Immunocytochemical and Neuro-Chemical Aspects of Sympathetic Ganglion Chemosensitivity

Abstract

Previous studies by Hanson et a1.⁸ demonstrated that acute hypoxic stress in vivo reduced the content of the neuropeptides, substance P and met-enkephalin, in decentralized superior cervical ganglia (SCG), and elevated glucose utilization in SCG exposed to hypoxia in vitro. Because similar changes were observed in the chemosensory tissue of the carotid body and not in nonchemosensory control tissue, these authors suggested that SCG contain intrinsic chemosensory mechanisms⁸.The subsequent studies of Cheng et al.² and Dalmaz et a1.³ added further support to this hypothesis. Dalmaz, Pequignot and their colleagues^3,15 showed that the turnover of dopamine (DA) was significantly increased in both the superior cervical ganglia (SCG) and carotid bodies from rats chronically (2 to 28 days) exposed to hypoxic gas mixtures. Their experiments also demonstrated that the turnover of norepinephrine (NE), the dominant biogenic amine contained in postganglionic SCG neurons, was not altered by chronic hypoxia, while its turnover in the carotid body was elevated between days 7 and 28 of the chronic exposure^3,15. A critical observation in these studies was that DA turnover in SCG remained elevated in hypoxic animals treated with guanethidine, an agent known to destroy primarily NE containing neuronal cell bodies ³.. Because nearly one-half of the DA in SCG is presumed to be contained in small intensely fluorescent (SIF) cells ¹², which remain intact following guanethidine treatment, it was suggested that these peculiar cells were acting as chemosensory in sympathetic ganglia. However, despite the fact that increased DA turnover persisted in the SCG following chronic carotid sinus nerve transection and preganglionectomy³, Dalmaz et a1.³