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Capsaicin‐Induced Ion Fluxes Increase Cyclic GMP but Not Cyclic AMP Levels in Rat Sensory Neurones in Culture
Author(s) -
Wood J. N.,
Coote P. R.,
Minhas A.,
Mullaney I.,
McNeill M.,
Burgess G. M.
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb07416.x
Subject(s) - capsaicin , dorsal root ganglion , calcium , medicine , endocrinology , extracellular , sodium nitroprusside , chemistry , pertussis toxin , tetrodotoxin , cyclic nucleotide , sensory neuron , forskolin , biophysics , biology , stimulation , biochemistry , sensory system , central nervous system , neuroscience , nitric oxide , g protein , receptor , nucleotide , gene
Capsaicin, which induces fluxes of sodilim, calcium, and potassium ions in a subset of both neonatal and adult rat dorsal root ganglion neurones, increased cyclic GMP (cGMP) levels by a factor of 20 (EC 50 0.07 μ) to 10‐20 pmol cGMP/mg protein in these cells. Cyclic AMP (CAMP) levels were unaffected. Nonneuronal cells derived from rat ganglia, and both neurones and nonneuronal cells from chick were unresponsive to capsaicin. Capsaicin‐induced cGMP elevation in rat dorsal root ganglion (DRG) neurones was unaffected by pertussis toxin, lowered by compounds that block voltage‐sensitive calcium channels, and was abolished by the removal of extracellular calcium. Calcium, guanidine, and rubidium fluxes were unaffected by treatment of DRG cells with sodium nitroprusside or dibutyryl cGMP. The cGMP response to capsaicin is thus a function of capsaicin‐evoked calcium uptake through voltage‐sensitive calcium channels. Elevated cGMP levels do not, however, contribute to capsaicin‐evoked ion fluxes or to their desensitisation.