MODULATION OF JUNCTIONAL CONDUCTANCE BETWEEN RAT CAROTID-BODY GLOMUS CELLS BY HYPOXIA, CAMP AND ACIDITY

Short-term cultures of glomus cells (up to seven days), were employed to study intercellular electrical communications. Bidirectional electr ic coupling was established under current clamping after impaling two adjacent glomus cells with microelectrodes, and alternate stimulation and recording. Their resting potential (V-m) and input resistance (R-o ) were thus measured. Both coupled cells were then voltage clamped at a level between their V(m)s. Current pulses applied to either cell eli cited a transjunctional voltage (V-j) and current (I-j), used to calcu late the junctional conductance (G(j)). G(j) was 1.52 +/- 0.29 nS (mea n +/- S.E.; n = 147). V-j linearly influenced G(j), suggesting ohmic j unctions. G(j) was not affected by V-m in 50% of the cases. However, t here was V-m-dependence in the others, but voltage changes had to be l arge (> +/-40 mV from the V-m). Therefore, physiologically or pharmaco logically induced glomus cell depolarization or hyperpolarization may not significantly affect intercellular coupling unless there are large variations in V-m. Hypoxia (induced by Na2S2O4 1 mM or 100% N-2) decr eased G(j) in 60-80% of the pairs while producing tighter coupling in the rest. Similar effects were obtained when the medium was acidified with lactic acid 1-10 mM. Cobalt chloride (3 mM) prevented, diminished or reversed the changes in G(j) observed during low PO2, suggesting t hat [Ca2+](i) changes are important in hypoxic uncoupling. However, no n-specific cationic effects of Co2+ have not been ruled out. Applicati ons of the membrane-permeant dB-cAMP 1 mM tightened coupling in almost all cell pairs. This is important because endogenous cAMP increases d uring hypoxia. Our results suggest that multiple factors modulate junc tional conductance between glomus cells. Changes in G(j) by 'natural' stimuli and/or cAMP may play an important role in chemoreception, espe cially in titrating the release of transmitters toward the carotid ner ve terminals. (C) 1998 Elsevier Science B.V.