Premium
Long‐term synaptic alteration in the rat hippocampal CA3 field following an entorhinal cortex lesion
Author(s) -
Miwa Chitoku,
Ueki Akinori,
Shinjo Hidetaka,
Simode Hiroko,
Morita Yoshio
Publication year - 2001
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1046/j.1440-1819.2001.00908.x
Subject(s) - entorhinal cortex , ibotenic acid , synaptophysin , hippocampal formation , dentate gyrus , hippocampus , neuroscience , lesion , acetylcholinesterase , cortex (anatomy) , pathology , medicine , immunohistochemistry , biology , central nervous system , biochemistry , enzyme
The entorhinal cortex is a key initial relay for cortical input to the hippocampus. To better understand hippocampal dysfunction resulting from early entorhinal cortex involvement in Alzheimer’s disease, we stereotaxically injected ibotenic acid to produce unilateral entorhinal cortex lesions in rats. We then serially examined the CA3 hippocampal region by neuronal counts, histochemistry for acetylcholinesterase, and synaptophysin immunohistochemistry. Over 12 months, the neuronal counts did not change. Acetylcholinesterase‐positive fibers were persistently but non‐progressively beginning at 3 months. Synaptophysin immunoreactivity progressively declined over 12 months. Since much of the entorhinal cortex output proceeds to CA3 via the dentate gyrus, transsynaptic degeneration is suspected.