to stressful events

increases risk of depressive reactions

190

How does hemispheric dominance affect depression?

strong relationship between happy mood and increased left prefrontal cortex activity

most people with depression have decreased activity in left, and increased activity in right prefrontal cortex

191

How do monoamine oxidase inhibitors (MAOIs) work?

block the enzyme monoamine oxidase (MAO) which metabolizes catecholamines and serotonins into inactive forms

allows presynaptic terminal to have more neurotransmitters available for release

192

How do tricyclics work?

block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine after release

prolongs presence of neurotransmitters in synaptic cleft where they can continue to stimulate post-synaptic cell

also blocks other receptors/channels which leads to side effects

193

How do selective serotonin reuptake inhibitors (SSRIs) work?

blocks reuptake of serotonin

similar to tricyclics, but specific to serotonin and with less side effects

194

How do serotonin norepinephrine reuptake inhibitors (SNRIs) work?

block reuptake of both serotonin and norepinephrine

same as SSRIs but additionally norephinephrine

195

Why must people who take MAOIs avoid foods with tyramine?

the combination leads to increases in blood pressure

196

What are atypical antidepressants?

includes everything other than the types just discussed

197

What is St. John's wort?

herb that acts as antidepressant

less expensive, available without prescription

side effect - decreases effectiveness of other drugs you may be taking

198

Why do antidepressants immediately produce effects on neurotransmitters but need at least 2 weeks to experience any major mood elevation?

many people with depression are low in BDNF that is key for synaptic plasticity and neuron proliferation in the hippocampus

antidepressants increase BDNF levels over weeks, the time it takes to see them take effect

new neurons make it easier to learn new ways of coping

199

What is electroconvulsive therapy (ECT)?

electrically inducing a seizure to relieve depression

increases proliferation of new neurons in hippocampus

alters expression of many genes in hippocampus and frontal cortex

acts faster and helps more people but is least likely to persist
- have to continue going back for treatment

temporary memory impairment

200

What are the benefits of therapy for depression?

increases metabolism in same brain areas as antidepressants

more likely to last

improve most when receiving a combination of therapy and drugs

201

How does exercise benefit depression?

regular, moderate-intensity exercise increases serotonin and BDNF levels and increases sensitivity to reward

202

What is electroconvulsive therapy (ECT)?

electrically inducing a seizure to relieve depression

given only in extreme cases

temporary memory impairment and high risk of relapse are side effects

203

What is transcranial magnetic stimulation?

magnetic field is applied to the scalp, stimulates axons near surface of the brain

204

What kind of sleep issues do people with depression typically have?

phase-advanced
- fall asleep but awaken early and can't get back to sleep

should adjust schedule to go to bed and wake earlier

205

How does sleep deprivation affect people with depression?

pulling an all-nighter leads depressed people to feel less depressed

deprivation causes astrocytes to release adenosine, which has antidepressant effects

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What is deep brain stimulation?

implanted battery power device into brain to deliver periodic stimulation to certain areas

extreme cases

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What is bipolar disorder?

alternate between 2 poles - depression and mania

type I - full-fledged manic episodes

type II - mild/hypomanic episodes

onset is usually teens/early 20s

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What is mania?

restless, excited, laughter, excessive self-confidence, rambling speech

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How can lithium salts treat bipolar disorder?

stabilizes mood

low dose is ineffective, high dose is toxic

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How do all medications affect bipolar disorder?

decrease AMPA glutamate receptors in hippocampus
- excessive glutamate activity responsible for some aspects of mania

blocks synthesis of arachidonic acid
- produced during brain inflammation, shown in excess in bipolar people
- counteracted by omega-3 fatty acids

get adequate sleep

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What is Seasonal Affective Disorder (SAD)?

depression during a particular season (usually winter)

most prevalent near poles where winter nights are long

phase-delayed sleep and temperature rhythms

have a mutation responsible for altering circadian rhythm

possible to treat with very bright lights

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According to the DSM-5, what symptoms do people have to show to be diagnosed with schizophrenia?

deteriorated in everyday functioning for 6+ months for reasons not attributable to other disorders

at least 2 symptoms including 1 from first 3
- delusions
- hallucinations
- disorganized speech
- disorganized behaviours
- weak signs of emotion and socialization

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What are positive symptoms?

symptoms that are present that should be absent

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What are negative symptoms?

behaviours that are absent that should be present

usually stable over time and difficult to treat

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What are cognitive symptoms?

