Nonselective cation conductance activated by muscarinic and purinergic receptors in rat spiral ganglion neurons.

1. Am J Physiol Cell Physiol. 2002 May;282(5):C1121-35.

Nonselective cation conductance activated by muscarinic and purinergic receptors
in rat spiral ganglion neurons.

Ito K(1), Dulon D.

Author information:
(1)Laboratoire de Biologie Cellulaire et Moléculaire de l’Audition, Institut
National de la Santé et de la Recherche Médicale EMI 99-27, Université de
Bordeaux 2, Hôpital Pellegrin, 33076 Bordeaux, France.

The present study characterizes the ionic conductances activated by acetylcholine
(ACh) and ATP, two candidate neuromodulators, in isolated spiral ganglion neurons
(SGNs). Brief application (1 s) of ACh evoked in a dose-dependent manner (EC(50)
= 4.1 microM) a reversible inward current with a long latency (average 1.3 s), at
holding potential (V(h)) = -50 mV. This current was reversibly blocked by
atropine and mimicked by muscarine. Application of ATP also evoked a reversible
inward current at V(h) = -50 mV, but the current showed two components. A fast
component with a short latency was largely reduced when N-methyl-D-glucamine
(NMDG) replaced extracellular sodium, implying a P2X-like ionotropic conductance.
The second component had a longer latency (average 1.1 s) and was presumably
activated by metabotropic P2Y-like receptors. The second component of ATP-evoked
current shared similar characteristics with the responses evoked by ACh: the
current reversed near 0 mV, displayed inward rectification, could be carried by
NMDG, and was insensitive to extracellular and intracellular calcium. This
ACh-/ATP-evoked conductance was reversibly inhibited by preapplication of
ionomycin. These results suggest that muscarinic receptors and purinergic
metabotropic receptors activate a similar large nonselective cation conductance
via a common intracellular pathway in SGNs, a candidate mechanism to regulate
neuronal excitability of SGNs.

DOI: 10.1152/ajpcell.00364.2001
PMID: 11940528 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus