The cholinergic influence on the function of the cat dorsal lateral geniculate nucleus (dLGN).

Abstract:

:The functional influence of the cholinergic input to cat dLGN has been examined by assessing the action of iontophoretically applied acetylcholine (ACh) on the visual responses of cells in layers A and A1. Iontophoretically applied pulses of ACh exerted a strong excitatory action on all 113 cells studied within these layers. In the presence of a sustained application of ACh, the excitatory responses to an optimal stimulus such as a spot of light located within the receptive field centre were greatly facilitated, but at the same time stimulus-specific inhibitory influences were also enhanced. The action of ACh on the stimulus-specific inhibitory influences had the consequence that the responses to non-optimal stimuli were not facilitated to the same extent as those to optimal stimuli and in some cases even diminished. The stimulus-specific inhibitory effects seen in the presence of ACh were very powerful and frequently resulted in complete suppression of the elevated background discharge. We suggest that the ACh directly excites both the relay cells and the Golgi type II inhibitory interneurones within the dLGN. The facilitation of the stimulus-specific inhibition may follow from a direct action on the presynaptic dendrites of the Golgi type II cells which arborize within the dendritic field of the relay cell. Supplementary observations on cells in the perigeniculate nucleus confirm previous findings showing that ACh has an inhibitory effect on these cells. We suggest a tripartite action for the cholinergic influence on the dLGN, involving direct facilitation of relay cells, enhancement of stimulus-specific inhibition via the Golgi type II cells, and disinhibition of the non-specific inhibitory influence form the perigeniculate nucleus.

journal_name

Brain Res

journal_title

Brain research

authors

Sillito AM,Kemp JA,Berardi N

doi

10.1016/0006-8993(83)90059-8

subject

Has Abstract

pub_date

1983-12-05 00:00:00

pages

299-307

issue

2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(83)90059-8

journal_volume

280

pub_type

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