Neurotransmitter Relationships in the Hypoxia-challenged Cat Carotid Body

The most fundamentally necessary substrate for life is oxygen.The human organism cannot be without it for more than a few minutes without doing irreversible damage to neural structures. This substrate is used to oxidize glucose, which process provides the organism with the energy required for all of life’s processes. Well-appreciated is the fact that the carotid body is the principal detector of systemic hypoxia. The aortic bodies also play a role, but appear to be in humans at least considerably less important. We have learned in this conference that the carotid body also increases its neural output to the nucleus tractus solitarius in response to reduced glucose in blood or perfusion fluids.lt is therefore somewhat amusing as well as frustrating that even though 250 years have passed since the first report of the carotid body in 1743, the precise steps describing how this all-important structure sends its message to the nucleus tractus solitarius continue to remain mysterious.Generations of investigators have tried to determine these mechanisms. And though considerable progress has been made, no definitive answer can yet be provided.interrelationship in the carotid body. Bairam and her colleagues (2000) using a different preparation also found that cholinergic agonists delivered exogenously controlled the release of catecholamines. That cholinergic mechanisms are found to control catecholaminergic release in the carotid body is not altogether surprising. The autonomic nervous system controls the heart’s stroke volume and rate with a balance and interaction of the sympathetic and parasympathetic nervous systems on the heart and on each other. In the central nervous system there are several instances of muscarinic and nicotinic modulation of dopamine and noradrenaline release (Clarke et al., 1996; DeKlippel et al., 1993; P. Izurieta-Sanchez et al, 2000; Smolders et al., 1997). One study suggested a potential source for the difference between release patterns for DA and NE. Presynaptic nicotinic receptors associated with striatal DA terminals differed pharmacologically from those on hippocampal NE terminals. Nigrostriatal DA neurons expressed mainly a4, a5, and 02 nicotinic receptor subunits, while hippocampal NE neurons expressed a3, p2, and P4 subunits. This situation is consistent with the reports of several other glomus cell heterogeneities. It seems entirely possible that not all glomus cells have exactly the same complement of neurotransmitters nor the same set of nicotinic receptors. Further study of neurotransmitter interrelationships will undoubtedly help to bring greater clarity to these interactions so fundamental to the chemotransduction of hypoxia, and perhaps reveal clues as to the mechanisms involved in the transduction of hypoglycemia.