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Aim:  Low frequency stimulation (LFS) inhibits neuronal hyperexcitability following epileptic activity. However, knowledge about LFS’ inhibitory mechanisms is lacking. Here, α 1  and α 2  adrenergic receptors’ roles in mediating LFS inhibitory action on high-K +  induced epileptiform activity (EA) was examined in rat hippocampal slices. Materials and methods:  LFS (1 Hz, 900 pulses) was applied to the Schaffer collaterals. Whole-cell, patch clamp recording was used to measure changes in CA1 pyramidal neurons’ excitability. By applying high-K +  on hippocampal slices, EA was induced, and neuronal excitability increased. Results:  When administered at the beginning of EA, LFS reduced neuronal excitability. In the presence of prazosin (10 µM, an α 1  adrenergic receptor antagonist) and yohimbine (5 µM, an α 2  adrenergic receptor antagonist), LFS’ typically has a restorative impact on EA-induced membrane potential hyperpolarization and spike firing frequency, but this effect was reduced after high-K +  washout; These antagonists did not have a significant effect on LFS’ inhibitory action on spike firing during EA. Conclusion:  These findings suggest that LFS’ anticonvulsant effect, on neuronal hyperexcitability following high-K +  EA, may be mediated partly through α adrenergic receptors in hippocampal slices.

Alpha adrenergic receptors have role in the inhibitory effect of electrical low frequency stimulation on epileptiform activity in rats