Status epilepticus differentially alters AMPA and kainate receptor subunit expression in mature and immature dentate granule neurons.
There is an increase in the birth of dentate granule neurons after status epilepticus (SE) and there are concurrent alterations in neurotransmitter receptor expression that may contribute to the development of spontaneous seizures. To determine whether newborn and/or mature dentate granule neurons have altered neurotransmitter receptor expression after SE, we dissected individual immature, PSA-NCAM-expressing, or mature, NeuN-expressing, dentate granule neurons 2 weeks after lithium-pilocarpine-induced SE in postnatal day 20 rats. Amplified single-cell RNA was used to probe reverse Northern blots containing alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and kainate neurotransmitter receptor subunits. Two weeks after lithium-pilocarpine-induced SE there were increases in AMPA GluR2 and kainate KA2 subunit mRNA and decreases in AMPA GluR3 and kainate GluR6 receptor subunit mRNA levels in mature dentate granule neurons. In contrast, only the kainate GluR6 subunit expression was reduced in immature dentate granule neurons after SE. Alterations in transcription of excitatory amino acid receptor subunits after SE occur primarily in the mature population of dentate granule neurons. Our findings suggest that neurotransmitter receptor gene expression is altered differently in immature and mature dentate granule neurons following SE, and may result in differential contributions of these two groups of dentate granule neurons to the subsequent development of epilepsy.
Porter
Brenda E
BE
The Children's Hospital of Philadelphia, PA, USA. Porterb@chop.edu
Cui
Xiao-Nan
XN
Brooks-Kayal
Amy R
AR
D000818:Animals; D000831:Animals, Newborn; D015152:Blotting, Northern / Q000379:methods; D015153:Blotting, Western / Q000379:methods; D018891:Dentate Gyrus / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D007150:Immunohistochemistry / Q000379:methods; D008094:Lithium / Q000633:toxicity; D039842:Neural Cell Adhesion Molecule L1 / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010751:Phosphopyruvate Hydratase / Q000378:metabolism; D010862:Pilocarpine / Q000633:toxicity; D021122:Protein Subunits / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D018091:Receptors, AMPA / Q000235:genetics / Q000378:metabolism*; D018092:Kainic Acid Receptors / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012794:Sialic Acids / Q000378:metabolism; D013226:Status Epilepticus / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*
D008094:Lithium; D039842:Neural Cell Adhesion Molecule L1; D010751:Phosphopyruvate Hydratase; D010862:Pilocarpine; D021122:Protein Subunits; D018091:Receptors, AMPA; D018092:Kainic Acid Receptors; D012794:Sialic Acids; C103469:polysialyl neural cell adhesion molecule