A cardioinhibitory area in the midbrain central tegmental field of cats

Anya M.Y. Lin, C. M. Pan, Y. F. Lin, J. S. Kuo, Samuel H.H. Chan, C. Y. Chai*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


A cardioinhibitory area in the central tegmental field of the midbrain (CIM) was studied in cats under chloralose-urethane anesthesia. Electrical and chemical (glutamate and DL-homocysteic acid) stimulations in this area produced marked bradycardia accompanied by mostly hypotension or minimal change in arterial pressure and by occasional hypertension particularly in the dorsal portion. CIM excitation potentiated the reflex bradycardia induced by IV phenylephrine, while bilateral electrolytic lesion of CIM neither changed the resting cardiovascular parameters nor the reflex bradycardia. The CIM bradycardia was not affected by supracollicular decerebration, but substantially reduced by unilateral vagotomy and completely eliminated by bilateral vagotomy. Destruction of the ambiguus nucleus (NA) and solitary and dorsal motor nuclei (NTS/DMV) abolished the bradycardia. Midline bisection at the midbrain-pontine level only slightly reduced the bradycardia while at the medullary level it was moderately attenuated. Electrolytic lesion of the cardioinhibitory area in gigantocellular reticular nucleus (GRN) abolished the bradycardia. These findings suggest that CIM is an independent mechanism which may send axons to GRN from which the axons may in turn synapse with the NTS/DMV complex and NA. Its final output may utilize both vagus nerves to modulate baroreceptor reflex in promoting bradycardia.

Original languageEnglish
Pages (from-to)699-707
Number of pages9
JournalBrain Research Bulletin
Issue number6
StatePublished - Jun 1987


  • Ambiguus nucleus
  • Cardioinhibition
  • Central tegmental field
  • Dorsal motor nucleus
  • Gigantocellular reticular nucleus
  • Midbrain
  • Reflex bradycardia
  • Solitary nucleus


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