Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2003-11-19
pubmed:abstractText
Valproate has been in clinical use for nearly 40 years for the treatment of a variety of neuropsychiatric illnesses, including bipolar disorder and epilepsy. Early reports linked its biochemical mechanism of action to alterations in gamma-aminobutyric acid (GABA)-ergic function. The definitive mechanism(s) mediating the clinical efficacy of this relatively simple molecule remain obscure. Although valproate does not directly interact with postsynaptic GABA receptors, it does increase regional neuronal concentrations of GABA by both inhibiting its metabolism and increasing its synthesis. The relevance of these effects to the clinical efficacy of valproate is unclear. Results of preclinical research, largely in rodents, have implicated ion channels, monoamines, corticotropin-releasing factor, and intracellular signaling proteins in the mechanism of action of valproate. This relative dearth of data in the area of valproate neuropharmacology is also evident when discussing the mechanism( s) of action of other mood stabilizers and anticonvulsants. Modern tools of basic and clinical neuroscience (eg, genomics, proteomics, functional brain imaging) will rapidly provide valuable insights into the precise mechanism(s) of action of valproate.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0048-5764
pubmed:author
pubmed:issnType
Print
pubmed:volume
37 Suppl 2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17-24
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Pharmacology of valproate.
pubmed:affiliation
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, Suite 4000, Atlanta, GA 30322, USA. mowens@emory.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't