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At present, long-term potentiation (LTP) of synaptic transmission is the leading neurophysiologic model for learning and memory processes, despite controversial results regarding its behavioral correlates. The evidence we present in this chapter demonstrates lasting plasticity at the level of local neuronal assemblies in both hippocampus and amygdala. Local circuit plasticity (LCP) is induced by tetanic stimulation of afferent fibers and is mediated, in the hippocampus, by a reduction in GAB A release. Different interneuronal populations are suggested to be involved in the LCP and LTP and at least one type of LCP correlates with age-related spatial memory abilities while the levels of LTP that can be induced initially were found unchanged in this respect. The results suggest that GABAergic interneurons play a major role in LCP and that the involved molecular/cellular modifications do not necessarily occur at the synaptic level. Overall, these data support the conception of LCP as a candidate mnemonic device that may be involved in more than one type of memory.
A general principle of biology is that any given behavior of an organism depends on a hierarchy of levels of organization. As applied to the brain, it means that one needs to identify the main levels of organization in order to provide a framework for understanding the principles underlying its construction and function. The study of brain and mind has led to the recognition of several important levels of analysis from large information processing blocks down to the finest details of molecular structure and subcellular biophysics.
The opinions expressed in the different chapters show a great variety and span the entire range from researchers who believe that long-term potentiation (LTP) is not a model of learning at all and could be an artifact (chapters by McEachern and Shaw, McNaughton, and Matzel and Shors) to those who do not see any problems with the concept of LTP as a model for learning mechanisms (Abraham, Cho and Eichenbaum, and Rogan et al.). Most authors, however, voice a more diversified opinion and suggest a “revised and improved” model of LTP and memory formation that tries to integrate our increased knowledge of how neurons communicate in living brains. Such a model could account for discrepancies observed between LTP inducibility and learning abilities that have been published so far.
Persisting with LTP As a Model for Learning and Memory Formation
While not discussing the lack of correlations between LTP inducibility and learning abilities in numerous publications, Abraham suggests in Chapter 1 that LTP [and long-term depression (LTD)] is still a useful model and the dominating theory for mechanisms of memory formation. He notes that LTP is not homogeneously expressed in areas of the brain. LTP in the dentate gyrus is usually detrimental, whereas CA1 LTP tends to be robust and nondetrimental. LTP in the cortex is difficult to induce but appears to be very stable once it has been induced. To him, these data indicate that genuine differences exist that might reflect different roles in different areas for LTP as a process of memory formation.
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