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Biological Psychology 402 > Chapter 15 Mood Disorders and Schizophrenia > Flashcards

Chapter 15 Mood Disorders and Schizophrenia Flashcards

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1
Q

Dizygote twin

A

fraternal (non-identical) twins derived from two eggs

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2
Q

DISC1 (disrupted in schizophrenia 1)

A

gene that controls production of dendritic spines and the generation of new neurons in the hippocampus

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3
Q

Antipsychotic (neuroleptic)

A

drugs that tend to relieve schizophrenia and similar conditions

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4
Q

Atypical antidepressants

A

miscellaneous group of drugs with antidepressant effects but only mild side effects

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5
Q

bipolar disorder (manic depressive)

A

a condition that alternates between depression and mania

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6
Q

Bipolar I disorder

A

a condition including full-blown episodes of mania

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7
Q

Bipolar II disorder

A

a condition with milder manic phases, characterized mostly by agitation or anxiety

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8
Q

Butyrophenones

A

a chemical family that includes antipsychotic drugs (haloperidol) that relieve the positive symptoms of schizophrenia

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9
Q

Chlorpromazine

A

(Thorazine) antipsychotic drug that relieves the positive symptoms of schizophrenia for most, though not all, patients

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10
Q

Concordance

A

similarity between individuals with regard to a trait

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11
Q

Delusions

A

unjustifiable beliefs

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12
Q

Differential diagnosis

A

one that rules other conditions out that have similar symptoms

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13
Q

Dizygote twins

A

fraternal or non identical twins

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14
Q

Dopamine hypothesis of schizophrenia

A

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

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15
Q

Electroconvulsive Therapy (ECT)

A

a treatment for depression by electrically inducing a seizure

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16
Q

Glutamate hypothesis of schizophrenia theory

A

proposal that schizophrenia relates in part to deficient activity at glutamate synapses, especially in the prefrontal cortex

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17
Q

Hallucinations

A

false sensory experiences

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18
Q

Monozygote twins

A

twins derived form one egg

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19
Q

Monoamine oxidase inhibitors (MAOIs)

A

drugs that block the enzyme monoamine oxidase (MAO), a presynaptic terminal enzyme that metabolizes catecholamines and serotonin into inactive forms

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20
Q

Mesolimbocortical system

A

a set of neurons that project from the midbrain tegmentum to the limbic system

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21
Q

Lithium

A

element whose salts are often used as therapy for bipolar disorder

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22
Q

Mania

A

a condition characterized by restless activity, excitement, laughter, self-confidence, rambling speech, and loss of inhibitions

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23
Q

Major Depression

A

a condition in which people feel sad and helpless every day for weeks at a time

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24
Q

Negative symptoms

A

absence of behaviors ordinarily seen in normal people (e.g., lack of emotional expression)

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25
Q

Neurodevelopmental hypothesis

A

proposal that schizophrenia begins with abnormalities in the prenatal or neonatal development of the nervous system, based on either genetics or other influences

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26
Q

NEUROTROPIN

A

a chemical that promotes the survival and activity of neurons

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27
Q

Phencyclidine (PCP) (angel dust)

A

drug that inhibits the NMDA glutamate receptors

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28
Q

Phenothiazines

A

a chemical family that includes antipsychotic drugs (chlorpromazine) that relieve the positive symptoms of schizophrenia

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29
Q

Positive Symptoms

A

presence of behaviors not seen in normal people

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30
Q

Schizophrenia

A

a psychotic disorder characterized by a deteriorating ability to function in everyday life and by some combination of hallucinations, delusions, thought disorder, movement disorder, and inappropriate emotional expressions

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31
Q

season of birth effect

A

tendency for people born in winter to have a slightly greater probability of developing schizophrenia than people born at other times of the year

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32
Q

Seasonal affective disorder

A

depression that recurs during a particular season, such as winter

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33
Q

Second generation antipsychotic drugs

A

drugs that alleviate schizophrenia without producing movement problems

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34
Q

Selective serotonin reuptake inhibitor (SSRI)

A

drug that blocks the reuptake of serotonin in the presynaptic terminal

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35
Q

Serotonin norepinephrine reuptake inhibitors (SNRIs)

A

drugs that block the reuptake of serotonin and norepinephrine

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36
Q

substance induced psychotic disorder

A

condition provoked by large, repeated doses of a drug

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37
Q

Tardive dyskinesia

A

a movement disorder characterized by tremors and other involuntary movements

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38
Q

Trycylic

A

antidepressant drug that blocks the reuptake of catecholamines and serotonin by presynaptic terminals

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39
Q

Unipolar disorder

A

mood disorder with only one extreme (or pole), generally depression

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40
Q

White Matter

A

area of the nervous system consisting mostly of myelinated axons

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41
Q

Which brain area is especially important for reinforcement and addictions? What is the effect of dopamine on neurons there?

A

nucleus accumbens

drugs activate the nucleus accumbens by releasing dopamine or norepinephrine

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42
Q

What is the effect of amphetamine of synapses?

A

Stimulate dopamine synapses in the nucleus accumbens

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43
Q

Compare the effects of cocaine with those of amphetamine. What are the similarities and differences

A

Both amphetamines and cocaine stimulate dopamine synapses in nucleus accumbens and else where by increasing presence of the dopamine in the presynaptic terminal.
-amphetamines and cocaine inhibit the transporter thus decreasing reuptake and prolonging the effects of released dopamine.

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44
Q

Why do amphetamine and cocaine users frequently report a crash a couple of hours after taking the drugs?

A

a few hours after taking a stimulant drug a user has a deficit of the transmitter and enters withdrawal state.

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45
Q

Why is methylphenidate (Ritalin) usually not abused?

A

Ritalin is prescribe for people with ADHD.

Effects are similar to cocaine but without the rapid rush-get gradual increase in effects=> decline.

46
Q

What are they physiological effects of MDMA (Ecstasy)?

A

stimulant in low doses, increasing released of dopamine and producing effects similar to amphetamines and cocaine.
at higher doses it also releases serotonin, altering perception and cognition like hallucinogenic drugs

47
Q

What is the basis of nicotines reinforcing effects? Is stimulation of all types of acetylcholine receptors reinforcing?

A

Nicotine-stimulates a family acetylcholine receptors known as nicotinic receptors.
Nicotine increases dopamine release.
Nicontine exposure is that receptors in the nucleus accumbens becomes more sensitive to nicotine (same with cocaine etc). enhanced reward to drug and decreased reward by anything else.

48
Q

How do opiates increase the release of dopamine?

A

familiar opiates: morphine, heroin and methadone

  • endorphins indirectly activate dopamine release
  • endorphins synapses inhibit neurons that release GABA
49
Q

What is the main psychoactive chemical in marijuana?

A

D^9 tetrahydrocannabinol

50
Q

Which two endogenous brain chemicals bind to cannabinoid receptors? How might marijuana decrease nausea?

A

anandamide
sn-2-arachidonylglycerol, abbreviated 2-AG
inhibiting serotonin type 3 synapses (5-HT3) which is known to be impt for nausea.

51
Q

Where in the brain are cannabinoid receptors located?

A

many areas of the brain except they are scarce in the medulla

52
Q

Why do large doses of marijuana not threaten breathing or heartbeat?

A

The medulla is the area of the brain that controls breathing and heartbeat. therefore even in large doses marijuana will not stop breathing and heartbeat. (no cannabinoid receptors here)

53
Q

What are cannabinoids effects on GABA and glutamate synapses? How might this affect brain damage after a stroke?

A

cannabinoids inhibit GABA release of dopamine in the ventral demential area of the midbrain-a major source of axons that release dopamine in the nucleus accumbens. By inhibiting GABA there , cannabinoids decrease inhibitions (therefore increase activity of neurons that release dopamine n the nucleus accumbens.)

54
Q

Which receptor does LSD stimulate? Can we explain the effects of LSD on behaviour?

A

Hallucinogenic drugs-LSD lysogenic acid diethyamide chemically resemble serotonin type 2A (5HT2a) receptor and provide stimulation at inappropriate times or for longer than usual durations

55
Q

What are two effects of alcohol on membranes? What type of receptor is made more responsive by alcohol?
Which other two type of synapses are affected?

A

facilitates response at the GABAa receptor the brains main inhibitory site.
Blocks activity at the glutamate receptors the brains main excitatory site.
Both lead to a decrease in brain activity.
Increases stimulation at dopamine receptors n the nucleus accumbens

56
Q

Difference between Type I and Type II alcoholism

A

Type I alcoholism develop alcohol problems gradually after age 25 may or may not have relatives with alcohol abuse
Type II more rapid onset usually before 25- most are men with close relatives with alcohol problems.

