The Biological Basis of Psychological Abnormality :pill: :pill: :pill:…
The Biological Basis of Psychological Abnormality :pill: :pill: :pill:
Changes at synapses
underlie learning, memory formation and many psychiatric disorders
change in receptor numbers, change in amount of transmitter release etc
change in structure of synapse
change in efficacy of second messenger systems
Drugs and Neurotransmission
blockade of NT production or storage
blockade of NT release
blockade re-uptake or degradation of NT
blockade or activation of receptors
increase of the number of receptors
changes in 2nd messenger systems
large role in brain function
code for receptors, Nts etc
enviro factors can determine whether a gene becomes switched on or not
induction - gene knockouts, pharmaceutics, lesion studies
measurement - beh. monitoring, neural recordings etc
structural & functional MRI,
however most poeple with disorders will be taking medications that alter brain function
Diminished interest in almost all activities
Depressed mood nearly every day
weight loss/gain/change in appetite
feelings of worthlessness/guilt
impaired ability to concentrate
recurrent thoughts of death
Unipolar - depression that altenates with normal emotional states
Bipolar - fluctuation between depressive and euphoric
Resistant to antidepressants
40's discovery of lithium
without lithium - cycle every 14 months, with - 9yrs
detailed mechanism unknown
Genes and depression
Adoption studies show higher rates of depression in
biological than adoptive parents.
No single gene for depression. Many genes contribute to a susceptibility, and environmental factor trigger depression
inhibits enzymes which break down monoamines
monoamines - dopamine, noradrenaline, serotonin
first introduced in 50s and 60s
only used in most resistant cases, bad side-effects
most modern drug treatment
less side-effects, more effective
affect serotonin selectively
similar effect to MAOIs but inhibit reputake
Neuroimaging of depression
incr. activity in neural systems supporting emotion processing eg amygdala
decr. activity in neural system supporting regulation of emotion eg dorsolateral PFC
grossly disorganised/catatonic beh
negative symptoms - affective flattening, alogia
++ and - symptoms (gained and lost beh)
respond diff to drug treatments - diff underlying cause
closer the biological relatedness, greater chance that the relative will also be schizophrenic - Gottesman 1991
genes implicated - neuregulin 1, COMT, G72
concordance - MZ = 50%, DZ = 17%
symptomatic twin frequently weighs less at birth
More physiological distress (affected twin has
experienced different environmental factors)
the most impaired individuals show the greatest disorganisation - Conrad 1991
Ventricular abnormalities, g matter loss, cellular disorganisation
The hypofrontality hypothesis: less activity in frontal lobes in schizophrenics. Holmes et al (2005)
Decreased cbf in anterior cingulate cortex during auditory discrimination task Holcomb et al. (2000)
Idea that schizophrenia is caused by an excess of dopamine
Large doses of amphetamine (a strong DA agonist) can cause psychosis, with similar symptoms to schizophrenia.
Treatment of Parkinson’s disease with L-dopa (a precursor to dopamine) may induce psychotic symptoms.
Dopamine receptor antagonists such as chlorpromazine or haloperidol are effective antischizophrenic drugs. These “neuroleptic” drugs bind to dopamine D2 receptors
Some studies have found an increase in dopamine receptors (especially D2) in schizophrenic persons, including those no longer taking neuroleptic drugs.
Atypical neuroleptics (i.e. clozapine) affect many receptor types, e.g. serotonin as well as D2 receptors. More effective at relieving negative symptoms than typical neuroleptics.
Some patients show no improvement when treated with DA antagonists.
Clozapine can also increase dopamine release in the frontal cortex.
Studies on D2 receptor levels in schizophrenics are inconsistent.
NMDA receptor - postsynaptic glutamate receptor.
NMDA receptor antagonists, e.g. phencyclidine,ketamine, produce phenomena resembling both - and + symptoms
• NMDA receptor agonists reported to improve + and - symptoms in schizophrenia - but can cause seizures
• Probably not just one NT system involved.