limitations of thought/reasoning

difficulty understanding abstract concepts

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How does schizophrenia arise?

new mutations, specifically microdeletion
- common in schizophrenics

disrupts brain development and increases probability of schizophrenia

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Who most commonly gets schizophrenia?

people in cities
- less sun (vitamin D)
- more exposure to toxins

immigrants
- loss of social support
- diet change, etc.

men
- more common and more intense

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How does DISC1 affect schizophrenia?

controls differentiation and migration of neurons, production of dendritic spines and hippocampal neurons

rare varients more common in schizophrenics

219

How does schizophrenia arise?

new mutations, specifically microdeletion
- common in schizophrenics

disrupts brain development and increases

220

Why does schizophrenia persist?

new mutations arise faster than natural selection can weed the new ones out, and disease persists

221

What is the neurodevelopmental hypothesis?

prenatal or neonatal influences produce abnormalities that leave brain vulnerable to other disturbances later in life

causes abnormalities in anatomy and behaviour

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What are intermediate risk factors of schizophrenia?

having an older (65+) father
living in a crowded city
infection with toxopasma gondii (from cats)

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What type of mild brain abnormalities exist in people with schizophrenia?

less grey and white matter

larger than average ventricles

smaller hippocampus

higher hippocampus metabolism
- indicates increased glutamate release, damages neurons

poor prefrontal cortex connections

right planun temporale is equal or larger
- usually left

lower activity in left hemisphere

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What is the season of birth effect?

tendency for people born in the winter to have greater probability of developing schizophrenia

particularly pronounced further from the equator

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Why does the season of birth effect exist?

higher chance of maternal infection in winter

excess cytokines impair baby brain development

fever slows neuron division

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What type of mild brain abnormalities exist in people with schizophrenia?

less grey and white matter

larger than average ventricles

smaller hippocampus

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How does schizophrenia progress?

show impairments at start of disorder and moderate loss through first couple years

then little-no deterioration

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What is the dopamine hypothesis of schizophrenia?

schizophrenia results from excess activity at dopamine synapses in certain brain areas

concentration of dopamine in whole brain is no higher than normal, but dopamine release is increased in basal ganglia

most effective drugs block dopamine receptors

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What does chlorpromazine do?

relieves positive symptoms for most patients

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What are phenothiazines and butyrophenones?

2 chemical families of antipsychotic drugs

behavioural benefits develop gradually

231

What is the dopamine hypothesis of schizophrenia?

schizophrenia results from excess activity at dopamine synapses in certain brain areas

concentration of dopamine in whole brain is

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What is substance-induced psychotic disorder?

extensive abuse of drugs induces the positive symptoms of schizophrenia

each drug increases/prolongs activity at dopamine synapses

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What is the glutamate hypothesis of schizophrenia?

schizophrenia caused by deficient activity at glutamate synapses in the prefrontal cortex

in many brain area dopamine inhibits glutamate release and glutamate inhibits dopamine release
- therefore produce same effects

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What is phencyclidine (PCP)?

drug that inhibits NMDA glutamate receptors

larger doses cause both positive and negative symptoms of schizophrenia

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What are some characteristics of autism spectrum disorder?

social/emotional exchange deficits
deficits in nonverbal communication
stereotyped behaviours (repetitive movements)
resistance to change in routine
overly weak or strong responses to change in stimuli

also many have
- ADD
- cerebellum abnormalities (clumsy)

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What is tardive dyskinesia?

tremors and other involuntary movements that develop gradually

can last long after someone quits drugs

when dopamine neurons are blocked in mesostriatal system that projects to basal ganglia

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What are second-generation antipsychotics?

less likely to produce movement problems

do produce other side effects

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What are topoisomerases? What is their role in autism?

enzymes that regulate the repair and regulation of DNA and RNA production

mutations impair many genes important for brain development, common result is autism
- maternal antibodies attack certain brain proteins prenatally

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What strength do people with autism spectrum disorder have?

better at detecting motion by visual stimuli

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What are some causes of autism?

mutations/microdeletions

older father

lack of folic acid (vitamin B9)
- important for development of nervous system

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What are topoisomerases? What is their role in autism?

enzymes that regulate the repair and regulation of DNA and RNA production

mutations impair many genes important for brain development, common result is autism

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What are some treatments for autism?

risperidone
- second-generation antipsychotic
- reduces stereotyped behaviours at risk of serious side effects

behavioural treatments to address social deficits
- eliciting attention
- reinforcing favourable behaviours, reinforcing competing behaviours to stereotyped behaviours