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Biological Basis of Psychological Disorders (Schizophrenia (Brain…
Biological Basis of Psychological Disorders
Synapses
The connections and means of communication between nerve cells
Each neurones can have thousands of synapses
Synaptic connection is mediated by the physical movement of chemicals (neurotransmitters)
Synaptic Transmission
AP of a presynaptic neuron
Transmitter release into cleft
Transmitter binds to receptor
Transmitter dissociates from receptor
Transmitter reuptake by transporters
Transmitter recycled
Synaptic Components
Pre & post synaptic receptors
Work as a 'lock & key' - one NT fits a certain receptor
Ion Channels or Gated 2nd messenger channels
Transporters
Enzymes that metabolise transmitters
Neurotransmitters
Amines - serotonin, adrenaline etc.
Amino Acids - GABA
Neuropeptides - Endorphins
Can be inhibitory (GABA) or excitatory (Glutamate)
Drugs & Neurotransmission
Pre-synaptic effects:
Block NT production or storage
Block NT release
Block re-uptake or degradation of NT
Post-synaptic effects:
Block activation of receptors
Increase number of receptors
Changes in 2nd messenger systems
Methodological approaches to study psychological abnormalities
Genetics
Code for receptors, enzymes & NTs etc.
Role varies overtime - some influences from birth, some later
Environmental factors can determine where a gene is 'switched on' or not
Animal Models
Induction:
Gene 'knockouts', pharmacological studies, lesion studies
Measurement:
Behavioural monitoring, neural recordings, neurochemistry
Human Studies
Genetics - twin studies etc.
Post-mortem studies
Structural MRI, fMRI, PET (changes in NT systems)
Depression
Depression
At least 5 of the symptoms must be present, during a 2 week period and have an effect on the individual's functioning
Unipolar
- Depression that alternates with 'normal' emotional states
Bipolar
- Fluctuation between depressive periods and euphoric episodes
Genes
Adoption studies show higher rates of depression in biological than adoptive parents
No single gene for depression - many contributing to susceptibility and environmental triggers
Treatments
MAOI's
Inhibit enzymes that break down monoamines (dopamine, serotonin etc.) - raising their levels at synapse
Tricyclic Antidepressants
Similar effects to MAOI's but different action
Inhibit reuptake of monoamine NTs - more to bind with receptors
SSRIs
Serotonin reuptake inhibitors
More effective and fewer side effects
Fournier et al.
- AD's do work
Neuroimaging of Depression
Increased activity in neural systems that support emotion processing
Decreased activity in neural systems that support regulation of emotion
Schizophrenia
Two (or more) of the following: delusions, hallucinations, disorganised speech and behaviour
NOT split personality
Gained behaviours: Hallucination, grandeur
Lost behaviours: Social withdrawal, poor focus
Genetics
The closer the relatedness = greater chance of both having SZ
Concordance: MZ = 50% DZ = 17%
Differing environmental factors due to SZ, lead to more stress resulting in the baby being born lighter
SZ acts differently which leads to different parental response
Brain Abnormalities
Ventricular Enlargement- Not related to length of illness
Grey matter loss
Cellular disorganisation in Hipocampus (chronic SZ)
Hypofrontality
Functional abnormality - Less activity in frontal lobes
SZ show decreased blood flow in ACC
The Dopamine Hypothesis
Idea that SZ caused by excess Dopamine
Treatment of Parkinsons with Dopamine - > Psychosis
Limitations:
Some patients show no improvement after DA
Studies are inconsistent
The Glutamate Hypothesis
NMDA Receptor is the post synaptic Glutamate receptor
Ketamine a glutamate Antagonist causing both positive and negative effects
The agonist improves positive and negative symptoms of SZ
Anxiety
Symptoms: Panic Disporders, Fobia, OCD, Stress etc
Fear is for immediate response, Anxiety is anticipatory
Diagnosed - Occurring for no reason, intense and long lasting
Increased amygdala activity (Brain fear system)
Decreased ACC activity (Fear regulation system)
Panic Disorder
Overwhelming anxiety, Feeling you are about to die, NS activation
Causes:
Psychological factors - Stress
Stimulants
Temporal Lobe abnormality
Ziemann et al:
Amygdala reacts to changes in Ph produced by high levels of CO2 therefore inhaling CO2 -> Fear
Hayano et al:
Smaller Amygdala = anxiety
PTSD
Symptoms:
Intrusive memories, Hyper vigilance, Intense physiological arousal and Flashbacks
Shin et al:
Vietnam veterans- Increased Amygdala, decreased frontal Gyius response
PTSD = Greater activation for all stimuli (unrelated to trauma) especially fearful faces
Psycho Biological model
Fear conditioning:
Failure of extinction mechanism caused my NMDA Antagonists
connected sites to the Amygdala may also fail when Amygdala fails
Hormones- High level of stress hormones may lead to cell death in important areas
Treatment
: Anti-Depressants, BZ's (Valium)- Bind to the GABA receptors increasing their inhibitory action