Stimulation within the rostral ventrolateral medulla can evoke monosynaptic GABAergic IPSPs in sympathetic preganglionic neurons in vitro. Deuchars, Susan A., K. Michael Spyer & Michael P. Gilbey. Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF.
APStracts 3:0227N, 1996.
The inhibitory responses of identified sympathetic preganglionic neurons (SPNs) to stimulation within the the rostral ventrolateral medulla (RVLM) were studied to determine their nature and pharmacology. Whole cell patch clamp recordings were made from 36 sympathetic preganglionic neurons (SPNs) in the upper thoracic segments of the spinal cord in a neonatal rat brainstem-spinal cord preparation. Neurons were identified as SPNs on the basis of their antidromic activation following stimulation of the ipsilateral segmental ventral root and their morphology and location in the intermediolateral cell column and intercalated nucleus. In all SPNs, electrical stimulation of the RVLM evoked fast EPSPs that were mediated by non-NMDA and NMDA receptors. These excitatory responses were the most prominent response in control aCSF and have been studied previously. In 22 of the SPNs, RVLM stimulation also elicited fast IPSPs that increased in amplitude as the membrane was depolarised. Five of these neurons were not studied further as they responded occasionally with IPSPs that had highly variable onset latencies indicating the involvement of a polysynaptic pathway. In the remaining SPNs (n = 17) the evoked IPSPs persisted in the presence of the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3,-dione (CNQX) and D,L-2-amino-5- phosphonopentanoic acid (AP-5). In eight of these SPNs it was necessary to block the EPSPs to reveal the IPSPs. In the 7 SPNs tested, the onset latencies of the IPSPs were not significantly different from the onset latencies of the fast EPSPs. The low sweep to sweep fluctuations in onset latency of individual IPSPs (absolute average deviation 0.4 ms) indicated that the IPSPs were elicited by activation of a monosynaptic pathway. The amplitudes of the IPSPs decreased in amplitude as the membrane was hyperpolarised and reversed in polarity at -70.3 +/- 1.7 mV which was close to the equilibrium potential for chloride ions. In addition, in 7 SPNs, bath applications of 5 [mu]M bicuculline, a GABA A antagonist, abolished or reduced the evoked IPSPs. Five SPNs were also studied which displayed ongoing IPSPs. The amplitudes of these IPSPs increased with membrane depolarisation and were blocked by bath applications of 5 [mu]M bicuculline suggesting that they were also mediated by activation of GABA A receptors. These results demonstrate the existence of a bulbospinal GABAergic pathway impinging directly onto SPNs. This pathway may be tonically active in the neonatal rat brainstem-spinal cord preparation.

Received 16 January 1996; accepted in final form 4 September 1996.
APS Manuscript Number J22-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996