Synaptic stimulation of nicotinic receptors in rat sympathetic ganglia is followed by slow activation of postsynaptic potassium or chloride conductances

Two slow currents have been described in rat sympathetic neurons during and after tetanization of the whole preganglionic input. Both effects are medi ated by nicotinic receptors activated by native acetylcholine (ACh). A firs t current, indicated as I-AHPsyn, is calcium dependent and voltage independ ent, and is consistent with an I-AHP-type potassium current sustained by ca lcium ions accompanying the nicotinic synaptic current. The conductance act ivated by a standard synaptic train was similar to 3.6 nS per neuron; it wa s detected in isolation in 14 out of a 52-neuron sample. A novel current, I -ADPsyn, was described in 42/52 of the sample as a post-tetanic inward curr ent, which increased in amplitude with increasing membrane potential negati vity and exhibited a null-point close to the holding potential and the cell momentary chloride equilibrium potential. I-ADPsyn developed during synapt ic stimulation and decayed thereafter according to a single exponential (me an tau = 148.5 ms) in 18 neurons or according to a two-exponential time cou rse (tau = 51.8 and 364.9 ms, respectively) in 19 different neurons. The me an peak conductance activated was similar to 20 nS per neuron. I-ADPsyn was calcium independent, it was affected by internal and external chloride con centration, but was insensitive to specific blockers (anthracene-9-carboxyl ic acid, 9AC) of the chloride channels open in the resting neuron. It is su ggested that g(ADPsyn) represents a specific chloride conductance activatab le by intense nicotinic stimulation; in some neurons it is even associated with single excitatory postsynaptic potentials (EPSCs). Both I-AHP and I-AD Psyn are apparently devoted to reduce neuronal excitability during and afte r intense synaptic stimulation.