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INHIBITION OF NEURONAL FIRING BY OPIATES: EVIDENCE AGAINST THE INVOLVEMENT OF CYCLIC NUCLEOTIDES
Author(s) -
KARRAS P.J.,
NORTH R.A.
Publication year - 1979
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1979.tb07877.x
Subject(s) - adenosine , myenteric plexus , cyclic nucleotide , phosphodiesterase inhibitor , intracellular , chemistry , phosphodiesterase , extracellular , cyclic adenosine monophosphate , ibmx , endocrinology , prostaglandin e , medicine , morphine , pharmacology , in vitro , nucleotide , biology , biochemistry , forskolin , enzyme , receptor , immunohistochemistry , gene
1 Extracellular recordings were made in vitro from single neurones of the myenteric plexus of the guinea‐pig ileum. 2 Neuronal firing was inhibited by morphine and normorphine (10 nM to 1 μ m ). Cyclic adenosine 3′,5′‐monophosphate (cyclic AMP) (100 μ m to 1 m m ) also inhibited the firing of the majority of the neurones. Prostaglandin E 2 usually caused a short‐lasting excitation of myenteric neurones and the phosphodiesterase inhibitor 3‐isobutyl‐l‐methylxanthine was usually without effect on firing rate. 3 The inhibition of neuronal firing by normorphine was unaffected by prior and/or concurrent administration of cyclic AMP, dibutyryl cyclic adenosine 3′,5′‐monophosphate, prostaglandin E 2 or 3‐isobutyl‐l‐methylxanthine. As these four treatments might be expected to elevate intracellular levels of cyclic AMP, the results lend no support to the notion that a reduction in intracellular cyclic AMP is essential to the inhibition of firing produced by morphine.