Modulation of Spike Repolarization in Hippocampal Neurones by Tumor-Promoting Phorbol Esters
Tumor-promoting pborbol esters (TPEs) are known to enhance synaptic transmitter release. This effect is likely to involve protein kinase C (PKC), which is directly activated by TPEs . In the hippocampus, TPEs induce synaptic enhancement which resembles, and occludes, long-term potentiation (LTP) , and LTP has been correlated with translocation of PKC . In Aplysia neurones, another protein kinase (PKA) mediates synaptic enhancement which underlies certain forms of learning . The proposed mechanism in Aplysia is inhibition of a K current, leading to a broadening of the presynaptic action potential, increased Ca influx, and enhanced transmitter release . I am investigating the possibility that a similar mechanism may contribute to synaptic plasticity in the hippocampus.
KeywordsHaas Phorbol Aminopyridine Tetraethylammonium
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