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Although it has been demonstrated in hippocampal slices that the reduction in excitability can be achieved through ATP/pannexin-1/adenosine/A 1 R/K ATP pathway simply by reducing the glucose concentration in the buffer without any addition of HB (105), a series of studies in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats, a genetic model of absence epilepsy, conducted by D'Agostino, Kovacs and colleagues revealed that HB itself seems to be able to elicit anticonvulsant effects through a mechanisms involving A 1 R

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