Spinal vs. supraspinal sites of action of the α2-adrenergic agonists clonidine and ST-91 on the acoustic startle reflex

Michael Davis, Randall L. Commissaris, Singal Yang, Kathryn R. Wagner, John H. Kehne, James V. Cassella, Nicholas M. Boulis

Research output: Contribution to journalArticlepeer-review


Previous work has shown that stimulation of α2-adrenergic receptors depresses the startle responses in rats. The present study suggests that this depressant effect involves supraspinal rather than spinal α2-adrenergic receptors because intraventricular but not intrathecal infusion of the hydrophilic α2-adrenergic agonist ST-91 depressed the acoustic startle reflex. To determine the point in the acoustic startle pathway where α2-adrenergic receptor activation might ultimately alter neural transmission, startle responses were elecited electrically from different points along the acoustic startle pathway after systemic administration of clonidine. Clonidine depressed acoustically-elicited startle and startle elicited by electrical stimulation of the ventral cochlear nucleus to a comparable magnitude and over a similar time course. It also partially depressed startle elicited by electrical stimulation of the nucleus reticularis pontis caudalis (RPC). Taken together, these data suggest that α2-adrenergic stimulation depresses startle by acting on supraspinal receptors, but that this effect is ultimately expressed, at least in part, by actions at both spinal and brainstem levels of the acoustic startle response pathway. The results are compared to other drugs known to affect the startle reflex.

Original languageEnglish (US)
Pages (from-to)233-240
Number of pages8
JournalPharmacology, Biochemistry and Behavior
Issue number1
StatePublished - May 1989
Externally publishedYes


  • Clonidine
  • Nucleus reticularis pontis caudalis
  • Reticular formation
  • ST-91
  • Spinal cord
  • Startle
  • Ventral cochlear nucleus
  • α-adrenergic receptors

ASJC Scopus subject areas

  • Biochemistry
  • Toxicology
  • Pharmacology
  • Clinical Biochemistry
  • Biological Psychiatry
  • Behavioral Neuroscience


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