EFFECTS OF DOPAMINE ON NEURONS OF THE LATERAL GENICULATE-NUCLEUS - ANIONTOPHORETIC STUDY

Citation
D. Albrecht et al., EFFECTS OF DOPAMINE ON NEURONS OF THE LATERAL GENICULATE-NUCLEUS - ANIONTOPHORETIC STUDY, Synapse, 23(2), 1996, pp. 70-78
Citations number
46
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
08874476
Volume
23
Issue
2
Year of publication
1996
Pages
70 - 78
Database
ISI
SICI code
0887-4476(1996)23:2<70:EODONO>2.0.ZU;2-4
Abstract
In urethane anesthetized rats, the iontophoretic administration of dop amine (DA) induced an inhibition of flash-evoked activity in the major ity of geniculate cells investigated. Excitatory effects of DA also we re found in some neurons of the dorsal lateral geniculate nucleus. The observed excitatory effects of DA were blocked selectively by D2 rece ptor antagonists, and the majority of inhibitory effects could be bloc ked by D1 receptor antagonists. In some neurons, the D2 receptor antag onist also blocked the DA-induced inhibition. Nine of 33 neurons teste d responded differently to DA according to the amount ejected: with lo wer iontophoretic currents they increased their rates of discharge, wh ereas higher DA ejecting currents resulted in a suppression of their a ctivity. Iontophoretic administration of a D1 agonist (SKF 38393) for the most part induced a decrease in baseline activity, whereas the D2 agonist (quinpirole) frequently induced an increase. These effects of agonists were dose-dependent and reproducible. Effects of the D1 and D 2 agonists could be reversed by the receptor-specific dopamine antagon ists. Presumed local circuit interneurons appeared to be involved in m ediation of some inhibitory effects of DA, since the D2-induced inhibi tions could be abolished by the GABA(A) antagonist, bicuculline. The m ajority of cells also was affected by DA antagonists given alone; thes e cells' responses to light usually were of an inhibitory nature. The results show that like other monoamines, DA also is involved in certai n aspects of visual processing at the level of the thalamus. (C) 1996 Wiley-Liss, Inc.