Brain research 2012-02-23

Sympathetic premotor neurones project to and are influenced by neurones in the contralateral rostral ventrolateral medulla of the rat in vivo.

Simon McMullan, Paul M Pilowsky

文献索引：Brain Res. 1439 , 34-43, (2012)

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摘要

The tonic activity of bulbospinal neurones in the rostral ventrolateral medulla (RVLM) is thought to underlie basal sympathetic nerve activity. A key research objective is to delineate the mechanisms that contribute to the firing of these neurones. In the current study we investigate the hypothesis that inputs arising in the contralateral RVLM converge on barosensitive bulbospinal neurones and contribute to their discharge pattern. Extracellular recordings were made from 24 barosensitive bulbospinal neurones in urethane anaesthetised, vagotomised and artificially ventilated rats during activation (glutamate or D,L-homocysteic acid microinjection, 50 nl, 50mM, or monopolar electrical stimulation) or inhibition (microinjection of GABA receptor agonists muscimol or isoguvacine, 50 nl, 10mM) of the contralateral RVLM. Chemical RVLM activation strongly increased (10/17) or inhibited (6/17) the spontaneous activity of neurones recorded in the contralateral RVLM. Electrical RVLM stimulation evoked a combination of short latency (median 6 ms) inhibitory and longer latency (median 9.1 ms, P<0.01) excitatory orthodromic responses in contralateral sympathetic premotor neurones and in some cases evoked antidromic action potentials that collided with spontaneous spikes. RVLM inhibition increased the discharge rate of sympathetic premotor neurones in the contralateral brainstem by 21 ± 13% (P<0.05) and reduced the variability of unit firing by 37 ± 12% (n=5, p<0.05). These findings indicate that sympathetic premotor neurones receive inhibitory and excitatory input from the contralateral RVLM, that inhibitory inputs predominate under baseline conditions, and that a population of sympathetic premotor neurones project to the contralateral RVLM in addition to their spinal targets.Copyright © 2012 Elsevier B.V. All rights reserved.