Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Long-term valproate treatment increases brain neuropeptide Y expression and decreases seizure expression in a genetic rat model of absence epilepsy.

Authors: Elms, J  Powell, KL  Van Raay, L  Dedeurwaerdere, S  O'Brien, TJ  Morris, MJ 
Citation: Elms J, etal., PLoS One. 2013 Sep 9;8(9):e73505. doi: 10.1371/journal.pone.0073505. eCollection 2013.
Pubmed: (View Article at PubMed) PMID:24039965
DOI: Full-text: DOI:10.1371/journal.pone.0073505

The mechanisms by which valproate, one of the most widely prescribed anti-epileptic drugs, suppresses seizures have not been fully elucidated but may involve up-regulation of neuropeptide Y (NPY). We investigated the effects of valproate treatment in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) on brain NPY mRNA expression and seizure control. GAERS were administered either valproate (42 mg.kg(-1) hr(-1)) or saline continuously for 5 days. Electroencephalograms were recorded for 24 hrs on treatment days 1, 3 and 5 and the percentage of time spent in seizure activity was analysed. NPY mRNA expression was measured in different brain regions using qPCR. Valproate treatment suppressed seizures by 80% in GAERS (p<0.05) and increased NPY mRNA expression in the thalamus (p<0.05) compared to saline treatment. These results demonstrate that long-term valproate treatment results in an upregulation of thalamic expression of NPY implicating this as a potential contributor to the mechanism by which valproate suppresses absence seizures.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 10448964
Created: 2015-12-09
Species: All species
Last Modified: 2015-12-09
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.