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Evidence for the Aetiological Theories: Neurochemical Abnormalities
How might these neurotransmitter abnormalities interact to produce symptoms?
In the normal brain:
Glutamatergic cells deliver a steady baseline stimulus to Dopaminergic neurons. These Dopaminergic neurons, in turn, release a steady baseline stream of Dopamine ("tonic firing") into the synaptic cleft.
Dopamine in the synaptic cleft will stimulate Dopamine autoreceptors (which dampen down Dopamine release) so that when the Dopamine pathway is activated by a particular stimulus, the burst of Dopamine ("burst firing") will be attenuated.
In the brain with schizophrenia:
There is some evidence that there is reduced baseline Glutamatergic stimulus - resulting in reduced Dopamine "tonic firing" - resulting in reduced concentrations of Dopamine in the synaptic cleft at rest.
This would result in reduced stimulation of the Dopamine autoreceptors. When the Dopamine pathway is then activated by a stimulus, the burst of Dopamine would be much greater than normal.
It is suggested that the low baseline levels of Dopamine activity in parts of the brain result in "negative" schizophrenic symptoms while the exaggerated burst firing results in "positive" schizophrenic symptoms.
see Grace et al. Tonic versus phasic dopamine release in the nucleaus accumbens. Schizophrenia Research (60) 2003