Download Biological explanation of schizophrenia (1)

BIOLOGICAL EXPLANATION
OF SCHIZOPHRENIA (1)
The function of neurotransmitters
• What is this?
• What does it do?
• Where are the
neurotransmitters?
• Can you name any
neurotransmitters?
LABEL THE DIAGRAM ON THE
FOLLOWING SLIDE. YOU CAN USE THE
TEXT BELOW TO HELP.
Neurotransmitter molecules are released from the end of the
presynaptic cell (the axon) into the space between the two
nerve cells (the synapse). Having travelled across the synaptic
gap or cleft, molecules may then be ‘taken up’ by specially
shaped receptor sites on the postsynaptic nerve cell (the
dendrite) and so the chemical message is passed on. The
relationship between the neurotransmitter molecule and the
receptor site is like a lock and key, molecules will only fit certain
receptor sites.
https://www.youtube.com/watch?v=WhowH0kb7n0
LETS REMIND OURSELVES HOW
NEUROTRANSMITTERS WORK
LETS REMIND OURSELVES HOW
NEUROTRANSMITTERS WORK
What happens
if the
neurotransmitt
ers are not
‘sponged
back up by
the
presynaptic
nerve?
What does
dopamine do?
What do you
think the
consequence
of too much
dopamine
would be?
BACKGROUND
• Patients who abused large amounts of amphetamine have often shown
positive symptoms of schizophrenia.
• Randrup and Munkvad (1966) raised dopamine levels in the brains of rats by
injecting them with amphetamine
• Rats behaviour changed – psychotic behaviour consistent with that shown in
patients with schizophrenia
• Research has suggested that the presence of an excess of dopamine
receptors and synapses in the brain contributes to schizophrenia
• Those treated with dopamine enhancing levodopa for Parkinson's disease can
experience psychotic side effects mimicking the symptoms of schizophrenia.
• Amphetamine, cocaine and similar drugs increase levels of dopamine in the brain and
can cause symptoms which resemble those present in psychosis, particularly after large
doses or prolonged use. This is often referred to as "amphetamine psychosis" or "cocaine
psychosis," but may produce experiences virtually indistinguishable from the positive
symptoms associated with schizophrenia.
• Up to 75% of patients with schizophrenia have increased signs and symptoms of their
psychosis upon challenge with moderate doses of methylphenidate or amphetamine or
other dopamine-like compounds, all given at doses at which control normal volunteers
do not have any psychologically disturbing effects Leiberman et al 1987)
• Lieberman et al. 1987 – 75% of patients with schizophrenia show new symptoms or
increase in symptoms of psychosis after using amphetamine (mimic the action of
dopamine)
• Not all users of amphetamine suffer from psychotic symptoms – Suggesting there is
something different about hope people’s brains react to dopamine
The Dopamine hypothesis states that the brain of
schizophrenic patients produces more dopamine
than normal brains.
Schizophrenia symptoms are due to excess activity of
the neurotransmitter – dopamine.
it is now thought that those with schizophrenia have
an abnormally high number of D2 receptors – rather
than just high dopamine levels.
• Post mortems of brains of people who had have had schizophrenia show a higher density of
dopamine receptors is in certain parts of the brain (cerebral cortex) than those who have not
suffered from schizophrenia (Owen et al. 1989)
• SZ- more sensitive to the action of dopamine
• Seeman (2013) People diagnosed with schizophrenia may have a higher number of D2 receptors
with a high affinity to dopamine
• More likely to bind to the neurotransmitter when it is present in the synapse
• More likely to overreact to the presence of the neurotransmitter
• This may result
• from a combination of increased presynaptic neural pruning, a high release of dopamine
• (Howes et al., 2012), altered numbers of dopamine D2 receptors (Seeman, 2013a, in press),
• and/or an increased sensitivity of the D2 receptor to dopamine (Seeman, 2011). This view is
• supported by the fact that the positive symptoms of delusions and hallucinations are
• alleviated in the majority of patients by D2-blocking medications.
The positive symptoms of schizophrenia include hallucinations
and delusions as a result of increased subcortical release of
dopamine, which augments D2 receptor activation
The mesolimbic pathway, sometimes referred to as the
reward pathway, is a dopaminergic pathway in the brain.
The pathway connects the ventral tegmental area (VTA_,
which is located in the midbrain, to the nucleus
accumbens (NA)
Positive
symptoms
Negative
symptoms
The negative symptoms of schizophrenia include lack of
motivation, avolition, diminished emotional expression, which
result from reduced D1 receptor activation in the prefrontal
cortex Okubo 1997
EVALUATION
• SCOAR
• Supporting research
• Application – treatment
• Reductionist – pg 293
It is further here suggested that dopaminergic overdrive is a
necessary step on the path
between initial causation and symptom expression. As such,
therapeutic interventions need
to focus on preventing dopamine overstimulation through a
combination of means:
biological (dampening dopamine release and transmission),
psychological (muting stress
that is mediated through dopamine pathways), and sociological
(alleviating poverty and
discrimination, which raise dopamine activity in large swaths of
the population). Seeman 2014