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Altered transporter‐mediated neocortical GABA release in R asmussen encephalitis
Author(s) -
Rassner Michael P.,
VelthovenWurster Vera,
Ramantani Georgia,
Feuerstein Thomas J.
Publication year - 2013
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/epi.12093
Subject(s) - veratridine , epilepsy , gaba transporter , chemistry , extracellular , transporter , pharmacology , neuroscience , biophysics , anesthesia , biology , medicine , biochemistry , sodium channel , sodium , organic chemistry , gene
Summary To learn whether epileptic seizures in R asmussen encephalitis ( RE ) may be promoted by insufficient γ‐aminobutyric acid ( GABA ) release. 3 H ‐ GABA was released from neocortical synaptosomes through transporter reversal following intrasynaptosomal N a + accumulation by veratridine that prevents inactivation of N a + channels. Tissues of three RE patients were compared with those of nine non‐ RE . In RE , the release was markedly reduced. In non‐ RE , the extracellular C a 2+ concentration ([ C a 2+ ] e ) was inversely related to the amount of release. In RE , the percental decline of additional release uponCa e2 +withdrawal was linked with the presurgical duration of epilepsy. Permanent opening of N a + channels by veratridine resembles maximal frequency of action potentials corresponding to epileptic seizures. These are preceded by a fall in [ C a 2+ ] e . Zero [ C a 2+ ] e increased release through the N a + / C a 2+ exchanger additionally elevating intrasynaptosomal N a + . This enhanced GABA release probably reflects an antiseizure mechanism. In RE , the additional release gets lost over epilepsy duration.