Clindamycin-induced alteration of ganglionic function. I. Direct effects on ganglion cell properties.

The influence of the lincosamide antibiotic, clindamycin, on the properties of bullfrog sympathetic ganglion B cells has been determined in vitro using conventional voltage recording methods or single microelectrode voltage-clamp recording techniques. Individual neurons were depolarized with both bath application or local perfusion of clindamycin. The amplitude of the depolarization was not altered by pretreatment with 50 microM (+)-tubocurarine, 10-microM atropine, or 1.5 microM tetrodotoxin (TTX), indicating that the clindamycin-induced depolarization does not result from either the activation of (1) nicotinic receptors, (2) muscarinic receptors, or (3) voltage-gated sodium channels. Clindamycin partially inhibited IM, an action which accounts for part of the clindamycin-induced depolarization. The duration of the hyperpolarizing afterpotential (HAP) following the action potential was decreased in the presence of clindamycin. Clindamycin decreased the amplitude and maximum rate of rise (MRR) of TTX-insensitive action potentials. As calcium influx is thought to contribute to the depolarizing phase of the TTX-insensitive spikes, we suggest that the decrease in HAP duration by clindamycin results from a decrease in the somal calcium current. Further, it is suggested that a decrease in IM and HAP duration may be responsible for the increased excitability exhibited during exposure to clindamycin.