Hypothesis: ACh is an essential excitatory neurotransmitter in the cat cb chemotransduction of hypoxia. Postulated model: neurotransmission in the superior cervical ganglion. In previous studies focused on the postsynaptic component - the nerve fiber apposed to the Type I cell - mecamylamine and atropine reduced the cb respone to a perfusion of hypoxic Krebs Ringer bicarbonate solution (KRB) in a dose-related way. Pirenzepinc- and gallamine-containing hypoxic KRB produced changes in neural activity consistent with a role for sEPSP and sIPSP in the cb, suggesting the presence of postsynaptic M1 and M2 muscarinic receptors. In this study focus is on the presynaptic element -the ACh-containing Type I cell. Nerve activity is recorded from the whole carotid sinus nerve (minus harorcceptor activity) in the anesthetized, paralyzed, artificially ventilated cat filled with a loop in the common carotid artery which allows intermittent, transient, selective perfusions of the cb. Previously we have shown that excluding calcium from the perfusate greatly reduced the cb's response to hypoxic KRB. Vesamicol and Cetiedil are two agents which prevent the packaging of ACh in vesicles and/or the release of ACh from the vesicles at the presynaptic membrane into the synaptic cleft. The inclusion of these agents reduced the cb response to hypoxic KRB in a dose-related manner . 1 hese data suggest that the steps in classical neurotransmission -entry of extracellular calcium into the presynaptic component and vesicular release of the neurotransmitter -apply to ACh in the cb. The data support the hypothesis.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology