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Chemoreception pp 255-261 | Cite as

Neurotransmitter Relationships in the Hypoxia-challenged Cat Carotid Body

  • Robert S. Fitzgerald
  • Hay-Yan Jack Wang
  • Serabi Hirasawa
  • Machiko Shirahata
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 536)

Abstract

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.

Keywords

Nicotinic Receptor Carotid Body Nucleus Tractus Solitarius Glomus Cell Cholinergic Mechanism 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. Alcayaga J., Iturriaga R., Varas R., Arroyo J., Zapata P., 1998. Selective activation of carotid nerve fibers by acetylcholine applied to the cat petrosal ganglion in vitro.Brain Res.786: 47–54.PubMedCrossRefGoogle Scholar
  2. Bairam A., Neji H., Marchal F., 2000. Cholinergic dopamine release from the in vitro rabbit carotid body.J. Appl. Physiol88: 1737–1744.PubMedGoogle Scholar
  3. Clarke P., Reuben M., 1996. Release of3H-noradrenaline from rat hippocampal synaptosomes by nicotine: mediation by different nicotinic receptor subtypes from striatal3H-dopamine release.Br. J. Pharmacol.117: 595–606.PubMedCrossRefGoogle Scholar
  4. DeKlippel N., Sarre S., Ebinger G., Michotte Y., 1993. Effect of M,- and M2-muscarinic drugs on striatal dopamine release and metabolism: an in vivo microdialysis study comparing normal and 6-hydroxy-dopamine-lesioned rats.Brain Res.630:57–64.CrossRefGoogle Scholar
  5. Fitzgerald R.S., 2000. Oxygen and carotid body chemotransduction: the cholinergic hypothesis - a brief history and new evaluation.Respir. Physiol.120: 89–104.PubMedCrossRefGoogle Scholar
  6. Fitzgerald R.S., Shirahata M., 1994. Acetylcholine and carotid body excitation during hypoxia in the cat.J. Appl Physiol76: 1566–1574.PubMedGoogle Scholar
  7. Fitzgerald R.S., Shirahata M., Ide T., 1997. Further cholinergic aspects of carotid body chemotransduction of hypoxia in cats.J. Appl. Physiol.82: 819–827.PubMedGoogle Scholar
  8. Fitzgerald R.S., Shirahata M., Ishizawa Y., 1996. The presynaptic component of a cholinergic mechanism in the carotid body chemotransduction of hypoxia in the cat.Adv. Exp. Med. Biol.410:245–252.PubMedCrossRefGoogle Scholar
  9. Fitzgerald R.S., Shirahata M., Wang H-Y., 1999. Acetylcholine release from cat carotid bodies.Brain Res.841:53–61.PubMedCrossRefGoogle Scholar
  10. Heymans C, Neil E., 1958. Reflexogenic Areas of the Cardiovascular System, p. 191. Boston: Little & Brown.Google Scholar
  11. Izurieta-Sanchez P., Sarre S., Ebinger G., Michotte Y., 2000. Muscarinic antagonists in substantia nigra influence the decarboxylation of L-dopa in striatum.Eur. J. Pharmacol.399: 151–160.PubMedCrossRefGoogle Scholar
  12. Nurse C.A., Zhang M., 1999. Acetylcholine contributes to hypoxic chemotransmission in co-cultures of rat type I cells and petrosal neurons.Respir. Physiol.115: 189–199.PubMedCrossRefGoogle Scholar
  13. Smolders I., Bogaert L., Ebinger G., Michotte Y., 1997. Muscarinic modulation of striatal dopamine, glutamate, and GABA release, as measured with in vivo microdialysisJ. Neurochem.68: 1942–1948.PubMedCrossRefGoogle Scholar
  14. Wang H-Y. (Jack), Fitzgerald R., 2002. Muscarinic modulation of hypoxia-induced release of catecholamines from the cat carotid body.Brain Res.927: 122–137.PubMedCrossRefGoogle Scholar
  15. Zhang M., Zhong H., Vollmer C, Nurse C.A., 2000. Co-release of ATP and ACh mediates hypoxic signalling at rat carotid body chemoreceptors.J. Physiol. Lond.525:143–158.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2003

Authors and Affiliations

  • Robert S. Fitzgerald
    • 1
  • Hay-Yan Jack Wang
    • 1
  • Serabi Hirasawa
    • 1
  • Machiko Shirahata
    • 1
  1. 1.Departments of Environmental Health Sciences (Division of Physiology), Physiology, Medicine, and Anesthesiology/Critical Care MedicineThe Johns Hopkins Medical InstitutionsBaltimoreUSA

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