Neuronal mechanisms of the attentional dysfunctions in senile dementia and schizophrenia: two sides of the same coin?

摘要: Deficits in early stages of information processing, specifically the inability to “disattend” irrelevant stimuli and selectively allocate processing resources (i.e., hyperattention), have been associated with development psychotic symptoms. Opposite deficits, i.e., failure attend select stimuli, divide attention hypoattention), represent a major variable dementia. The hypothesis that hyperattention hypoattention are mediated via cortical cholinergic hyperactivity hypoactivity, respectively, is discussed. Several lines evidence support role symptoms, including therapeutic effects anticholinergic drugs schizophrenic patients, chronic exposure irreversible cholinesterase inhibitors, worsening symptoms as result treatment cholinomimetic compounds. potent impairments attentional abilities administration muscarinic antagonists intact subjects, compounds demented patients two examples supports hypofunction cognitive A neuronal model dopamine-GABAergic modulation acetylcholine proposed on basis indicating nucleus accumbens dopamine, GABAergic pathway substantia innominata basal forebrain, modulates release. available confirms several predictions derived from this model, dopaminergic regulation (ACh) release, bidirectional release by benzodiazepine receptor (BZR) agonists inverse agonists, antipsychotic BZR agonists. Bidirectional deviations activity inputs hypothesized substrate dysfunctions with, or even underlying,