57
Q

Turnover of what neurotransmitter has been linked to Type I I alcoholism?

A

one identified genen controls variations in dopamine type 4 receptor which has two common forms short and long.
Long form is less sensitive and seek out more alcohol to compensate for receiving less than normal reinforcement.

58
Q

What is the genetic risk factor for alcoholism.

A

another key gene controls COMT, an enzyme that breaks down dopamine after its release. Some people have less active form of the enzyme and others have mere active form.
More active form breaks down more dopamine and therefore tends to decrease reinforcement. People with that gene tend to be more impulsive.
Prenatal environment also contributes to alcohol risk.

59
Q

What is the biochemical sects of Antabuse? What is the physiological effect when combined with alcohol use?

A

disulfuram (aka Antabuse) antagonizes the effects of acetaldehyde dihydrogenase by binding to its copper ion
Take pill and drink alcohol=getting sick

60
Q

How may Antabuse work, in addition to its physiological effects?

A

Ethyl alcohol=>acetaldehye=>(via acetaldehyde dehydrogenase) acetic acid
Anatabuse exaggerates this effect.

61
Q

What are two characteristics of sones of alcoholics that may predispose them to alcoholism

A
  1. less than aver intoxication after drinking a moderate amount of alcohol
  2. have brain peculiarities-smaller than average amygdala in the right hemisphere.
62
Q

List the symptoms of major depression

A

feel sad and helpless for weeks at a time
little energy
feel worthless
contemplate suicide
have trouble sleeping
cannot concentrate
find little pleasure and can hardly imagine being happy again.

63
Q

what is the evidence for a genetic predisposition for depression?

A

studies of twins show moderate degree of heritability.
Several genes linked to depression but none of the genes by itself has a large effect
Early onset depression people have high probability of other relatives with depression.
late onset >45 have relatives with circulatory problems

64
Q

Are men or women more vulnerable?

A

Childhood male and female equally vulnerable.

more females beyond age of 14.

65
Q

What is the main role of hormones in depression

A

fluctuating him ones play a role.

66
Q

What seems to be the role of traumatic experiences in the onset of episodes of depression?

A

first episode is usually triggered by a highly stressful event.
For later episodes people don’t usually pinpoint a trigger

67
Q

What hemisphere dominance have been associated with happy moods in normal people?

A

Happy mood = increased activity in left prefrontal cortex.

68
Q

What is Borna disease? What evidence links it to depression?

A

a viral infection of farm animals produces periods of frantic activity alternating with period of inactivity.
many were tested for disease and had major depression as well.

69
Q

Name three groups of antidepressants

A

trycyclics
selective serotonin reuptake inhibitors
monoamine oxidase inhibitors.

70
Q

Tricylic Antidepressants-how does it work

A

blocks transporter proteins that reabsorb serotonin dopamine and norepinephrine into the presynaptic neuron after their release. Result is prolong presence of neurotransmitter in synaptic cleft.

71
Q

selective serotonin reuptake inhibitors (SSRI)

A

specific to serotonin acts like TCA but milder side effects
(blocks transporter proteins that reabsorb serotonin, dopamine and norepinephrine into the presynaptic neuron after their release. Result is prolonged presence of neurotransmitter in synaptic cleft.)

72
Q

Monoamine oxidase inhibitors (MAOIs)

A

blocks enzyme monamine oxidase.

a presynaptic termina enzyme that metabolizes catecholamines and serotonin in to inactive forms.

73
Q

Why is fluoxetine (Prozac) preferred over the tricyclics and the monoamine oxidate inhibitors?

A

Prozac-fluorxetine is a selective serotonin reuptake inhibitor
It has milder side effects than the TCA’s but effectiveness is about the same.

74
Q

What are atypical antidepressants? For whom are they used?

A

misc are a misc group-everythign else.
e.g. bupropion-which inhibits reuptake of dopamine and to some extent norepinephrine but not serotonin.
St Johns wart.

75
Q

How effective is St John’s wort in relieving depression? Which class of antidepressants produces effects similar to those of St. Johns’s wort? What is one potential problem with use of St. Johns wort?

