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Permethrin modulates cholinergic mini-synaptic currents by partially blocking the calcium channel.

Ying Yan¹, Ying Yang, Jing You

¹Department of Anatomy and Neurobiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.

Toxicology Letters

|January 22, 2011

Summary

Permethrin, a pyrethroid insecticide, may disrupt neuronal activity by partially blocking calcium channels, affecting cholinergic signaling in Drosophila. This contrasts with the known effects on voltage-gated sodium channels.

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Area of Science:

Neuroscience
Insect toxicology
Pharmacology

Background:

Pyrethroid insecticides are known to affect neuronal excitability, primarily by modulating voltage-gated sodium channels (VGSCs).
Emerging evidence suggests alternative mechanisms, potentially involving other neuronal targets, contribute to pyrethroid neurotoxicity.
Cholinergic neurotransmission is crucial for central nervous system function in insects and mammals.

Purpose of the Study:

To investigate the effects of the pyrethroid permethrin on calcium currents and cholinergic synaptic transmission in the Drosophila brain.
To explore whether permethrin acts as a calcium channel antagonist and its impact on cholinergic signaling.

Main Methods:

Electrophysiological recordings were used to measure calcium currents and cholinergic mini-synaptic currents in Drosophila neurons.
Permethrin was applied at a concentration of 2.5μM to assess its effects.
Calcium was removed from the external solution to evaluate its role in synaptic transmission.

Main Results:

Permethrin (2.5μM) significantly reduced both calcium currents and cholinergic mini-synaptic currents in the Drosophila brain.
The inhibitory effect of permethrin on calcium current was not complete, indicating partial blockade.
Removal of external calcium markedly decreased cholinergic mini-synaptic transmission, confirming calcium's essential role.

Conclusions:

The findings support the hypothesis that permethrin modulates cholinergic mini-synaptic currents through partial blockade of calcium channels.
This suggests that calcium channel modulation is a potential mechanism contributing to the neurotoxic effects of pyrethroids, in addition to VGSC interactions.