Overexpression of and RNA interference with the CCAAT enhancer-binding protein on long-term facilitation of Aplysia sensory to motor synapses

Citation
Ja. Lee et al., Overexpression of and RNA interference with the CCAAT enhancer-binding protein on long-term facilitation of Aplysia sensory to motor synapses, LEARN MEM, 8(4), 2001, pp. 220-226
Citations number
24
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
LEARNING & MEMORY
ISSN journal
1072-0502 → ACNP
Volume
8
Issue
4
Year of publication
2001
Pages
220 - 226
Database
ISI
SICI code
1072-0502(200107/08)8:4<220:OOARIW>2.0.ZU;2-P
Abstract
In the marine mollusk Aplysia, the CCAAT/enhancer-binding protein, ApC/EBP, serves as in immediate early gene in the consolidation of long-term facili tation in the synaptic connection between the sensory and motor neurons of the gill-withdrawal reflex. To further examine the role of ApC/EBP) as a mo lecular switch of a stable form of long-term memory, we cloned the full-len gth coding regions of two alternatively spliced forms, the short and long f orm of ApC/EBP. Overexpression of each isoform by DNA microinjection result ed in a 16-fold increase in the expression of the coinjected luciferase rep orter gene driven by in ERE promoter. In addition, when we overexpressed Ap C/EBP in Aplysia sensory neurons, we found that the application of a single pulse of 5-HT that normally induced only short-term facilitation now induc ed long-term facilitation. Conversely, when we attempted to block the synth esis of native ApC/EBP by microinjecting double-strand RNA or antisense RNA , we blocked long-term facilitation in a sequence-specific manner. These da ta support the idea that ApC/EBP is both necessary and sufficient to consol idate short-term memory into long-term memory. Furthermore, our results sug gest that this double-strand RNA interference provides,I powerful tool in t he study of the genes functioning in learning and memory in Aplysia by spec ifically inhibiting both the constitutive and induced expression of the gen es.