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Peptide‐mediated glial responses to Leydig neuron activity in the leech central nervous system
Author(s) -
Schmidt Joachim,
Deitmer Joachim W.
Publication year - 1999
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.1460-9568.1999.00731.x
Subject(s) - neuron , neuropil , neuroscience , hyperpolarization (physics) , biology , neuroglia , leech , neurotransmission , membrane potential , hirudo medicinalis , neuromodulation , central nervous system , chemistry , biochemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy , world wide web , computer science
Neuronal activity may lead to a variety of responses in neighbouring glial cells; in general, an ensemble of neurons needs to be active to evoke a K + ‐ and/or neurotransmitter‐induced glial membrane potential change. We have now detected a signal transfer from a single neuromodulatory Leydig neuron to the giant neuropil glial cells in the central nervous system of the leech Hirudo medicinalis. Activation of a Leydig neuron, two of which are located in each segmental ganglion, elicits a hyperpolarization in the giant neuropil glial cells. This hyperpolarization could be mimicked by bath application of the peptide myomodulin A (1 n m –1.0 μ m ). Myomodulin‐like immunoreactivity has recently been found to be present in a set of leech neurons, including Leydig neurons (Keating & Sahley 1996, J. Neurobiol., 30, 374–384). The glial responses to Leydig neuron stimulation persisted in a high‐divalent cation saline, when polysynaptic pathways are suppressed, indicating that the effects on the glial cell were direct. The glial responses to myomodulin A application persisted in high‐Mg 2+ /low‐Ca 2+ saline, when chemical synaptic transmission is suppressed, indicating a direct effect of myomodulin A on the glial membrane. The glial hyperpolarization evoked by myomodulin A was dose dependent (EC 50 = 50 n m ) and accompanied by a membrane conductance increase of ≈ 25%. Ion substitution experiments indicated that myomodulin A triggered a Ca 2+ ‐independent K + conductance. Thus, our results suggest, for the first time, direct signal transmission from an identified modulatory neuron to an identified glial cell using a myomodulin‐like peptide.