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A Prion Like-Protein, Protein Kinase Mzeta and Memory Maintenance

Posted in Alzheimer's Disease, Cell Biology, Signaling & Cell Circuits, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Genome Biology, Innovations in Neurophysiology & Neuropsychology, Proteomics, tagged behavioral performance, Ebonyi StateUniversity, learning, memory, memory encoding, neuronal astrocyte, neuronal plasticity, Prion, protein kinase, synaptic function on October 19, 2012| Leave a Comment »

English: diagram based on Squire and Zola (1996) about decalarative and non-declarative memory (Photo credit: Wikipedia)

Larry H Bernstein, MD, FCAP, Reporter

An interesting paper recently published.

I only show abstract and part of introduction.

Available online http://www.interesjournals.org/JMMS

Martin Ezeani, Maxwell Omabe, J.C. Onyeanusi, I.N. Nnatuanya, Elom S.O.
*1Department of Neurosciences, University of Sussex UK
*2Molecular Pathology Division, Department of Medical Laboratory Sciences, Faculty of Health Sciences, Ebonyi State
University.
*3Department of Medical Biochemistry, Faculty of Basic Medical Sciences, Ebonyi State University.

ABSTRACT
Molecular studies of both declarative and non-declarative memory in Aplysia californica, lymaea stagnalis and hippocampal slices implicate experience-dependent 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 conditions like Alzheimer’s there is lack of the ability to recreate the past. From this perspective, memory literally is the glue that binds our mental life, the scaffolding that holds our personal history and that makes it possible to change throughout life. What causes memory persistence after labile phase 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 become 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 behavioural performance are the result of a fundamental physiological phenomenon.

The fundamental physiological 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 (PKMζ) in memory maintenance.
Keywords: Memory Maintenance, NMDARs and AMPARs, CPEB, Neuronal Lacate and Protein Kinase Mzeta.

INTRODUCTION
Memory defines the ability to retain, store and recall events. Memory maintenance is the process of keeping optimally these events. For instance, the beautiful nature of Sussex genomic center and its Medical School are
examples of explicit or declarative memory. Memories such as these are stored very well in the brain for recall of details later in life. Apart from these explicit or
declarative memories another type of memory is implicit or non-declarative memory. In this latter type of memory, motor skills and other type of tasks are done through performance with no conscious recall of past experience.
For instance riding a bicycle and driving a car.

Studies suggest that experience-dependent changes of synaptic strength, growth, structure and fundamental mechanism are ways of which these memories are encoded, processed and stored within the brain (Hawkins et al.,
2006; Bailey et al., 2004; and Beckinschtein et al., 2010). In these processes of initial memory formation and consolidation, memory basically exists in forms. These forms may include; short term memory (STM), intermediate memory (IM) and Long term memory (LTM) (Beckinschtein et al., 2010). There is also early and late LTM. Memories are maintained because, if all these memories are formed by similar molecular process, then what accounts for these types of basic memory?