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Psychology (7,776)
PSYB65H3 (519)
Ted Petit (310)
Lecture

PSYB65 Lec06.docx

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Department
Psychology
Course
PSYB65H3
Professor
Ted Petit
Semester
Fall

Description
Lec06 Outline  Psychiatric disorders o Schizophrenia o Depression o Mania o Bipolar disorders  Alzheimer’s disease o Neurodegenerative disease  Classic neuropsychology o Deals with brain and how each part of the brain works  Different lobes  PSYB65 o Biochemical neurotransmitter problems  Psychiatric o Neurodegenerative problems Schizophrenia  Characterized by o Verbal hallucinations o Delusions  What it looks like  History of schizophrenia o Freud  Absentee fathers  Overprotective mothers o Genetic studies  1/100-200 people have schizophrenia  Immediate family  Rate of schizophrenia appears to increase among family members  ~10-15% higher rate of schizophrenia o Suggest genetic component o Suggest environmental component  Parents act one way  children act one way o Twin studies  To find out if it is genetic or environmental  Non-identical twins  Incidence rate 10-15%  Identical twins  Incidence rate 40-75%  Suggests genetic component although other factors play a part  It is not 100% incidence rate  Classic neuropsychology of schizophrenia o Is there any part of the brain that don’t function very well or don’t seem structurally common?  Poor performance on tests of frontal lobe function  Reduced ability in terms of verbal and non-verbal memory  Enlarged ventricles  Genetics o Not isolated for one ‘schizophrenic gene’ but a family of genes, once activated, results in schizophrenia  Polygenetic  Psychopharmacology o Antihistamines used for colds o Calmed down schizophrenics o Certain drugs are better suited to treat schizophrenia  Block sites for biogenic amines (monoamines)  Norepinephrine  Dopamine  Serotonin o Dopamine antagonists  Block dopamine o Phenothiazines o Chloropromazines  Effectiveness directly related to ability to block dopamine receptors  Receptor blockers most effective  not dopamine itself o Dopamine stimulants  E.g. amphetamine  Did two things o Schizophrenic  No symptoms at the moment  Immediately become psychotic / schizophrenic o Normal people  Show schizophrenic types of behaviors  Show symptoms  don’t have schizophrenia  Looking at brains of schizophrenics o Wait until they are dead  Have normal amounts of dopamine  Found abnormal amounts of dopamine receptors and sub-type receptors  6x the amount of D2 / D4 receptors  Onset of about 30 years of age  Side effects o Drugs don’t work as well as they could be o Suppress dopamine receptors too much  Likely to end up with symptoms of parkinsons Depression  Depression o Problems in sleeping o Problems with food intake o Suicidal tendencies  Treatment o Reserpine  Blood pressure medication  get depressed  Causes neurotransmitter monoamines to leak from presynaptic vesicles  Problems in packages  Fewer biogenic amines o If leaked out  biochemically degraded  Reduction of monoamines  cause of depression o Aldomat  Lowers blood pressure  Blocks synthesis of norepinephrine  Caused depression  Reduction of norepinephrine  depression  Autopsy suicide patients o Reduction in 5HIAA  Serotonin metabolite o Serotonin reduction  depression  Tricyclic vs tetracyclic antidepressants o Block reuptake of norepinephrine and serotonin  Dopamine o Did not seem to affect depression  Tryptophan o Precursor of serotonin o Also stops depression  Monoamineoxidase o MAO o Degradation of monoamines o MAOi  Monoamineoxidase inhibitors
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