Abstract
A rodent model of diencephalic amnesia, pyrithiamine-induced thiamine deficiency (PTD), was used to investigate diencephalic-hippocampal interactions. Acetylcholine (ACh) release, a marker of memory-related activation, was measured in the hippocampus of PTD-treated and control rats prior to, during, and after spontaneous alternation test. During behavioral testing, all animals displayed increases in ACh release. However, both the percent increase of ACh release during spontaneous alternation testing and the alternation scores were higher in control rats relative to PTD-treated rats. Thus, when rats are tested on a task with demands dependent on the hippocampus, it appears that the hippocampus is not fully activated after diencephalic damage.
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