RELATIONSHIP BETWEEN CHANGES OF GLOMUS CELL CURRENT AND NEURAL RESPONSE OF RAT CAROTID BODY. CHENG, PHILLIP M., DAVID F. DONNELLY. Department of Pediatrics, Section of Respiratory Medicine, Yale University School of Medicine, New Haven, CT 06510.
APStracts 2:0235N, 1995.
SUMMARY AND CONCLUSIONS
1. Mature rat carotid bodies were harvested and sinus nerve activity was recorded, in vitro , during superfusion with Ringer's saline. Membrane currents of glomus cells were simultaneously recorded using conventional whole-cell or perforated-patch whole-cell recording. Presumptive glomus cells were identified by the presence of a rapidly-activated, voltage-dependent outward current above a threshold of - 20mV. 2. Outward current of presumptive glomus cells was inhibited by tetraethylammonium chloride (20mM) and by verapamil (5-10[mu]M), consistent with previous studies using isolated glomus cells. Somal capacitance, calculated from the current transient following a step hyperpolarization, was 7.47+/-0.54 pF (n=52, mean+/-SEM). Membrane resistance for perforated-patch recordings was 820+/-187 Mohms. 3. In perforated-patch recordings, brief periods of hypoxia (30-45s) caused a marked increase in nerve activity to 21.6+/-2.7 times baseline spiking frequency (n=59) but no significant change in membrane resistance or outward current. No change in holding current was detected, although the low amplifier gain precluded high resolution measurement. Similar results were obtained using conventional whole cell recording, except outward current significantly decreased during hypoxia but failed to recover in the immediate post-hypoxia period. 4. Tetraethylammonium (20mM) rapidly inhibited outward current to 55+/-7% (n=15) of pre-drug current, but nerve activity only slightly increased to 2.0+/-0.3 times baseline spike frequency (n=15). Brief anoxia (40s duration) in the presence of TEA evoked a brisk increase in nerve activity to 30+/-13 times baseline frequency (n=3), demonstrating that organ function was not blocked by TEA. 5. Charybdotoxin (10nM) significantly reduced outward current by 12.1+/-3.0% (n=11) but did not significantly alter nerve activity, holding current or membrane resistance. Apamin (100nM) did not significantly affect nerve activity, membrane resistance or holding current. Outward current decreased by 11.4+/-6.1% (n=13). 6. These results show a dissociation between changes in glomus cell voltage-gated outward currents and changes in afferent nerve activity. This suggests that modulation of glomus cell K + current by hypoxia is not the primary step in initiating the nerve response to hypoxia in the rat carotid body. 

Received 24 October 1994; accepted in final form 24 June 1995.
APS Manuscript Number J668-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 August 1995.