The neural pathway involved in "efferent inhibition" of chemoreceptors in the cat carotid body.
This study was done to determine whether a pathway of efferent axons in the carotid sinus nerve is necessary for the phenomenon of "efferent inhibition" (inhibition induced in carotid body chemoreceptors by electrical stimulation of the carotid sinus nerve). Our approach was to eliminate efferent axons in the carotid sinus nerve of cats without destroying the sensory axons. This was achieved by cutting the ipsilateral glossopharyngeal and vagus nerves central to their sensory ganglia and/or by removing the nodose and superior cervical ganglia. In neurophysiological studies we found that the response of chemoreceptors in cats 10 days after surgery was the same as that in controls. chemoreceptor activity was decreased by electrical stimulation of the carotid sinus nerve and was increased by hypoxia and cyanide. In operated cats as in control animals, "efferent inhibition" was abolished by haloperidol and dihydroergotamine, drugs that block the inhibitory action of dopamine. Electron microscopic studies disclosed that the number of nerve endings in glomus cell/sheath cell complexes was not measurably different in control and experimental carotid bodies. By contrast, 10 days after the carotid sinus nerve was cut the number of nerve endings next to such ells was reduced by more than 99%. cutting the nerve roots and excising the ganglia eliminated most nerve endings on blood vessels: The number of noradrenergic-type nerve endings was reduced 99% and other types of nerve endings (presumptive cholinergic and peptidergic types) were reduced by more than 90%. Our experiments indicate that "efferent inhibition" is not abolished by operations that destroy inputs to blood vessels and to carotid boy glomus cells from (1) the nodose ganglion, (2) superior cervical ganglion, or from (3) neurons in the brain stem whose axons run in the glossopharyngeal or vagus nerves. We conclude that " efferent inhibition" may be caused by antidromic stimulation of sensory axons.
D000818:Animals; D002344:Carotid Body / Q000502:physiology* / Q000648:ultrastructure; D002415:Cats; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004087:Dihydroergotamine / Q000494:pharmacology; D004525:Efferent Pathways / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology*
D004087:Dihydroergotamine; D006220:Haloperidol