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 electric 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_ms. Current pulses applied to either cell elicited a transjunctional voltage (V_j) and current (I_j), used to calculate the junctional conductance (G_j). G_j was 1.52±0.29 nS (mean±S.E.; n=147). V_j linearly influenced G_j, suggesting ohmic junctions. G_j was not affected by V_m in 50% of the cases. However, there was V_m-dependence in the others, but voltage changes had to be large (>±40 mV from the V_m). Therefore, physiologically or pharmacologically 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% N₂) decreased 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 that Ca²⁺]_i changes are important in hypoxic uncoupling. However, non-specific cationic effects of Co²⁺ have not been ruled out. Applications of the membrane-permeant dB-cAMP 1 mM tightened coupling in almost all cell pairs. This is important because endogenous cAMP increases during hypoxia. Our results suggest that multiple factors modulate junctional conductance between glomus cells. Changes in G_j by ‘natural' stimuli and/or cAMP may play an important role in chemoreception, especially in titrating the release of transmitters toward the carotid nerve terminals.