Basal forebrain cholinergic input is not essential for lesion-induced plasticity in mature auditory cortex.
The putative role of the basal forebrain cholinergic system in mediating lesion-induced plasticity in topographic cortical representations was investigated. Cholinergic immunolesions were combined with unilateral restricted cochlear lesions in adult cats, demonstrating the consequence of cholinergic depletion on lesion-induced plasticity in primary auditory cortex (AI). Immunolesions almost eliminated the cholinergic input to AI, while cochlear lesions produced broad high-frequency hearing losses. The results demonstrate that the near elimination of cholinergic input does not disrupt reorganization of the tonotopic representation of the lesioned (contralateral) cochlea in AI and does not affect the normal representation of the unlesioned (ipsilateral) cochlea. It is concluded that cholinergic basal forebrain input to AI is not essential for the occurrence of lesion-induced plasticity in AI.
Kamke
Marc R
MR
School of Psychology, Psychiatry, and Psychological Medicine, Monash University, Victoria 3800, Australia. Marc.Kamke@med.monash.edu.au
Brown
Mel
M
Irvine
Dexter R F
DR
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001303:Auditory Cortex / Q000503:physiopathology*; D001927:Brain Diseases / Q000139:chemically induced / Q000503:physiopathology; D001931:Brain Mapping; D002415:Cats; D002799:Cholinergic Fibers; D003051:Cochlea / Q000293:injuries*; D000922:Immunotoxins; D009473:Neuronal Plasticity; D016548:Prosencephalon / Q000378:metabolism*; D014947:Wounds and Injuries / Q000503:physiopathology
D000922:Immunotoxins; D000109:Acetylcholine