In neurons, an active system of protein synthesis is present not only in cell body and dendrites, but also in axonal and presynaptic domains. In squid model systems, axonal and presynaptic RNAs derive from nearby glial cells (1). Using synaptosomal fractions, brain plastic events have been shown to elicit modification of synaptic protein synthesis. Notably, in rats trained for a two-way active avoidance task, the local expression of two synaptic proteins is significantly enhanced (2). In addition, in rats with permanent brain ischemia the rate of synaptic protein synthesis undergoes a massive and prolonged increase (3). To investigate synaptosomal protein synthesis under pathological conditions of brain plasticity, rats were rendered epileptic by pharmacological treatment. Our preliminary data show a decreased rate of synaptosomal protein synthesis and a modified profile of newly-synthesized synaptic proteins in rats treated with pentylentetrazole in comparison with controls. On the other hand, treatment with kainic acid did not reveal comparable effects, suggesting a different action mechanism. The present data suggest a potential involvement of synaptic protein synthesis in epileptic events.

1. Physiol. Rev 88: 515–555, 2008. 2. Brain Res. 1132: 148–157, 2007. 3. Neurosci. Lett. 415: 77–80, 2007.