A
Ketogenic Diet (KD) mimics the
anticonvulsant effects of fasting, which are known to suppress
seizures. The purinergic system has been investigated in the matter of
epilepsy development, especially the
nucleoside adenosine, which has been considered a natural brain
anticonvulsant. During epileptic
seizures, extracellular
adenosine concentration rises rapidly to micromolar levels.
Adenosine can exert its
anticonvulsant functions, after its release by
nucleoside bidirectional transport, or by production through the sequential catabolism of
ATP by ectonucleotidases, such as E-NTPDases (ectonucleoside
triphosphate diphosphohydrolases) and
ecto-5'-nucleotidase. Here, we have investigated the effect of a
ketogenic diet on the
nucleotide hydrolysis and NTPDases expression in the
lithium-
pilocarpine (Li-Pilo) model of
epilepsy. For the induction of Status Epileticus (SE), 21-day-old female Wistar rats received an i.p. injection of
lithium chloride (127 mg/kg) and 18-19 h later an i.p. injection of
pilocarpine hydrochloride (60 mg/kg). The control groups received an injection of saline. After induction of SE, the control and Li-Pilo groups received standard or
ketogenic diets for 6 weeks. The
lithium-
pilocarpine exposure affected the
ATP (a decrease of between 8 % and 16 %) and
ADP (an increase of between 18 % and 22 %) hydrolysis in both groups whereas the diet did not impact the
nucleotide hydrolysis.
NTPDase2 and 3
mRNA expressions decreased in the Li-Pilo group (41 % and 42 %). This data highlights the participation of the purinergic system in the pathophysiology of this model of
epilepsy, since
nucleotide hydrolysis and NTPDase expressions were altered by Li-Pilo exposure, with no significant effects of the
ketogenic diet. However, the interaction between purinergic signaling and a
ketogenic diet on
epilepsy still needs to be better elucidated.