RELATIONSHIP BETWEEN CHANGES OF GLOMUS CELL CURRENT AND NEURAL RESPONSE OF RAT CAROTID-BODY

1. Mature rat carotid bodies were harvested and sinus nerve activity w as recorded in vitro during superfusion with Ringer saline. Membrane c urrents of glomus cells were simultaneously recorded using conventiona l whole cell or perforated-patch whole cell recording. Presumptive glo mus cells were identified by the presence of a rapidly activated, volt age-dependent outward current above a threshold of -20 mV. 2. Outward current of presumptive glomus cells was inhibited by tetraethylammoniu m chloride (TEA) (20 mM) and by verapamil (5-10 mu M), consistent with previous studies in which isolated glomus cells were used. Somal capa citance, calculated from the current transient following a step hyperp olarization, was 7.47 +/- 0.54 (SE) pF (n = 52). Membrane resistance f or perforated-patch recordings was 820 +/- 187 M Ohm. 3. In perforated -patch recordings, brief periods of hypoxia (30-45 s) caused a marked increase in nerve activity to 21.6 +/- 2.7 times baseline spiking freq uency (n = 59) but no significant change in membrane resistance or out ward current. No change in holding current was detected, although the low amplifier gain precluded high-resolution measurement. Similar resu lts were obtained using conventional whole cell recording, except that outward current significantly decreased during hypoxia but failed to recover in the immediate posthypoxia period. 4. TEA (20 mM) rapidly in hibited outward current to 55 +/- 7% (n = 15) of predrug current, but nerve activity only slightly increased to 2.0 +/- 0.3 times baseline s pike frequency (n = 15). Brief anoxia (40 s in duration) in the presen ce 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 (10 nM) significantly reduced outwar d current by 12.1 +/- 3.0% (n = 11) but did not significantly alter ne rve activity, holding current, or membrane resistance. Apamin (100 nM) 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 vo ltage-gated outward currents and changes in afferent nerve activity. T his suggests that modulation of glomus cell K+ current by hypoxia is n ot the primary step in initiating the nerve response to hypoxia in the rat carotid body.