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Effect of normorphine and enkephalin on spontaneous potentials in the vas deferens
Abstract:
Spontaneous excitatory junction potentials were recorded intracellularly from the smooth muscle of the mouse vas deferens. Exposure of the vas deferens to either normorphine (1 muM) or methionine-enkephalin (0.5 muM) did not alter the frequency or amplitude distribution of the spontaneous potentials. The possible mechanisms by which the narcotic agonists depress the release of noradrenaline on nerve stimulation without inhibiting the spontaneous release of noradrenaline are discussed.
Insights
Narcotic agonists like normorphine and methionine-enkephalin do not affect spontaneous excitatory junction potentials in mouse vas deferens smooth muscle. This suggests these drugs selectively inhibit nerve-stimulated noradrenaline release, not spontaneous release.
Area of Science:
- Neuropharmacology
- Smooth Muscle Physiology
- Autonomic Nervous System
Background:
- Opioid receptors are present in the vas deferens.
- Noradrenaline is a key neurotransmitter in regulating smooth muscle contraction.
- Spontaneous neurotransmitter release occurs independently of nerve stimulation.
Purpose of the Study:
- To investigate the effect of normorphine and methionine-enkephalin on spontaneous neurotransmission in the mouse vas deferens.
- To differentiate the mechanisms of opioid action on stimulated versus spontaneous noradrenaline release.
Main Methods:
- Intracellular recording of spontaneous excitatory junction potentials (SEJP) from mouse vas deferens smooth muscle.
- Application of normorphine (1 muM) and methionine-enkephalin (0.5 muM).
- Analysis of SEJP frequency and amplitude distribution.
Main Results:
- Neither normorphine nor methionine-enkephalin altered the frequency or amplitude of SEJPs.
- Opioid agonists did not inhibit spontaneous noradrenaline release.
Conclusions:
- Opioid-induced depression of noradrenaline release in the vas deferens is not mediated by a reduction in spontaneous release.
- The findings suggest a selective presynaptic mechanism for opioid inhibition of evoked neurotransmission.