On LTP
Nevertheless, they conclude that "most evidence firmly supports a role for LTP in learning and memory" (also see Eichenbaum & Otto 1993). This conclusion is based, in part, on a commonly echoed assertion that although no direct evidence links LTP to memory, no better mechanism has been postulated.
it cannot be said with certainty that LTP can not be induced in a particular brain region, but it is safe to say that phenomena fitting the general description of LTP occur ubiquitously throughout the nervous system.
even in tasks dependent on the hippocampus for acquisition, the structure is typically not required for later retrieval.
As operationally defined by Bliss and Lomo (1973), LTP is a persistent (hours) enhancement of an excitatory postsynaptic potential (EPSP) following brief high-frequency (tetanic) stimulation of afferent pathways
If enhanced synaptic efficacy is, in fact, the mechanism underlying memory formation (a topic that we cannot fully address here), and all forms of enhanced synaptic efficacy are deemed to be LTP, the hypothesis that LTP underlies memory formation cannot be disproved and serves no heuristic value. In the end, the term "LTP" becomes no more than a synonym for memory formation .
The point is that one should not assume that a single mechanism is shared by all; rather, the length and breadth of the list of modulators suggests that they could not impinge on a single mechanism or even a single class of mechanisms
One defining feature of LTP is its dependence on high levels of postsynaptic calcium, a common feature of most learning-induced neuronal modifications. In and of itself, a definition which includes "calcium dependence" provides little insight since a wide range of cellular functions require calcium and still more are dependent on elevations of intracellular Ca2+ above basal levels
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posted by eline @ 3:24 AM
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