LAUSR

Capsaicin, a compound found in chili peppers, causes burning sensations by acting on the peripheral sensory system. However, it has also been reported to exert substantial effects on central neurons. The aim of this patch-clamp study was to test the antiepileptic potential of capsaicin in prefrontal cortical pyramidal neurons. Capsaicin at a concentration of 60 μM inhibited neuronal excitability. Moreover, later spikes in response to 50-second-long current steps were much smaller in amplitude in the presence of 60 μM capsaicin than in control solution. The tested compound did not influence the membrane potential. Voltage-clamp recordings showed that capsaicin markedly enhanced the use-dependent block of sodium channels (sodium currents were evoked at frequencies of 0,5 Hz and 10 Hz). The presence of the compound shifted the steady-state inactivation curve of sodium channels towards hyperpolarization, which suggests greater inactivation of sodium channels at rest in the presence of capsaicin. Moreover, capsaicin inhibited epileptiform events evoked in three different proepileptic solutions. Capsaicin abolished interictal-like events lasting less than 1 second recorded in zero magnesium solution with an increased potassium ion concentration. The drug also abolished long ictal events evoked in zero magnesium solution containing 4-AP. Moreover, ictal events recorded in zero magnesium solution containing picrotoxin was substantially shortened in the presence of capsaicin. We suggest that capsaicin exerts an antiepileptic effect. The important mechanism behind this phenomenon seems to be the inhibition of sodium channels, which is an effect of many antiepileptic drugs.