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Second messenger cascade of glial responses evoked by interneuron activity and by a myomodulin peptide in the leech central nervous system
Author(s) -
Britz Frank C.,
Hirth Ingolf C.,
Deitmer Joachim W.
Publication year - 2004
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 - 10.1111/j.0953-816x.2004.03192.x
Subject(s) - adenylyl cyclase , biology , second messenger system , neuron , stimulation , neuroglia , protein kinase a , cyclic nucleotide , neuroscience , camp dependent pathway , interneuron , microbiology and biotechnology , endocrinology , medicine , signal transduction , central nervous system , kinase , biochemistry , nucleotide , gene , inhibitory postsynaptic potential
The giant glial cell in the neuropil of segmental ganglia of the leech Hirudo medicinalis responds to the activity of the Leydig interneuron and to a peptide of the myomodulin family, the presumed transmitter mediating the Leydig neuron‐to‐giant glial cell transmission, with a membrane hyperpolarization due to an increased membrane K + conductance [Britz et al . (2002) Glia , 38, 215–227]. We have now studied the second messenger cascade initiated by Leydig neuron stimulation and by the endogenous myomodulin (MM Hir ) in the voltage‐clamped giant glial cell. Glial responses to both stimuli are mediated by a G‐protein‐coupled receptor linked to adenylyl cyclase by the following criteria: (i) injection of GDP‐β‐S, but not GDP, resulted in an irreversible decrease of the glial responses to both stimuli; (ii) the responses to both stimuli were reversibly inhibited by the adenylyl cyclase inhibitor SQ22,536; and (3) bath‐applied di‐butyryl‐cyclic AMP, but not di‐butyryl‐cyclic GMP, elicited an outward current, which reduced the responses elicited by neuronal stimulation or myomodulin. A cocktail of protein kinase (PK) inhibitors (H‐8, KT5720), the PKA antagonist Rp‐cAMPS, or presumed inhibitors of cyclic nucleotide channels, LY83583 and l ‐ cis ‐diltiazem, had no effect on the glial responses. Our results suggest that Leydig neuron stimulation and MM Hir activate a cAMP‐mediated K + conductance in the glial cell, which appeared neither to be due to the activation of PKA nor of known cyclic nucleotide‐gated channels directly.