Introduction: Active compounds derived from plants are able to inhibit nerve conduction. Cardamonin, a naturally occurring chalcone, manifests anti-nociceptive, anti-inflammatory and anti-neuropathy properties. Consequently, cardamonin may potentially inhibit nerve action potential, whereby, it affects the nerve conduction. Compound action potential is the sum of the activity which is measured from a nerve trunk. Objective: The experiment was carried out to investigate the inhibitory effect of cardamonin on compound action potentials and its possible mechanism of action on frog sciatic nerve. Methodology: LabTutor software was used to record compound action potentials in frog sciatic nerve. Sciatic nerve was isolated from the frog and soaked in Ringer's solution. Stimulating electrodes were used to stimulate the nerve and recording electrodes were used to record compound action potentials. Compound action potential of the nerve were recorded before and after treatments [vehicle, cardamonin (0.5, 1 & 2 mg/ml) & morphine (3mg/ml)]. Participation of opioid system was investigated by pre-treating the nerve with naloxone and followed by cardamonin. All the data were recorded and analysed via LabTutor software. The data were analysed by using Two-way ANOVA followed by Bonferonni's post hoc test with significant value at P < 0.05. Results: The outcomes showed that all the doses of cardamonin significantly reduced the peak amplitude of compound action potential in frog sciatic nerves. Besides, co-treatment of naloxone and cardamonin significantly (P < 0.001) reversed the effect of cardamonin on peak amplitude of compound action potential, suggesting the involvement of opioid receptors to inhibit nerve conduction. Conclusion: Cardamonin reduces the nerve signal conduction via activation of opioid receptors to modulate pain and contribute to the analgesic effects.

Melicope ptelefolia is a medicinal plant from the Rutaceae, also known as 'tenggek burung' in Malaysia. Traditionally, natives ingest M. ptelefolia to treat a wide range of illnesses. This study aimed to investigate the effects of M. ptelefolia aqueous extract (MPAE) on compound action potentials (CAPs) in frog sciatic nerves and its mechanism involving the opioid receptors. The effects of MPAE on CAPs in frog sciatic nerves were examined using the AD Instrument Nerve Chamber. The frog sciatic nerves were dissected from the lumbar plexus to the knee of the frog and placed in Ringer's solution. Three treatment groups with different dosages (1, 3 and 10 mg/mL) of MPAE, including negative (vehicle) and positive control group (3 mg/mL of morphine) were tested on the frog sciatic nerves by placing them in a nerve organ chamber. Following this, the involvement of opioid receptors in the effects of MPAE on CAPs was investigated by using naloxone hydrochloride as a non-selective opioid receptor antagonist. Our results showed that the peak amplitudes of CAPs were significantly (p<0.001) reduced when treated with MPAE (3 and 10 mg/mL) in frog sciatic nerves. The MPAEinduced CAPs inhibition was reversed when pre-treated with naloxone, suggesting the involvement of the opioidergic system. These results indicated the modulatory action of MPAE on nerve conduction, which may provide important leads in the development of new therapeutic drugs through the involvement of opioid receptors.

Boesenbergia rotunda, traditionally used to relieve stomach, abdomen, joint, muscle, and rheumatic pain was also reported for its antinociceptive effect on a mouse model. However, the possible pain relief effect of Boesenbergia rotunda ethanolic extract (BREE) via the inhibition to the neural pain pathway remains to be elucidated. This study investigated the inhibitory effect of BREE on compound action potentials (CAPs) and the possible involvement of the opioid receptors. The changes in the CAPs amplitudes of the frog's sciatic nerves were evaluated following the exposure to three different dosages of BREE (1, 3 and 10 mg/ml and morphine (3 mg/ml). In another set of experiment, the nerves were pretreated with a non-selective opioid receptor antagonist, naloxone (0.1 mg/ml), before exposing the nerve to BREE (1 mg/ml) to investigate the involvement of opioid receptors in the CAPs inhibitory mechanism. The outcome showed a reduction in the CAPs amplitudes when treated with BREE (1, 3 and 10 mg/ml) whereby the effect was reversible. The CAPs inhibition by BREE was absent when the opioid receptors were blocked. Taken together, these findings suggest that BREE-induced CAPs amplitude reduction involves the activation of opioid receptors.