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
Copyright © 2012 International Research Journals
Review
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?
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PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.