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Synaptic stimulation of nicotinic receptors in rat sympathetic ganglia is followed by slow activation of postsynaptic potassium or chloride conductances
Author(s) -
Sacchi Oscar,
Rossi Maria Lisa,
Canella Rita
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00144.x
Subject(s) - chemistry , postsynaptic potential , biophysics , excitatory postsynaptic potential , neuron , neuroscience , tetanic stimulation , stimulation , nicotinic agonist , synaptic potential , reversal potential , calcium , potassium , receptor , patch clamp , biochemistry , biology , organic chemistry
Two slow currents have been described in rat sympathetic neurons during and after tetanization of the whole preganglionic input. Both effects are mediated by nicotinic receptors activated by native acetylcholine (ACh). A first current, indicated as I AHPsyn , is calcium dependent and voltage independent, and is consistent with an I AHP ‐type potassium current sustained by calcium ions accompanying the nicotinic synaptic current. The conductance activated by a standard synaptic train was ∼ 3.6 nS per neuron; it was 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 current, which increased in amplitude with increasing membrane potential negativity and exhibited a null‐point close to the holding potential and the cell momentary chloride equilibrium potential. I ADPsyn developed during synaptic stimulation and decayed thereafter according to a single exponential (mean τ = 148.5 ms) in 18 neurons or according to a two‐exponential time course (τ = 51.8 and 364.9 ms, respectively) in 19 different neurons. The mean peak conductance activated was ∼ 20 nS per neuron. I ADPsyn was calcium independent, it was affected by internal and external chloride concentration, but was insensitive to specific blockers (anthracene‐9‐carboxylic acid, 9AC) of the chloride channels open in the resting neuron. It is suggested that g ADPsyn represents a specific chloride conductance activatable by intense nicotinic stimulation; in some neurons it is even associated with single excitatory postsynaptic potentials (EPSCs). Both I AHP and I ADPsyn are apparently devoted to reduce neuronal excitability during and after intense synaptic stimulation.