Martin Ezeani, Maxwell Omabe, J.C. Onyeanusi, I.N. Nnatuanya, Elom S.O
Molecular studies of both declarative and non-decla rative memory in Aplysia californica, lymaea stagnalis and hippocampal slices implicate experience-depende nt changes of synaptic structure and strength as the fundamental basis of memory storage and maintenance. The essential outcome of these changes in synaptic structure and strength is our ability to remember what we are thought. Remembrance is of critical importance. In disease c onditions like Alzheimer’s there is lack of the ability to recreate the past. From this perspective , memory literally is the glue that binds our menta l life, the scaffolding that holds our personal histo ry and that makes it possible to change throughout life. What causes memory persistence after labile p hase of memory is not yet fully known. Elegant discoveries have explained why labile memory phase could persist over time into long term memory phase. Synaptic connections are not fixed but becom e modified by learning. These modifications in synaptic structure and strength persist and become the fundamental component of memory storage after learning. Learning-induced changes in behavio ural performance are the result of a fundamental physiological phenomenon. The fundamental physiolog ical phenomenon is neuronal plasticity. In the process of neuronal plasticity, we review only the emerging aspect of the roles of prion like-protein, neuronal astrocyte and protein kinase Mzeta (PKM ζ ) in memory maintenance
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