A

appears to be as effective as antidepressants but dangerous side effects are that St Johns wort increases the effectiveness of a liver enzyme that breaks dow most meds. Therefore it decreases effectiveness of other drugs you are taking.

76
Q

What neurotropin is produced as a result of repeated use of antidepressants? In which brain areas is it produced?

A

Increase in the presence of serotonin at synapse

77
Q

How is electroconvulsive therapy (ECT) applied today? How is this an improvement over practices in the 1950s?

A
  • With informed consent only-in the 50s they did it without consent
  • usually use it only on patients with severe depression who have not responded to antidepressants
  • applied every other day for about 2 weeks
  • also administered with muscle relaxants
78
Q

For which two groups of patients is ECT most often used?

A

-severe depression when no meds work

79
Q

What are the advantages and disadvantages of ECT?

A

most people wake calmly without remembering it can help those that nothing else works for.
temporary memory loss
relapse is likely

80
Q

What are the effects of ECT on neurotransmitter receptors? what newer treatment is similar to ECT?

A

increased proliferation of new neurons in hippocampus.
repetative transcranial magnetic stimulation
intense magnetic field is applied to the scalp, stimulating the axons near the surface of the brain.

81
Q

How does the onset of REM sleep differ in depressed people, compared to non depressed individuals? How may this be related to body temperature cycles?

A

enter REM sleep within 45 mins after going to sleep

Fall asleep but awaken early.

82
Q

What change in sleepignschedules has been found to alleviate depression? How long do the benefits last?

A

sleep deprivation alleviates depression but effects are temporary-depression returns after next night of sleep.
sleep earlier to get 7-8 hours sleep
relieves depression for about a week.

83
Q

What is the difference between unipolar and bipolar disorder? what is another term for bipolar disorder?

A

unipolar-normal and depression

bipolar-mania and depression (manic depressive)

84
Q

Describe the symptoms of mania. What is hypomania? What is the difference between bipolar I and bipolar II disorder?

A

mania: restless activity, excitement, laughter, self confidence rambling speech and loss of inhibitions.
Hypomania-milder mania phases
bipolar I disorder-full blown mania
Bipolar II disorder-Milder manic phases

85
Q

What can we say about genetic factors in bipolar disorder?

A

twin studies show evidence for genetic link
two gens that appear to increase probability of bipolar II disorder
Genes only show increased risk
None show strong relationship.

86
Q

What is the most effective therapy for bipolar disorder? what can we say about its mode of action?

A

Lithium-stabilizes mood, preventing relapse into mani/depression
dose has to be regulated carefully
valproate and carbemazepine also help.

87
Q

What other drugs are used to treat bipolar disorder other than Li? What are three possible mechanisms by which these frogs achieve their effects?

A

Valproate-(Depakene, Depakote and others)
Carbamazepine
decreased number of AMPA type glutamate receptors in the hippocampus.

88
Q

What is seasonal affective disorder? How is it treated?

A

SAD-depression that recurs during a particular season—usually winter.

89
Q

How are the sleep and temperature rhythms of SAD patients different from this of other depressed patients

A

SAD patients have phase delayed sleep and temp rhythms becoming sleepy and wakeful later normal
Treatment with bright lights.

90
Q

What is the origin of the term schizophrenia?

A

Greek for split mind but is not related to dissociative identity disorder (multiple personality disorder)
Bleuer meant by schizophrenia was split between emotional and intellectual aspects of the experience.

91
Q

What are the negative symptoms of schizophrenia? how stable are they?

A

behaviours that are absent that should be present.

92
Q

What are the two clusters of positive symptoms of schizophrenia? How stable are thye

A

behaviours that are present that should be absent.
delusions
hallucinations
disorganized speech
grossly disorganized behaviour
weak or absent signs of emotion speech and socialization.

93
Q

What is the overall incidence of schizophrenia? does this incidence vary among ethnic groups and sexes?

A

worldwide 1%
all ethnic groups but more common in cities than rural
more common for males than females

94
Q

How does the prevalence of schizophrenia today compare with that of the mid-1900s? Give two reasons why Third World countries might have a lower incidence of schizophrenia that do the developed countries.

A

Since mid-1900s =>incidence
Third weld countries-difference in record keeping
-also could be social support/diet.

