Short Term Memory May Be the Depletion of Releasable Pool--论文代写范文精选

尽管许多研究表明，有两个阶段的感官性质，在某种程度上,缺乏连接认知底层生物化学的细节。下面的paper代写范文进行讲述。

Abstract
The Tagging/Retagging model of short term memory was introduced earlier (1) to explain the linear relationship that exists between response time and correct response probability for word recall and recognition: At the initial stimulus presentation displayed words are tagged by creating a set of neurons in an excitation equilibrium which is the particular brain’s “definition” of the word. This tagging level drops logarithmically with time to 50% after 14 seconds and to 20% after 220 seconds. When a probe word is reintroduced the tagging level has to increase for the word to be properly identified leading to a delay in response time. 

This delay is proportional to the tagging loss which is in turn directly related to the decrease in probability of correct word recall and recognition. Evidence suggests that the tagging level is the level of depletion of the Readily Releasable Pool (RRP) of neurotransmitter vesicles at presynaptic terminals. The evidence includes the linear relationship between tagging level and time as well as the logarithmic decay of the tagging level. The activation of a short term memory may thus be the depletion of RRP (exocytosis) and short term memory loss the ensuing recycling of the neurotransmitter vesicles (endocytosis).

Introduction 
An immense amount of fascinating work has been performed by cognitive psychologists attempting to quantify the properties of short term memory (for a review see (2)). Unfortunately this work has not led to a theoretical convergence. For example, various models of memory stores have been introduced and survive in text books even though “numerous studies suggesting that there are two phases of sensory storage with very different properties: a brief afterimage lasting up to several hundred milliseconds, and a more processed (i.e. perceptually resolved) memory preserving sensory features for up to 15 or 20 seconds” ( (3). 

Presumably this is due, in part, to a lack of connection of the cognitive literature to the details of the underlying biochemistry. Without this “harder science” connection it may be hard to convince various parts of the community of the supremacy of one theoretical model over another. In a recent contribution (1) the current author showed that short term memory correct recall and recognition probabilities are linearly related to response times over a large time range (from 6 to 600 seconds). I interpreted this observation according to a new tagging model of short term memory in which long term memory locations were tagged and as time passes the tagging decays. Only when the memory locations are fully retagged does a subject respond with an affirmative answer to recall or recognition. 

In addition I found that both recall and recognition probabilities decay logarithmically with time. (We also know that for very weak, subliminal stimulation, there should be no short term memory.) The current paper addresses what might be the biological underpinnings of short term memory that have the two properties (a) linear tagging time and (b) logarithmic decay time. I will attempt to trace these cognitive properties of short term memory through the tagging model to their microscopic biochemistry. I start by describing the tagging model and the evidence for the tagging being linear in time and the loss of the tagging being logarithmic in time. Then I trace the tagging process to the depletion of presynaptic neurotransmitter vesicles. A brief summary concludes the paper.

The Tagging Model
The linear curves found are the central findings of the earlier paper. Their simplicity suggests that they describe a core property of short term memory. I explained the relationships by introducing the Tagging/Retagging model of short term memory: When presented with a word, a subject tags that word by marking long term memory locations (Figure 4). The tagging level, defined as the probability of a correct identification, then slowly drops (Figure 5) until the word is reintroduced, at which point the tagging level goes back up (the same word is read again and subjected to the same procedure as the first time it was presented see Figure 6). The retagging time can be inferred from the delay in the response and is found to be proportional to the tagging level drop from the linear relationship between response time and probability of recall and recognition. When the tagging level of the probe word drops to x%, the tagging level of the reference to the initial list (for recognition) and of the word association (for recall) also drops to x%. As the exposure to the probe word retags the probe word, the tagging levels of the list reference and word association are not increased and the subject only responds correctly x% of the time.

The strikingly linear relationship between response probability and response time is likely a fundamental property of our short term memory. The tagging model is a compelling explanation of the data. But any memory process is one of biochemistry. What could possibly be a biochemical mechanism explaining the tagging model? We know that long term memory is related to long term synaptic changes presumably via protein synthesis (6). Short term behavior in the very simple slug aplysia can also be related to changes in the synapses: “serotonin leads to an increase in presynaptic cAMP, which activates PKA and leads to synaptic strengthening through enhanced transmitter release produced by a combination of mechanisms” (6). Thus it is tempting to search for something that quickly tags synapses and more slowly untags them and does so in a reversible fashion (if the changes are not reversible, it would be long term memory rather than short term). Such a system is the cycle of exocytosis and endocytosis of neurotransmitter vesicles in the presynaptic terminal.

The Cycle of Exocytosis and Endocytosis 
Neurotransmitter is stored in small vesicles in the presynaptic terminal (for an introduction please see (7) pp. 105-7 and the introduction in (8) and on can surmise that “all presynaptic functions, directly or indirectly, involve synaptic vesicles” (9) (exocytosis and endocytosis has been reviewed elsewhere ( (9) and (16)). . When an action potential comes along the presynaptic neuron in, say, hippocampus, the Ca2+ channels open and in 10-20% of cases ( (10) and (11)) cause one (typical in the hippocampus, see (11)) of these vesicles to fuse to the plasma membrane of the presynaptic terminal and open up a pore into the synaptic cleft and release neurotransmitter into the synaptic cleft (exocytosis). 

It occurs via a synchronous (within 1 msec) and an asynchronous component (12) (which persists for tens of msecs) and the asynchronous component can after repeated stimulation completely deplete the available vesicles in what is called the Readily Releasable Pool of vesicles (RRP, for reviews of the RRP see (13) and (9)). Neurotransmitters cross over to the receptors in the postsynaptic terminal and make an action potential more likely in the postsynaptic neuron. The neurotransmitter in the synaptic cleft is quickly broken down by enzymes. Exocytosis is a possible candidate for the tagging process. In Figure 9 is shown the average time course for exocytosis (depletion of the Readily Releasable Pool of neurotransmitter vesicles) in a rat hippocampal culture (11). It is linear in the beginning just like the tagging process and the overall time is a little over 1 second, consistent with the tagging time in the experiments quoted (calculated in (1) to be 0.2 to 1.8 seconds). Full tagging corresponds to a state of the synapse in which the presynaptic neurons are no longer actively influencing the postsynaptic neuron, in effect, limiting the size of the overall neural excitation corresponding to the recalled or recognized word.(paper代写)

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