Cardiovascular depressor responses to stimulation of substantia nigra and ventral tegmental area.
Experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of L-glutamate (Glu) stimulation of the substantia nigra (SN) and ventral tegmental area (VTA) on arterial pressure (AP) and heart rate (HR). Glu stimulation of the SN pars compacta (SNC) elicited decreases in both mean AP (MAP; -18.9 +/- 1.3 mmHg; n = 52) and HR (-26.1 +/- 1.6 beats/min; n = 46) at 81% of the sites stimulated. On the other hand, stimulation of the SN pars lateralis or pars reticulata did not elicit cardiovascular responses. Stimulation of the adjacent VTA region elicited similar decreases in MAP (-18.0 +/- 2.6 mmHg; n = 20) and HR (-25.4 +/- 3.8 beats/min; n = 17) at approximately 74% of the sites stimulated. Intravenous administration of the dopamine D2-receptor antagonist raclopride significantly attenuated both the MAP (70%) and the HR (54%) responses elicited by stimulation of the transitional region where the SNC merges with the lateral VTA (SNC-VTA region). Intravenous administration of the muscarinic receptor blocker atropine methyl bromide had no effect on the magnitude of the MAP and HR responses to stimulation of the SNC-VTA region, whereas administration of the nicotinic receptor blocker hexamethonium bromide significantly attenuated both the depressor and the bradycardic responses. These data suggest that dopaminergic neurons in the SNC-VTA region activate a central pathway that exerts cardiovascular depressor effects that are mediated by the inhibition of sympathetic vasoconstrictor fibers to the vasculature and cardioacceleratory fibers to the heart.
Kirouac
G J
GJ
Department of Physiology, University of Western Ontario, London, Canada.
Ciriello
J
J
D000704:Analysis of Variance; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001931:Brain Mapping; D018492:Dopamine Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D018738:Hexamethonium / Q000494:pharmacology; D008297:Male; D008636:Mesencephalon / Q000187:drug effects / Q000502:physiology*; D008845:Microinjections; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D020891:Raclopride; D051381:Rats; D017208:Rats, Wistar; D017448:Receptors, Dopamine D2 / Q000502:physiology; D012457:Salicylamides / Q000494:pharmacology; D013268:Stimulation, Chemical; D013378:Substantia Nigra / Q000187:drug effects / Q000502:physiology*; D013681:Tegmentum Mesencephali / Q000187:drug effects / Q000502:physiology*
D001552:Benzazepines; D018492:Dopamine Antagonists; D018727:Muscarinic Antagonists; D018733:Nicotinic Antagonists; D017448:Receptors, Dopamine D2; D012457:Salicylamides; D018738:Hexamethonium; D018698:Glutamic Acid; D020891:Raclopride; D001285:Atropine