THE NEURAL PATHWAY INVOLVED IN EFFERENT INHIBITION OF CHEMORECEPTORS IN THE CAT CAROTID-BODY
THE NEURAL PATHWAY INVOLVED IN EFFERENT INHIBITION OF CHEMORECEPTORS IN THE CAT CAROTID-BODY
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DOI:
10.1002/cne.902010310
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发表时间:
1981-01-01
影响因子:
2.5
通讯作者:
MITCHELL, RA
中科院分区:
文献类型:
--
作者:
MCDONALD, DM;MITCHELL, RA
Whether a pathway of efferent axons in the carotid sinus nerve is necessary for efferent inhibition (inhibition induced in carotid body chemoreceptors by electrical stimulation of the carotid sinus nerve) is studied. Efferent axons in the carotid sinus nerve of cats were eliminated 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, 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. EM studies disclosed that the number of nerve endings in glomus cell/sheath cell complexes was not measurably different in control and experimental carotid bodies. After the carotid sinus nerve was cut [10 days] the number of nerve endings next to such cells was reduced by > 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 by 99% and other types of nerve endings (presumptive cholinergic and peptidergic types) were reduced > 90%. Efferent inhibition probably is not abolished by operations that destroy inputs to blood vessels and to carotid body glomus cells from the nodose ganglion, superior cervical ganglion or from neurons in the brain stem whose axons run in the glossopharyngeal or vagus nerves. Efferent inhibition may be caused by antidromic stimulation of sensory axons.