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 (Vm) and input resistance (Ro) were thus measured. Both coupled cells were then voltage clamped at a level between their Vms. Current pulses applied to either cell elicited a transjunctional voltage (Vj) and current (Ij), used to calculate the junctional conductance (Gj). Gj was 1.52+/-0.29 nS (mean+/-S.E.; n=147). Vj linearly influenced Gj, suggesting ohmic junctions. Gj was not affected by Vm in 50% of the cases. However, there was Vm-dependence in the others, but voltage changes had to be large (>+/-40 mV from the Vm). Therefore, physiologically or pharmacologically induced glomus cell depolarization or hyperpolarization may not significantly affect intercellular coupling unless there are large variations in Vm. Hypoxia (induced by Na2S2O4 1 mM or 100% N2) decreased Gj 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 Gj 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 Gj 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.
Abudara
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Departments of Physiology, University of Utah School of Medicine, Research Park, Salt Lake City, UT 84108, USA.
Eyzaguirre
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D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002344:Carotid Body / Q000503:physiopathology*; D002478:Cells, Cultured; D003035:Cobalt / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology*; D004594:Electrophysiology; D006863:Hydrogen-Ion Concentration; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007365:Intercellular Junctions / Q000502:physiology*; D007700:Kinetics; D008564:Membrane Potentials / Q000502:physiology; D008839:Microelectrodes; D009431:Neural Conduction / Q000502:physiology*; D018408:Patch-Clamp Techniques; D051381:Rats
D002121:Calcium Channel Blockers; D003035:Cobalt; D003994:Bucladesine; D000242:Cyclic AMP