A series of human and animal investigations has suggested that altered
expression and function of the alpha 7-nicotinic cholinergic receptor
may be responsible for the auditory sensory gating deficit characteri
zed in schizophrenia patients and their relatives as diminished suppre
ssion of an auditory-evoked response (P50) to repeated stimuli. This f
inding, in conjunction with evidence for familial transmission of this
sensory gating deficit; suggests a pathogenic role of the gene for th
e alpha 7-nicotinic receptor in schizophrenia. This article considers
the possible effects of this dysfunction in a broader context. Not onl
y is this dysfunction consistent with difficulties in sensory gating,
but it might also predispose patients to problems with learning effici
ency and accuracy. Such learning problems could underlie schizophrenia
patients' delusional thinking, hallucinations, and social dysfunction
, In addition, heavy smoking in many schizophrenia patients is consist
ent with the high concentration of nicotine necessary to activate the
receptor and with the receptor's extremely rapid desensitization. Fina
lly, the receptor's possible role in cell. growth and differentiation
should be considered in connection with developmental deficits and oth
er cellular abnormalities in schizophrenia.