Long-term Potentiation Memory Research Articles

Hormones and the hippocampus.

Hippocampal lesions produce memory deficits, but the exact function of the hippocampus remains obscure. Evidence is presented that its role in memory may be ancillary to physiological regulation. Molecular studies demonstrate that the hippocampus is a primary target for ligands that reflect body physiology, including ion balance and blood pressure, immunity, pain, reproductive status, satiety and stress. Hippocampal receptors are functional, probably accessible to their ligands, and mediate physiological and cognitive changes. This argues that an early role of the hippocampus may have been in sensing soluble molecules (termed here 'enteroception') in blood and cerebrospinal fluid, perhaps reflecting a common evolutionary origin with the olfactory system ('exteroception'). Functionally, hippocampal enteroception may reflect feedback control; evidence is reviewed that the hippocampus modulates body physiology, including the activity of the hypothalamus-pituitary-adrenal axis, blood pressure, immunity, and reproductive function. It is suggested that the hippocampus operates, in parallel with the amygdala, to modulate body physiology in response to cognitive stimuli. Hippocampal outputs are predominantly inhibitory on downstream neuroendocrine activity; increased synaptic efficacy in the hippocampus (e.g. long-term potentiation) could facilitate throughput inhibition. This may have implications for the role of the hippocampus and long-term potentiation in memory.

LTP: Memory, arousal, neither, both

The neurophysiological phenomenon of LTP (long term potentiation) is considered by many to represent an adequate mechanism for acquiring or storing memories in the mammalian brain. In our target article, we reviewed the various arguments put forth in support of the LTP/memory hypothesis. We concluded that these arguments were inconsistent with the purported data base and proposed an alternative interpretation that we suggested was at least as compatible with the available data as the more widely held view. In doing so, we attempted to illustrate that the inadequacy of present experimental designs did not permit us to distinguish between equally viable hypotheses. In the four years since we wrote the first draft of our target article, hundreds of additional studies on LTP have been published and their results have been incorporated into current theories about memory. A diverse group of commentators responded to our target article with their own theories of how memories might be stored in the brain, some of which rely on LTP. Some commentators doubted whether memories can be stored through modifications of synaptic strength. Some assert that it will never be possible to understand the neural mechanisms of memory; still others remain hopeful that we will accomplish some semblance of a resolution, provided we appreciate LTP's role in a subset of seemingly amorphous memory systems. In summary, although it is commonly written that “LTP is a memory storage device,” the divergence of views among the commentators suggests, at least as strongly as our target article, that such conviction is unwarranted and fails to acknowledge both the lack of consensus regarding the role of LTP in memory and the complexity of the phenomenon of memory itself.

Long-term potentiation and learning.

Long-term potentiation (LTP), a relatively long-lived increase in synaptic strength, remains the mot popular model for the cellular process that may underlie information storage within neural systems. The strongest arguments for a role of LTP in memory are theoretical and involve Hebb's Postulate, Marr's theory of hippocampal function, and neural network theory. Considering LTP research as a whole, few studies have addressed the essential question: Is LTP a process involved in learning and memory? The present manuscript reviews research that attempts to link LTP with learning and memory, focusing on studies utilizing electrophysiological, pharmacological, and molecular biological methodologies. Most evidence firmly supports a role for LTP in learning memory. However, an unequivocal experimental demonstration of a contribution of LTP to memory is hampered by our lack of knowledge of the biological basis of memory and of the ways in which memories are represented in ensembles of neurons, the existence of a variety of cellular forms of LTP, and the likely resistance of distributed memory stores to degradation by treatments that incompletely disrupt LTP.