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• W1549203779 abstract "1 Excitatory junction potentials (e.j.ps) were recorded with intracellular microelectrodes from smooth muscle cells of the mouse isolated vas deferens. The amplitude of the e.j.p. was used as a measure of transmitter release evoked by applying single pulse stimuli to the intramural nerves. 2 Cyclic adenosine 3′,5′-monophosphate (cyclic AMP) and dibutyryl cyclic AMP (db cyclic AMP, up to 1 mm) depressed the amplitude of e.j.ps, probably by interacting with extracellular sites on the nerve terminals, similar to those responsive to adenosine. 3 The phosphodiesterase inhibitors, 1-methyl-3-isobutyl xanthine (IBMX) and 1-ethyl-4-hydrazino-1H-pyrazolo(3,4-b)pyridine-5-carboxylic acid, ethylester, hydrochloride (SQ20,006) increased e.j.p. amplitude; this increase was much greater when the phosphodiesterase inhibitor was applied together with db cyclic AMP. 4 Neither the cyclic nucleotides nor the phosphodiesterase inhibitors altered the resting membrane potential of smooth muscle cells. 5 The amplitude of the e.j.p. was depressed by normorphine, d-Ala2-Met5-enkephalinamide (DAEA) and d-Ala2-d-Leu5-enkephalin (DADL) with respective EC50s of 560 nm, 49 nm and 510 pm. 6 There was no change in the EC50 for normorphine in the presence of cyclic AMP (1 mm) or in the presence of a combination of IBMX (50 μm) and db cyclic AMP (500 μm). Similarly, the depression of the e.j.p. by DAEA or DADL was not affected by the combination IBMX (500 μm) and db cyclic AMP (250 μm). 7 These findings provide evidence against the hypothesis that a reduction in cyclic AMP levels in nerve terminals is an essential step in the inhibition by opiates and opioid peptides of transmitter release." @default.
• W1549203779 created "2016-06-24" @default.
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• W1549203779 date "1980-01-01" @default.
• W1549203779 modified "2023-09-26" @default.
• W1549203779 title "A STUDY OF THE ROLE OF CYCLIC ADENOSINE 3′,5′-MONOPHOSPHATE IN THE DEPRESSION BY OPIATES AND OPIOID PEPTIDES OF EXCITATORY JUNCTION POTENTIALS IN THE MOUSE VAS DEFERENS" @default.
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• W1549203779 doi "https://doi.org/10.1111/j.1476-5381.1980.tb10940.x" @default.
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