There is growing pharmacological evidence from several animal models of
seizure disorders that
adenosine possesses endogenous
anticonvulsant activity. Apart from being released from cells,
adenosine can be produced by the degradation of
adenine nucleotides by ectoenzymes or soluble
nucleotidases. These
enzymes constitute an important mechanism in synaptic modulation, as they hydrolyze
ATP, an excitatory
neurotransmitter, to
adenosine, a neuroprotective compound. We recently demonstrated an increase in ectoenzyme activity in rat brain synaptosomes after
pentylenetetrazol-kindling in rats resistant to kindling, suggesting a role for ectonucleotidases in the seizure control. The present work investigates the effect of
seizures induced by
pentylenetetrazol kindling on the
enzymes that could be playing a role in
ATP,
ADP and
AMP hydrolysis to
adenosine in rat blood serum. Animals received
injections of PTZ (30 mg/kg, i.p., dissolved in
0.9% saline) once every 48 h, totaling 10 stimulations and the controls animals were injected with saline. The hydrolysis of
ATP,
ADP and
AMP were significantly increased (42, 40, and 45%, respectively), while
phosphodiesterase activity was unchanged. These results suggest once more that an increase in the
ATP diphosphohydrolase and
5'-nucleotidase activities and, possibly, in
adenosine levels, could represent an important compensatory mechanism in the development of chronic
epilepsy. Moreover, the fact that this increase can also be measured in serum could mean that these
enzymes might be useful as plasma markers of
seizures in
epilepsy.