Synaptic stimulation of nicotinic receptors in rat sympathetic ganglia is followed by slow activation of postsynaptic potassium or chloride conductances
O. Sacchi et al., Synaptic stimulation of nicotinic receptors in rat sympathetic ganglia is followed by slow activation of postsynaptic potassium or chloride conductances, EUR J NEURO, 12(8), 2000, pp. 2651-2661
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.