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As long-term memory is subject to fading in the natural Forgetting process, several recalls/retrievals of memory may be needed for long-term memories to last for years, dependent also on the depth of processing. Individual retrievals can take place in increasing intervals in accordance with the principle of Spaced Repetition . This can happen quite naturally through reflection or deliberate recall, often dependent on the perceived importance of the material. CAPACITY Current research indicates that long term memory's capacity is potentially unlimited. SLEEP Some theories consider Sleep to be an important factor in establishing well-organized long-term memories. ''(See also Sleep And Learning .)'' According to Tarnow's theory, long term memories are stored in Dream format (reminiscent of the Penfield & Rasmussen’s findings that electrical excitations of cortex give rise to experiences similar to dreams). During waking life an executive function interprets long term memory consistent with reality checking (Tarnow, 2003). Tarnow, E. (2003) ''How Dreams And Memory May Be Related'' Neuro-Psychoanalysis 5(2), 177-182 and also http://cogprints.org/2068/ TYPES OF MEMORY The and Procedural Memory . # Declarative Memory refers to all memories that are consciously available. These are encoded by the Hippocampus , Entorhinal Cortex , and perirhinal cortex, but consolidated and stored elsewhere in the cortex. The precise location of storage is unknown, but the temporal cortex has been proposed as a likely candidate. Declarative memory also has two major prostate subdivisions:
# Procedural Memory refers to the use of objects or movements of the body, such as how exactly to use a pencil or ride a bicycle. This type of memory is encoded and probably stored by the Cerebellum and the Striatum . #Emotional memory is the memory for events that evoke a particularly strong emotion. Emotion And Memory is a domain that can involve both declarative and procedural memory processes. Emotional memories are consciously available, but elicit a powerful, unconscious physiological reaction. They also have a unique physiological pathway that involves strong connections from the Amygdala into the Prefrontal Cortex , but much weaker connections running back from the prefrontal cortex to the amgydala. DISORDERS OF MEMORY Minor everyday slips and lapses of memory are fairly commonplace, and may increase naturally with age, when ill, or when under stress (Reason J.)Reason, J. (1995) Self-report questionnaires in cognitive psychology: have they delivered the goods? in Attention: Selection, Awareness, and Control (Eds.) Alan Baddeley & Lawrence Weiskrantz . Some women may experience more memory lapses following the onset of the menopause {Link without Title} . More serious problems with memory generally occur due to Traumatic Brain Injury or Neurodegenerative Disease {Link without Title} : Traumatic brain injury The majority of findings about memory have been the result of studies that Lesion ed specific brain regions in rats or primates, but some of the most important work has been the result of accidental or inadvertent brain trauma. The most famous case in memory studies is the case study of HM , who had parts of his hippocampus, parahippocampal cortices, and surrounding tissue removed in an attempt to cure his epilepsy. His subsequent total Anterograde Amnesia and partial Retrograde Amnesia provided the first evidence for the localization of memory function, and further clarified the differences between declarative and procedural memory. Neurodegenerative diseases Very many neurodegenerative diseases can cause memory loss. Some of the most prevalent (and consequently, most intensely researched) include Alzheimer's Disease , Dementia , Huntington's Disease , Multiple Sclerosis , and Parkinson's Disease . None act specifically on memory; instead memory loss is often a casualty of generalized neuronal deterioration. Currently, these illnesses are irreversible, but research into stem cells, psychopharmacology, and genetic engineering hold much promise. BIOLOGICAL UNDERPINNINGS AT THE CELLULAR LEVEL Long term memory is dependent upon the construction of new proteins within the cellular body, particularly transmitters, receptors, and new synapse pathways that reinforce the communicative strength between neurons. The production of new proteins devoted to synapse reinforcement is triggered after the release of certain signaling substances (such as calcium within hippocampal neurons) in the cell. In the case of hippocampal cells, this release is dependent upon the expulsion of magnesium (a binding molecule) that is expelled after significant and repetitive synaptic signaling. The temporary expulsion of magnesium frees NMDA receptors to release calcium in the cell, a signal that leads to gene transcription and the construction of reinforcing proteins. Neihoff, Debra (2005) "The Language of Life 'How cells Communicate in Health and Disease'" Speak Memory, 210-223. For more information see Long-term Potentiation (LTP). One of the newly synthesized proteins in LTP is also critical for maintaining long-term memory. This protein is an autonomously active form of the enzyme Protein Kinase C (PKC), known as PKMζ . PKMζ maintains the activity-dependent enhancement of synaptic strength and inhibiting PKMζ erases established long-term memories, without affecting short-term memory or, once the inhibitor is eliminated, the ability to encode and store new long-term memories. REFERENCES
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