A glutamatergic deficiency model of schizophrenia.
Although the presence of hyperdopaminergia has been demonstrated in the brains of people with schizophrenia, at least in some circumstances, other neurotransmitters are important in this disorder, and a glutamatergic deficiency model of schizophrenia is proposed. It is suggested that the amount of sensory input allowed to reach the cerebral cortex is restricted by an inhibitory effect of the striatal complexes on the thalamus, thereby protecting it from being overwhelmed. Several strands of evidence are presented to support the concept that a weakened glutamatergic tone increases the risk of sensory overload and of exaggerated responses in the monoaminergic systems that could result in psychosis.
Carlsson
A
A
Department of Pharmacology, University of Göteborg, Sweden.
Hansson
L O
LO
Waters
N
N
Carlsson
M L
ML
D015306:Biogenic Monoamines / Q000378:metabolism; D002540:Cerebral Cortex / Q000378:metabolism; D018492:Dopamine Antagonists / Q000378:metabolism; D018698:Glutamic Acid / Q000172:deficiency*; D006801:Humans; D018377:Neurotransmitter Agents / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D012559:Schizophrenia / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology
D015306:Biogenic Monoamines; D018492:Dopamine Antagonists; D018377:Neurotransmitter Agents; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid