Encoding
Encoding
Memory has the ability to encode, store andrecall information. Memories give an organism the capability to learn and adapt from previous experiences as well as build relationships. Encoding allows the perceived item of use or interest to be converted into a construct that can be stored within the brain[citation needed] and recalled later fromshort-term or long-term memory. Working memory stores information for immediate use or manipulation which is aided through hooking onto previously archived items already present in the long-term memory of an individual.
Types
Visual, elaborative, organizational, acoustic, and semantic encodings are the most intensively used. Other encodings are also used.
Visual encoding
Visual encoding is the process of encoding images and visual sensory information. This means that people can convert the new information that they stored into mental pictures (Harrison, C., Semin, A.,(2009). Psychology. New York p. 222) Visual sensory information is temporarily stored within ouriconic memory[1] and working memory before being encoded into permanent long-term storage.[2][3] Baddeley's model of working memory states that visual information is stored in the visuo-spatial sketchpad.[1] Theamygdala is a complex structure that has an important role in visual encoding. It accepts visual input in addition to input from other systems and encodes the positive or negative values of conditioned stimuli.[4]
Elaborative encoding
Elaborative encoding is the process of actively relating new information to knowledge that is already in memory. Memories are a combination of old and new information, so the nature of any particular memory depends as much on the old information already in our memories as it does on the new information coming in through our senses.[citation needed] In other words, how we remember something depends on how we think about it at the time. Many studies have shown that long-term retention is greatly enhanced by elaborative encoding.[5]
Acoustic encoding
Acoustic encoding is the encoding of auditory impulses. According to Baddeley, processing of auditory information is aided by the concept of the phonological loop, which allows input within our echoic memory to be sub vocally rehearsed in order to facilitate remembering.[1] When we hear any word, we do so by hearing to individual sounds, one at a time. Hence the memory of the beginning of a new word is stored in our echoic memory until the whole sound has been perceived and recognized as a word.[6] Studies indicate that lexical, semantic and phonological factors interact in verbal working memory. The phonological similarity effect (PSE), is modified by word concreteness. This emphasizes that verbal working memory performance cannot exclusively be attributed to phonological or acoustic representation but also includes an interaction of linguistic representation.[7] What remains to be seen is whether linguistic representation is expressed at the time of recall or whether the representational methods used (such as recordings, videos, symbols, etc.) participate in a more fundamental role in encoding and preservation of information in memory.[7]
Other senses
Tactile encoding is the processing and encoding of how something feels, normally through touch. Neurons in the primary somatosensory cortex (S1) react to vibrotactile stimuli by activating in synchronisation with each series of vibrations.[8] Odors and tastes may also lead to encode.
Organizational encoding is the course of classifying information permitting to the associations amid a sequence of terms.
In general encoding for short-term storage (STS) in the brain relies primarily on acoustic rather than semantic encoding.
Semantic encoding
Semantic encoding is the processing and encoding of sensory input that has particular meaning or can be applied to a context. Various strategies can be applied such aschunking and mnemonics to aid in encoding, and in some cases, allow deep processing, and optimizing retrieval.
Words studied in semantic or deep encoding conditions are better recalled as compared to both easy and hard groupings of nonsemantic or shallow encoding conditions with response time being the deciding variable.[9]Brodmann's areas 45, 46, and 47 (the left inferior prefrontal cortex or LIPC) showed significantly more activation during semantic encoding conditions compared to nonsemantic encoding conditions regardless of the difficulty of the nonsemantic encoding task presented. The same area showing increased activation during initial semantic encoding will also display decreasing activation with repetitive semantic encoding of the same words. This suggests the decrease in activation with repetition is process specific occurring when words are semantically reprocessed but not when they are nonsemantically reprocessed.[9] Lesion and neuroimaging studies suggest that theorbitofrontal cortex is responsible for initial encoding and that activity in the left lateral prefrontal cortex correlates with the semantic organization of encoded information.[10]
Long-term potentiation
Encoding is a biological event that begins withperception. All perceived and striking sensations travel to the brain's thalamus where all these sensations are combined into one single experience.[11] The hippocampus is responsible for analyzing these inputs and ultimately deciding if they will be committed to long-term memory; these various threads of information are stored in various parts of the brain. However, the exact way in which these pieces are identified and recalled later remains unknown.[11]
Encoding is achieved using a combination of chemicals and electricity. Neurotransmitters are released when an electrical pulse crosses the synapse which serves as a connection from nerve cells to other cells. The dendrites receive these impulses with their feathery extensions. A phenomenon called long-term potentiation allows a synapse to increase strength with increasing numbers of transmitted signals between the two neurons. For that to happen, NMDA receptor, which influences the flow of information between neurons by controlling the initiation of long-term potentiation in most hippocampal pathways, need to come to the play. For these NMDA receptors to be activated, there must be two conditions. Firstly, glutamate has to be released and bound to the NMDA receptor site on postsynaptic neurons. Secondly, excitation has to take place in postsynaptic neurons.[12] These cells also organise themselves into groups specializing in different kinds of information processing. Thus, with new experiences the brain creates more connections and may 'rewire'. The brain organizes and reorganizes itself in response to one's experiences, creating new memories prompted by experience, education, or training.[11] Therefore, the use of a brain reflects how it is organised.[11] This ability to re-organize is especially important if ever a part of the brain becomes damaged. Scientists are unsure of whether the stimuli of what we do not recall are filtered out at the sensory phase or if they are filtered out after the brain examines their significance.[11]
Mapping activity
Positron emission tomography (PET) demonstrates a consistent functional anatomical blueprint of hippocampal activation during episodic encoding and retrieval. Activation in the hippocampal region associated with episodic memory encoding has been shown to occur in the rostral portion of the region whereas activation associated with episodic memory retrieval occurs in the caudal portions.[13] This is referred to as theHippocampal memory encoding and retrievalmodel or HIPER model.