95
Q

What evidence form twin studies suggests a genetic basis for schizophrenia? what are concordance rates?

A

agreement

monozygotic 50% concordance

96
Q

What other factor may explain the greater concordance for monozygotic over dizygotic twins for dizygotic twins over non-twin siblings.

A

monozygotes-one egg split
-could differ because a genes is activated
greater concordance for dizygotic twins because they re more genetically related than just siblings.

97
Q

What can we conclude about the role of genetics in schizophrenia.

A

strong link

98
Q

What three lines of evidence suggest that schizophrenia may result from abnormalities in the early development of the brain?

A

Increased schizophrenia is elevated among people who had problems that could have affected their brain development including poor nutrition of mother during pregnancy, premature birth and low birth weight.
Mother exposed to extreme stress

99
Q

What specific prenatal and neonatal conditions have been associated with increased risk for schizophrenia?

A

role of schizophrenia is elevated among pople who had problems that could have affected their brain development including poor nutrition of other during pregnancy, premature birth , low birth weight.

100
Q

in what season of birth is there slightly greater likely hood of developing schizophrenia?

A

people born in winter due to influenza and other viruses in the fall.

101
Q

What brain abnormalities have been linked with schizophrenia?

A

less than average fray matter and white matter

Larger than average ventricles (the fluid filled spaces within the brain)

102
Q

Which brain areas have been most strongly implicated with schizophrenia? What are some psychological functions of those areas? Do schizophrenics show impairment of those functions?

A

strongest deficits were in the left temporal and frontal area of the cortex and most cortical areas
Thalamus is also smaller
Deficits of memory and attention

103
Q

Why do researchers believe the abnormalities in schizophrenia resulted from developmental effects rather than from gradual brain damage in adulthood

A

compare brain abnormalities in patients right after diagnosis to later in life and brain abnormalities are not worse.
Therefore researchers do not believe it is due to brain damage later in life

104
Q

How might one explain the late onset of schizophrenic symptoms, if the brain damage occred during early development?

A

other symptoms during childhood deficits of attention memory and impulse control.
Prefrontal cortex an area that shows consisted signs of deficit in schizophrenia is an area that is one of the slowest brain areas to mature.

105
Q

What is the dopamine hypothesis of schizophrenia? what are the main lines if evidence favouring it?

A

Schizophrenia results from excess activity at dopamine synapses in certain brain areas.
although the [dopamine] is no higher than normal the turnover is elevated esp in the basal ganglia.
Elevated dopamine release occurs in people showing 1st symptoms of schizophrenia

106
Q

Which drugs can induce a state similar to schizophrenia? What is their major mechanism of action?

A

amphetamines
metamphetamines or cocaine each of these drugs increases the activity at dopamine synapses
also LSD is best know for its effects on serotonin synapses also stimulates dopamine synapse.

107
Q

What other neurotransmitter has been hypothesized to be abnormal in schizophrenia? What are three types of interactions between these two neurotransmitters?

A

glutamate deficient activity at glutamate synapses expo in the prefrontal cortex
in many brain areas dopamine inhibits glutamate release or glutamate stimulates neurons that inhibit dopamine release. Therefore increase dopamine produces same effect as decreased glutamate.

108
Q

Why may blockade of dopamine receptors have beneficial effects, if the original problem is deficient glutamate

A

Blocking the dopamine receptor => increase glutamate available.

109
Q

What is phencyclidine? what are its effects on receptors? What are its psychological effects?

A

PCP aka angel dust
A drug that inhibits this NMDA glutamate receptors
at low dose CP produces both positive and neg symptoms of schizophrenia

110
Q

What kinds of evidence suggest an abnormality in glutamate release or receptors?

A

mice with a deficiency of glutamate receptors show some abnormal behaviours including increased anxiety, impaired memory and impaired social behaviour
effects of PCP-angel dust-a drug that inhibits NMDA.

111
Q

Why would it be unwise to administer glutamate to schizophrenic people? What kind of drug has been found to block the behavioural effects of PCP in rats?

A

strokes kill neurons by overstimulating glutamate synapses

increased in overall brain synapses is risky

112
Q

What is glycine? How does it affect NMDA receptors? What were the clinical finings conceding glycine or cycloserine?

A

NMDA glutamate receptors has a primary site that ??

Biological Psychology 402 (15 decks)

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