Abstract
Recent data show that, while the enhancement of both Glu/Asp-mediated excitation and GABA-mediated inhibition underlies absence attacks, the breakdown of GABAergic inhibition is prerequisite of convulsive and partial seizures. The subsequent activation of NMDA receptors with massive Ca2+ entry into the neurons produces longlasting plastic changes, reinforcing the epileptogenic condition that becomes more and more resistant to therapy as seizures keep recurring. Thus, the rational development of new AEDs against convulsive and partial seizures should be based on: I. prevention of GABAergic breakdown by enhancement of GABA-mediated inhibition; II. impairment of excitatory transmission by decrease of Glu/Asp release or NMDA receptor antagonism; III. Ca2+ antagonists.
| Translated title of the contribution | Convulsive generalized seizures and partial seizures: The cellular bases for the development of new drugs |
|---|---|
| Original language | Italian |
| Title of host publication | Bollettino - Lega Italiana contro l'Epilessia |
| Pages | 407-409 |
| Number of pages | 3 |
| Edition | 66-67 |
| Publication status | Published - 1989 |
| Externally published | Yes |
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