One study used PET to measure cerebral blood flow during encoding and recognition of faces in both young and older participants. Young people displayed increased cerebral blood flow in the right hippocampus and the left prefrontal and temporal cortices during encoding and in the right prefrontal and parietal cortex during recognition.[14] Elderly people showed no significant activation in areas activated in young people during encoding, however they did show right prefrontal activation during recognition.[14]Thus it may be concluded that as we grow old, failing memories may be the consequence of a failure to adequately encode stimuli as demonstrated in the lack of cortical and hippocampal activation during the encoding process.[14]
Recent findings in studies focusing on patients with post traumatic stress disorder demonstrate that amino acid transmitters, glutamate and GABA, are intimately implicated in the process of factual memory registration, and suggest that amine neurotransmitters, norepinephrine and serotonin, are involved in encoding emotional memory.[15]
Molecular perspective
The process of encoding is not yet well understood, however key advances have shed light on the nature of these mechanisms. Encoding begins with any novel situation, as the brain will interact and draw conclusions from the results of this interaction. These learning experiences have been known to trigger a cascade of molecular events leading to the formation of memories.[16] These changes include the modification of neural synapses, modification of proteins, creation of new synapses, activation of gene expression and new protein synthesis. However, encoding can occur on different levels. The first step is short-term memoryformation, followed by the conversion to along-term memory, and then a long-term memory consolidation process.[17]
Synaptic plasticity
Synaptic plasticity is the ability of the brain to strengthen, weaken, destroy and create neural synapses and is the basis for learning. These molecular distinctions will identify and indicate the strength of each neural connection. The effect of a learning experience depends on the content of such an experience. Reactions that are favoured will be reinforced and those that are deemed unfavourable will be weakened. This shows that the synaptic modifications that occur can operate either way, in order to be able to make changes over time depending on the current situation of the organism. In the short term, synaptic changes may include the strengthening or weakening of a connection by modifying the preexisting proteins leading to a modification in synapse connection strength. In the long term, entirely new connections may form or the number of synapses at a connection may be increased, or reduced.[17]
The encoding process
A significant short-term biochemical change is the covalent modification of pre-existing proteins in order to modify synaptic connections that are already active. This allows data to be conveyed in the short term, without consolidating anything for permanent storage. From here a memory or an association may be chosen to become a long-term memory, or forgotten as the synaptic connections eventually weaken. The switch from short to long-term is the same concerning both implicit memory and explicit memory. This process is regulated by a number of inhibitory constraints, primarily the balance between protein phosphorylation anddephosphorylation.[17] Finally, long term changes occur that allow consolidation of the target memory. These changes include new protein synthesis, the formation of new synaptic connections and finally the activation of gene expression in accordance with the new neural configuration.[18] The encoding process has been found to be partially mediated by serotonergic interneurons, specifically in regard to sensitization as blocking these interneurons prevented sensitization entirely. However, the ultimate consequences of these discoveries have yet to be identified. Furthermore, the learning process has been known to recruit a variety of modulatory transmitters in order to create and consolidate memories. These transmitters cause the nucleus to initiate processes required for neuronal growth and long term memory, mark specific synapses for the capture of long-term processes, regulate local protein synthesis and even appear to mediate attentional processes required for the formation and recall of memories.
Encoding and genetics
Human memory, including the process of encoding, is known to be a heritable trait that is controlled by more than one gene. In fact, twin studies suggest that genetic differences are responsible for as much as 50% of the variance seen in memory tasks.[16] Proteins identified in animal studies have been linked directly to a molecular cascade of reactions leading to memory formation, and a sizeable number of these proteins are encoded by genes that are expressed in humans as well. In fact, variations within these genes appear to be associated with memory capacity and have been identified in the
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