The endocannabinoid system is an important form of interneuronal communication made of presynaptic cannabinoid type-1 (CB1) receptors and endogenous cannabis compounds (CBs) which share structural analogies with esocannabinoids derived from Cannabis Sativa (Δ9- tetrahydrocannabinol and others). The CB1 receptor is considered to be the most abundant G-protein-coupled receptor in the mammalian brain, in particular in the hippocampus, and its activation by CBs in different brain sites decreases both inhibitory (GABA) and excitatory (glutamate) neurotransmitter release. It has been recently shown, in an animal model of febrile seizures, that a single episode of experimental prolonged febrile seizure during early postnatal development persistently enhances, in the rat hippocampus, the retrograde inhibition of GABA release by endogenous cannabinoids. The potentiation of endocannabinoid signalling results from selective increase in the number of CBl receptors modulating GABA release, without an effect on the endocannabinoid- mediated inhibition of glutamate release. This selective long-term plasticity of endocannabinoid signaling induces a chronic suppression of inhibition resulting in a lower seizure threshold. Because of the association of mesial temporal sclerosis with prolonged febrile seizures in infancy, we can hypothesize an analogous endocannabinoid-mediated mechanism in the epileptogenesis of this epileptic syndrome. It seems thus interesting to measure the CB1 receptors' expression and activity in the hippocampus of patients with epilepsy associated with mesial temporal sclerosis that underwent temporal lobectomy.
|Translated title of the contribution||Study proposal on epilepsy associated with mesial temporal sclerosis and the endocannabinoid system|
|Number of pages||2|
|Journal||Bollettino - Lega Italiana contro l'Epilessia|
|Publication status||Published - 2005|
ASJC Scopus subject areas
- Clinical Neurology