Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-8-4
pubmed:abstractText
In the present study, we investigated the cellular and synaptic mechanisms underlying the neuroprotective action of lamotrigine and remacemide. Both drugs, in fact, have been reported to exert a neuroprotective action in in vivo animal models of ischemia. To address this issue, electrophysiological recordings and cell swelling measurements were performed from striatal neurons in control condition and during combined oxygen and glucose deprivation (in vitro ischemia) in a brain slice preparation. Lamotrigine, remacemide, and the active desglycinyl metabolite of remacemide, D-REMA, induced a concentration-dependent reduction of both repetitive firing discharge and excitatory postsynaptic potentials. However, while remacemide and D-REMA exerted their inhibitory action on glutamatergic transmission by blocking NMDA receptors, lamotrigine exerted a preferential presynaptic action, as indicated by its ability to increase paired-pulse facilitation. Both remacemide and lamotrigine were found to be neuroprotective against the irreversible field potential loss and cell swelling induced by in vitro ischemia, and coadministration of low concentrations of these drugs exerted an additive neuroprotective action. A combined use of lamotrigine and remacemide could be employed in clinical trials to enhance neuroprotection in neurological disorders involving an abnormal striatal glutamatergic transmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
182
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
461-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12895457-Acetamides, pubmed-meshheading:12895457-Animals, pubmed-meshheading:12895457-Anticonvulsants, pubmed-meshheading:12895457-Brain Ischemia, pubmed-meshheading:12895457-Cell Hypoxia, pubmed-meshheading:12895457-Corpus Striatum, pubmed-meshheading:12895457-Dose-Response Relationship, Drug, pubmed-meshheading:12895457-Drug Synergism, pubmed-meshheading:12895457-Electric Stimulation, pubmed-meshheading:12895457-Electrophysiology, pubmed-meshheading:12895457-Excitatory Amino Acids, pubmed-meshheading:12895457-Excitatory Postsynaptic Potentials, pubmed-meshheading:12895457-Glucose, pubmed-meshheading:12895457-Neurons, pubmed-meshheading:12895457-Neuroprotective Agents, pubmed-meshheading:12895457-Patch-Clamp Techniques, pubmed-meshheading:12895457-Rats, pubmed-meshheading:12895457-Rats, Wistar, pubmed-meshheading:12895457-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:12895457-Triazines
pubmed:year
2003
pubmed:articleTitle
Lamotrigine and remacemide protect striatal neurons against in vitro ischemia: an electrophysiological study.
pubmed:affiliation
Clinica Neurologica, Dipartimento di Neuroscienze, Università di Roma Tor Vergata, Via Montpellier 1, 00133 Rome, Italy. calabre@uniroma2.it
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't