Co-Authors:
Meiri, N., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel
Abstract:
Signal-transduction mechanisms leading to neuronal plasticity involve a series of phosphorylation steps, which lead to transcription and de-novo protein synthesis. However, it is not clear how the specificity of the signal transduction achieved. Here, we evaluated the role of 14-3-3ε, a chaperone of phosphorylation and cellular-localization determination, in thermal control establishment, which represents hypothalamic plasticity, in chicks. As with other sensory mechanisms, there is a critical period in the development of temperature control. Neuroanatomically, body temperature is balanced by the preoptic anterior hypothalamus (PO/AH) and controlled by thermosensitive neurons. Hot or cold exposure during the critical period of temperature control development causes a plastic change in the ratio between hot- and cold-sensitive cells and can modulate temperature tolerance throughout life. It has been found that both mRNA and protein of isoform 14-3-3ε, but not other 14-3-3 isoforms, are induced during hot and cold conditioning in the PO/AH, with a peak at 24 h of conditioning. To determine whether 14-3-3ε has a general role in neuronal plasticity, we checked its expression after passive avoidance learning in the relevant neuroanatomical areas, i.e. the mesopallium intermediomediale and the striatum mediale. It was established that in these areas its expression was not altered after learning. The present study suggests that the correlative induction of both 14-3-3ε mRNA and protein many hours after learning is involved in plasticity in the hypothalamus but not in passive avoidance-related plasticity, which might indicate that specificity in the signal-transduction mechanism is at least partially mediated by 14-3-3. © 2007 Wiley Periodicals, Inc.
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