Premium
Glutamate receptor 1‐immunopositive neurons in the gliotic CA1 area of the mouse hippocampus after pilocarpine‐induced status epilepticus
Author(s) -
Tang Feng Ru,
Chia Shwn Chin,
Zhang Si,
Chen Peng Min,
Gao Hong,
Liu Chun Ping,
Khanna Sanjay,
Lee Wei Ling
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04071.x
Subject(s) - dentate gyrus , subiculum , epileptogenesis , hippocampal formation , neuroscience , calretinin , status epilepticus , pilocarpine , ampa receptor , calbindin , hippocampus , parvalbumin , entorhinal cortex , glutamate receptor , biology , chemistry , medicine , pathology , epilepsy , receptor , immunohistochemistry
Abstract Significant reduction in glutamate receptor 1 (GluR1)‐ and GluR2/3‐immunopositive neurons was demonstrated in the hilus of the dentate gyrus in mice killed on days 1, 7 and 60 after pilocarpine‐induced status epilepticus (PISE). In addition, GluR1 and GluR2/3 immunostaining in the strata oriens, radiatum and lacunosum moleculare of areas CA1–3 decreased drastically on days 7 and 60 after PISE. Neuronal loss observed in the above regions may account, at least in part, for a decrease in GluR immunoreactivity. By contrast, many GluR1‐immunopositive neurons were observed in the gliotic area of CA1. Of these, about 42.8% were immunopositive for markers for hippocampal interneurons, namely calretinin (7.6%), calbindin (12.8%) and parvalbumin (22.4%). GluR1 or GluR2/3 and BrdU double‐labelling showed that the GluR1‐ and GluR2/3‐immunopositive neurons at 60 days after PISE were neurons that had survived rather than newly generated neurons. Furthermore, anterograde tracer and double‐labelling studies performed on animals at 60 days after PISE indicated a projection from the hilus of the dentate gyrus to gliotic areas in both CA3 and CA1, where the projecting fibres apparently established connections with GluR1‐immunopositive neurons. The projection to CA1 was unexpected. These novel findings suggest that the intrinsic hippocampal neuronal network is altered after PISE. We speculate that GluR1‐immunopositive neurons in gliotic CA1 act as a bridge between dentate gyrus and subiculum contributing towards epileptogenesis.