EFFECTS OF IL-1-BETA ON NEURONAL ACTIVITIES IN THE DORSAL MOTOR NUCLEUS OF THE VAGUS IN RAT-BRAIN SLICES

Citation
Zl. Mo et al., EFFECTS OF IL-1-BETA ON NEURONAL ACTIVITIES IN THE DORSAL MOTOR NUCLEUS OF THE VAGUS IN RAT-BRAIN SLICES, Brain research bulletin, 41(4), 1996, pp. 249-255
Citations number
38
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03619230
Volume
41
Issue
4
Year of publication
1996
Pages
249 - 255
Database
ISI
SICI code
0361-9230(1996)41:4<249:EOIONA>2.0.ZU;2-I
Abstract
Effects of recombinant human interleukin-1 beta (IL-1 beta) on the neu ronal activities in the rat dorsal motor nucleus of the vagus (DMV) we re investigated by extra- and intracellular recordings in slice prepar ations. Twelve (52%) of 23 spontaneously firing neurons recorded extra cellularly, 7 of which were electrophysiologically identified as vagal motoneurons, were inhibited by a bath application of IL-1 beta at a d ose of either 5.8 x 10(-8) or 5.8 x 10(-9) M. The duration of the resp onses ranged widely from about 10 min to more than 2 h. Two (9%) of th e 23 neurons were excited, whereas the remaining 9 (39%) were not affe cted by IL-1 beta. Of 42 DMV neurons recorded intracellularly, 19 (45% ) showed a hyperpolarization following an application of 5.8 x 10(-8) M IL-1 beta, which still persisted in a TTX-containing solution. Two ( 5%) displayed depolarization and 21 (50%) were unaffected. The hyperpo larization in 16 of the 19 neurons (84%) ranged from -5 to -10 mV and lasted for more than 30 min without changing the input resistance. The IL-1 beta-induced hyperpolarization was completely blocked by concurr ent perfusion with sodium salicylate. The remaining three neurons show ed a short-lasting (5-14 min) hyperpolarization (ranging from -6 to -1 5 mV) with a decrease in the input resistance. These findings indicate that IL-1 beta mainly inhibits the vagal motoneurons in the DMV, at l east partly through prostaglandin synthesis. This provides a mechanism that could account for the central action of IL-1 beta on visceral pr ocesses such as the inhibition of gastric acid secretion. Copyright (C ) 1996 Elsevier Science Inc.