Dendritic BC1 RNA: modulation by kindling-induced afterdischarges.

Local protein synthesis in dendrites is thought to provide a mechanism for long-lasting modifications of synapses in response to physiological activity and behavioral experience. New synthesis of dendritic proteins may be triggered by various paradigms, including induction of epileptiform activity. Prerequisite for such modulated synthesis is a mechanism that limits translation of synaptodendritic mRNAs to times of demand. Recently identified as a translational repressor that is localized to dendrites, small untranslated BC1 RNA has been implicated in the regulation of postsynaptic protein synthesis. Here we show that translational repressor BC1 RNA is itself undergoing modulation as a result of neuronal stimulation. Induction of hippocampal epileptiform activity resulted in a significant decrease of BC1 RNA in the CA3 region over several hours after excitation. The observed decrease was cell-wide, thus indicating reduced expression rather than intracellular redistribution. We suggest that a downregulation of the translational repressor BC1 RNA serves to modulate postsynaptic protein complements in response to the induction of epileptiform activity. Such increased protein synthesis in dendrites may be required for the consolidation of enduring epileptogenic mechanisms.