The translocation of protein kinase C isozymes was investigated in an animal model of cognitive deficit and lack of induction of long-term potentiation (LTP). In MAM rats, presynaptic α, β, ε PKC showed enhanced translocation, while postsynaptic γ PKC displayed decreased translocation when compared to control levels. This imbalance of PKC isozyme translocation between the pre- and post-synaptic compartment might therefore represent a possible molecular cause for the lack of synaptic plasticity observed in these animals.

Differential translocation of protein kinase C isozymes in rats characterized by a chronic lack of LTP induction and cognitive impairment / A. Caputi, S. Rurale, L. Pastorino, M. Cimino, F. Cattabeni, M.M.G. Di Luca. - In: FEBS LETTERS. - ISSN 0014-5793. - 393:1(1996), pp. 121-123.

Differential translocation of protein kinase C isozymes in rats characterized by a chronic lack of LTP induction and cognitive impairment

F. Cattabeni;M.M.G. Di Luca
1996

Abstract

The translocation of protein kinase C isozymes was investigated in an animal model of cognitive deficit and lack of induction of long-term potentiation (LTP). In MAM rats, presynaptic α, β, ε PKC showed enhanced translocation, while postsynaptic γ PKC displayed decreased translocation when compared to control levels. This imbalance of PKC isozyme translocation between the pre- and post-synaptic compartment might therefore represent a possible molecular cause for the lack of synaptic plasticity observed in these animals.
Protein kinase C; Synaptic plasticity; Translocation
Settore BIO/14 - Farmacologia
FEBS LETTERS
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2434/183823
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