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PURPOSE In limbic or mesial temporal lobe epilepsy, much attention has been given to specific regions or cell populations (e.g., the hippocampus or dentate granule cells). Epileptic seizures may involve broader changes in neural circuits, and evidence suggests that subcortical regions may play a role. In this study we examined the midline thalamic regions(More)
The limbic/mesial temporal lobe epilepsy syndrome has been defined as a focal epilepsy, with the implication that there is a well defined focus of onset, traditionally centered around the hippocampus. The pathology of the hippocampus in this syndrome has been well described and a number of physiological abnormalities have been defined in this structure in(More)
CA1 is the major output area for the hippocampus, and current evidence shows that it is excited primarily from ipsilateral and contralateral CA3 pyramidal cells in the rat. Direct connections from the midline thalamic nuclei to the hippocampus have been described anatomically, but the physiological role of these connections has not been reported until the(More)
The midline thalamus has a role in memory formation and has well described projections to multiple limbic sites including the hippocampus, amygdala, and entorhinal cortex. Stimulation of this region evokes excitatory responses in the CA1 region of the hippocampus, but nothing is known about the nature of thalamic influence on other limbic sites such as the(More)
OBJECTIVE The optimal sites and stimulation protocols for brain stimulation in epilepsy have not been found. Clinical trials, which have shown modest benefit in seizure reduction, have involved patients with poorly localized intractable focal epilepsy and stimulation sites without clear relations to specific underlying seizure circuits. The medial dorsal(More)
PURPOSE Uncontrolled epilepsy remains a significant health concern and requires new approaches to therapy. N-methyl-d-aspartate (NMDA) receptor blockade has been considered, but the adverse cognitive and behavioral effects of conventional NMDA-receptor antagonists have prevented the development of clinically useful compounds. An alternative approach may be(More)
In one computational model of hippocampal function, the entorhinal cortical input to CA1 is hypothesized to play a key role in the ability of CA1 to decode CA3 recodings. Here, we develop a modification of this CA1 decoder hypothesis that is applicable to several computational theories of hippocampal function, and then we electrophysiologically investigate(More)
The physiology and pharmacology of CA1 is changed in epilepsy. There is evidence that the thalamic input to CA1 has a somewhat different physiological effect compared with the CA3 input. In this study we sought to determine whether this difference in physiology persists in epilepsy, and whether there are changes in the pharmacologic profile of these(More)
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