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Apamin blocks certain neurotransmitter-induced increases in potassium permeability
Nature
|November 22, 1979
Summary
Apamin, a bee venom neurotoxin, blocks ATP-induced potassium channel activity in smooth muscle. This finding suggests apamin is not a specific ATP receptor blocker but rather inhibits potassium permeability changes.
Area of Science:
- Neuropharmacology
- Smooth Muscle Physiology
- Bee Venom Research
Background:
- Apamin, a neurotoxic polypeptide from bee venom, has a known structure.
- Previous studies suggested ATP is a neurotransmitter in non-adrenergic inhibitory nerve supply to visceral smooth muscle.
- Apamin was tentatively identified as a specific postsynaptic blocker of this purinergic inhibition.
Purpose of the Study:
- To investigate the mechanism of action of apamin on visceral smooth muscle.
- To determine if apamin acts as a specific postsynaptic blocking agent for ATP-mediated inhibition.
- To clarify apamin's role in non-adrenergic, purinergic inhibition.
Main Methods:
- Experimental confirmation of apamin's effect on ATP and nerve stimulation-induced inhibition.
- Investigation of apamin's impact on potassium permeability.
- Utilized nanomolar concentrations of apamin in visceral smooth muscle preparations (guinea pig stomach and taenia coli).
Main Results:
- Apamin at nanomolar concentrations reduced inhibition by both externally applied ATP and non-adrenergic nerve stimulation.
- Apamin was found to inhibit the increase in potassium permeability induced by ATP.
- The results suggest apamin's action is not specific to ATP receptors.
Conclusions:
- Apamin inhibits the increase in potassium permeability caused by ATP and other agents.
- Apamin is not a specific postsynaptic blocker of ATP receptors.
- Apamin's broader effect on potassium permeability underlies its inhibitory action on non-adrenergic, purinergic smooth muscle inhibition.
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