EXTRINSIC INHIBITORY INNERVATION TO RUBRAL NEURONS IN RAT BRAIN-STEM SLICES

Citation
Ys. Fu et al., EXTRINSIC INHIBITORY INNERVATION TO RUBRAL NEURONS IN RAT BRAIN-STEM SLICES, Experimental neurology, 137(1), 1996, pp. 142-150
Citations number
24
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
137
Issue
1
Year of publication
1996
Pages
142 - 150
Database
ISI
SICI code
0014-4886(1996)137:1<142:EIITRN>2.0.ZU;2-T
Abstract
Synaptic connections between the neurons in the red nucleus (RN) and i ts extrinsic neurons were studied using rat brain-stem slices. Intrace llular records were obtained from the RN neurons. Ipsilateral stimuli to areas in the dorsolateral mesencephalic reticular formation (DLMRF) or substantia nigra (SN) elicited monosynaptic hyperpolarizing postsy naptic potentials (PSPs) in about 95% of RN neurons recorded. The hype rpolarizing PSPs could be reversibly blocked by bicuculline, indicatin g that they were GABA(A) receptor-mediated-Cl--inhibitory PSPs. The si tes of most inhibitory synapses arising from DLMRF and SN are possibly located on the proximal half of the soma-dendritic membrane of RN neu rons, according to the analysis of the IPSPs with Rall's model. In add ition, tracing dyes were employed to examine the morphological pathway s. After rhodamine B, a retrograde tracer, was applied to the RN in br ain slices, the cell bodies of a number of neurons in DLMRF and SN wer e labeled. These labeled neurons were also immunopositive for glutamic acid decarboxylase (GAD) as revealed from double labeling with an ant i-GAD antiserum. The anterograde tracer, tetramethylrhodamine dextran, was applied to the DLMRF or SN and taken up by many neurons in the ar eas. A portion of these cells extended their processes toward and term inated within the RN. Moreover, electron microscopic examination confi rmed that the tetramethylrhodamine dextran-decorated synaptic terminal s were present in the RN. The results indicate that the rubral neurons receive direct GABA(A) receptor-mediated inhibitory inputs from neuro ns in the DLMRF and SN, which may participate in modulation of rubral outputs. (C) 1996 Academic Press, Inc.