Dysregulation of thalamic sensory 'transmission' in schizophrenia:
neurochemical vulnerability to hallucinations
Ralf-Peter Behrendt*
The Retreat Hospital, Heslington Road, York, UK.
* To whom correspondence should be addressed.
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Abstract |
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Cholinergic arousal mechanisms predispose thalamic and cortical neurons to fire
action potentials at gamma rhythms, which have a tendency to resonate in thalamocortical
networks, thereby forming coherent assemblies under constraints of sensory input to
specific thalamic nuclei, on the one hand, and prefrontal and limbic attentional
mechanisms, on the other. Perception may be based on sustained assemblies of coherent
gamma oscillations in thalamocortical circuits. In schizophrenia, the impact of sensory
input on self-organization of thalamocortical activity may be generally reduced. As a
result, processes underlying perception can become uncoupled from sensory input,
particularly at times of hyperarousal, leading to domination of attentional mechanisms
and the emergence of hallucinations. Evidence is reviewed that implicates excessive
neuronal noise in specific thalamic nuclei in the generation of hallucinations in
schizophrenia. Nicotinic receptor abnormalities, dopaminergic hyperactivity and
glutamate-receptor hypofunction are reconciled within a model of psychotic symptom
generation that places crucial emphasis on dysfunction of the reticular thalamic nucleus.
Key Words:
acetylcholine, alpha-7 nicotinic receptor, antipsychotics, dopamine, hallucinogens, reticular thalamic nucleus, stress-vunerability models, psychosis
