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
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