Pilocarpine-induced status epilepticus increases Homer1a and changes mGluR5 expression

Summary Homer1a regulates expression of group I metabotropic glutamate receptors type I (mGluR1 and mGluR5) and is involved in neuronal plasticity. It has been reported that Homer1a expression is upregulated in the kindling model and hypothesized to act as an anticonvulsant. In the present work, we...

Full description

Saved in:
Bibliographic Details
Published in:Epilepsy research 2012-09, Vol.101 (3), p.253-260
Main Authors: Cavarsan, C.F, Tescarollo, F, Tesone-Coelho, C, Morais, R.L.T, Motta, F.L.T, Blanco, M.M, Mello, L.E
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Carrier Proteins - genetics
Carrier Proteins - metabolism
Epilepsy
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Hippocampus
Homer Scaffolding Proteins
Homer1a
Immediate early genes
Male
Medical sciences
Nervous system (semeiology, syndromes)
Neurology
Neuropharmacology
Neuroprotective agent
Pharmacology. Drug treatments
Pilocarpine - toxicity
Pilocarpine model
Rat
Rats
Rats, Wistar
Receptor, Metabotropic Glutamate 5
Receptors, Metabotropic Glutamate - genetics
Receptors, Metabotropic Glutamate - metabolism
Seizures - chemically induced
Seizures - metabolism
Status Epilepticus - chemically induced
Status Epilepticus - genetics
Status Epilepticus - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Summary Homer1a regulates expression of group I metabotropic glutamate receptors type I (mGluR1 and mGluR5) and is involved in neuronal plasticity. It has been reported that Homer1a expression is upregulated in the kindling model and hypothesized to act as an anticonvulsant. In the present work, we investigated whether pilocarpine-induced status epilepticus (SE) would alter Homer1a and mGluR5 expression in hippocampus. Adult rats were subjected to pilocarpine-model and analyzed at 2 h, 8 h, 24 h and 7 d following SE. mRNA analysis showed the highest expression of Homer1a at 8 h after SE onset, while immunohistochemistry demonstrated that Homer1a protein expression was significantly increased in hippocampus, amygdala and piriform and entorhinal cortices at 24 h after SE onset when compared to control animals. The increased Homer1a expression coincided with a significant decrease of mGluR5 protein expression in amygdala and piriform and entorhinal cortices. The data suggest that during the critical periods of epileptogenesis, overexpression of Homer1a occurs to counteract hyperexcitability and thus Homer1a may be a molecular target in the treatment of epilepsy.
ISSN:0920-1211
1872-6844
DOI:10.1016/j.eplepsyres.2012.04.011