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Increase in GAP‐43 and GFAP immunoreactivity int the rat hippocampus subsequent to perforant path kindling
Author(s) -
Dalby N. O.,
Rondouin G.,
LernerNatoli M.
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490410507
Subject(s) - fascia dentata , perforant path , kindling , glial fibrillary acidic protein , hippocampus , hippocampal formation , neuroscience , sprouting , gap 43 protein , perforant pathway , helix pomatia , biology , chemistry , epilepsy , microbiology and biotechnology , immunohistochemistry , dentate gyrus , immunology , snail , botany , ecology
Kindling is an animal model of epilepsy which is accompanied by morphological and biochemical changes in the brain, including sprouting of fibers and increased transmitter release. Here we have examined the immunocytochemical expression of (1) GAP‐43, a growth‐associated protein, which is a neuron‐specific PKC substrate, particularly expressed in development and regeneration and (2) glial fibrillary acidic protein (GFAP), part of the astrocytic cytoskeleton, after perforant path kiraling. Subsequent to kindling, GAP‐43 imimunoreacliviiy was increased in CAI stratum lacunosum‐moleculare and the inner and outer molecular layer of the fascia dentata. Other hippocampal subregions showed a lower increase. GFAP immunoreactivity was increased in the entire hippocampus, but especially in stratum lacunosum‐moleculare of the CAI and the hilus of fascia dentata. The difference between the number of GFAP‐positive profiles in the hippocampus of control rats and in fully kindled rats was found to be non‐significant. We interpret these findings as being related to both plastic neuronal changes and possible neuronal degeneration. © 1995 Wiley‐Liss, Inc.