Spinal GABA(A) receptors do not mediate the sympathetic baroreceptor reflex in the rat

Ann K. Goodchild, Bart T.M. Van Deurzen, Qi Jian Sun, John Chalmers, Paul M. Pilowsky

Research output: Contribution to journalArticlepeer-review

16 Citations (Scopus)


Activation of baroreceptors causes efferent sympathetic nerve activity (SNA) to fall. Two mechanisms could account for this sympathoinhibition: Disfacilitation of sympathetic preganglionic neurons (SPN) and/or direct inhibition of SPN. The roles that spinal GABA and glycine receptors play in the baroreceptor reflex were examined in anesthetized, paralyzed, and artificially ventilated rats. Spinal GABA(A) receptors were blocked by an intrathecal injection of bicuculline methiodide, whereas glycine receptors were blocked with strychnine. Baroreceptors were activated by stimulation of the aortic depressor nerve (ADN), and a somatosympathetic reflex was used as control. After an intrathecal injection of vehicle, there was no effect on any measured variable or evoked reflex. In contrast, bicuculline caused a dose-dependent increase in arterial pressure, SNA, phrenic nerve discharge, and it significantly facilitated the somatosympathetic reflex. However, bicuculline did not attenuate either the depressor response or sympathoinhibition evoked after ADN stimulation. Similarly, strychnine did not affect the baroreceptor-induced depressor response. Thus GABA(A) and glycine receptors in the spinal cord have no significant role in baroreceptor-mediated sympathoinhibition.

Original languageEnglish
Pages (from-to)R320-R331
Number of pages12
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number1
Publication statusPublished - 1 Jul 2000
Externally publishedYes


  • Aortic depressor nerve
  • Arterial pressure
  • Phrenic nerve discharge
  • Sympathetic nerve activity


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