Abstract
Sensitization of the gill- and siphon-withdrawal reflex in Aplysia is thought to result from a set of molecular processes with different time courses1: short-term sensitization is explained by cyclic AMP-dependent modulation of ion-channel function in sensory neurons lasting minutes2; memory that endures for hours or longer, by the expression and distribution within the neurons of new gene products3. Because gene induction and axonal transport are relatively slow, there may also be a need for a distinct form of intermediate memory to bridge the short- and long-term processes4. We now report that a protocol producing long-term sensitization results in a decrease in the amount of regulatory subunits of the cAMP-dependent protein kinase in animals 24 h after training, with no effect on the catalytic subunit. The loss appears to be post-translational. Because a decrease in the ratio of regulatory to catalytic subunits would result in elevated kinase activity after cAMP has returned to its unstimulated concentration in sensory cells, it could be the molecular mechanism of intermediate memory.
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Greenberg, S., Castellucci, V., Bayley, H. et al. A molecular mechanism for long-term sensitization in Aplysia. Nature 329, 62–65 (1987). https://doi.org/10.1038/329062a0
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DOI: https://doi.org/10.1038/329062a0
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