ABSTRACT
Intercellular coupling by gap junctions is one of the main features of glial cells, but very little is known about this aspect of satellite glial cells (SGCs) in sympathetic ganglia. We used the dye coupling method to address this question in both a prevertebral ganglion (superior mesenteric) and a paravertebral ganglion (superior cervical) of mice. We found that in control ganglia, the incidence of dye coupling among SGCs that form the envelope around a given neuron was 10-20%, and coupling between SGCs around different envelopes was rare (1.5-3%). The dye injections also provided novel information on the structure of SGCs. Following peripheral inflammation, both types of coupling were increased, but most striking was the augmentation of coupling between SGCs forming envelopes around different neurons, which rose by 8-14.6-fold. This effect appeared to be non-systemic, and was blocked by the gap junction blocker carbenoxolone. These changes in SGCs may affect signal transmission and processing in sympathetic ganglia.
Subject(s)
Gap Junctions/physiology , Neurogenic Inflammation/pathology , Neuroglia/physiology , Superior Cervical Ganglion/pathology , Animals , Dinitrofluorobenzene/adverse effects , Dinitrofluorobenzene/analogs & derivatives , Disease Models, Animal , Female , Freund's Adjuvant/adverse effects , Gap Junctions/pathology , Isoquinolines/metabolism , Male , Mice , Mice, Inbred BALB C , Mice, Inbred C57BL , Neurogenic Inflammation/etiologyABSTRACT
Modest decreases in extracellular osmolarity induce brain hyperexcitability that may culminate in epileptic seizures. At the cellular level, moderate hyposmolarity markedly potentiates the intrinsic neuronal excitability of principal cortical neurons without significantly affecting their volume. The most conspicuous cellular effect of hyposmolarity is converting regular firing neurons to burst-firing mode. This effect is underlain by hyposmotic facilitation of the spike afterdepolarization (ADP), but its ionic mechanism is unknown. Because blockers of K(V)7 (KCNQ) channels underlying neuronal M-type K(+) currents (K(V)7/M channels) also cause spike ADP facilitation and bursting, we hypothesized that lowering osmolarity inhibits these channels. Using current- and voltage-clamp recordings in CA1 pyramidal cells in situ, we have confirmed this hypothesis. Furthermore, we show that hyposmotic inhibition of K(V)7/M channels is mediated by an increase in intracellular Ca(2+) concentration via release from internal stores but not via influx of extracellular Ca(2+). Finally, we show that interfering with internal Ca(2+)-mediated inhibition of K(V)7/M channels entirely protects against hyposmotic ADP facilitation and bursting, indicating the exclusivity of this novel mechanism in producing intrinsic neuronal hyperexcitability in hyposmotic conditions.
