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....

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Bibliographic Details
Published in:Brain research. Molecular brain research. 2005-01, Vol.133 (1), p.110-118
Main Authors: Nimmrich, Volker, Hargreaves, Eric L., Muslimov, Ilham A., Bianchi, Riccardo, Tiedge, Henri
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Autoradiography - methods
Biological and medical sciences
Brain - cytology
Brain - physiology
Dendrites - metabolism
Electric Stimulation
Electroencephalography - methods
Epilepsy
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation - physiology
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Immunohistochemistry - methods
In Situ Hybridization - methods
Kindling
Kindling, Neurologic - metabolism
Kindling, Neurologic - physiology
Local protein synthesis
Male
Medical sciences
Nervous system (semeiology, syndromes)
Neurology
Rats
Rats, Sprague-Dawley
RNA, Small Cytoplasmic - genetics
RNA, Small Cytoplasmic - metabolism
Vertebrates: nervous system and sense organs
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Summary: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.
ISSN:0169-328X
1872-6941
DOI:10.1016/j.molbrainres.2004.10.008