Endocannabinoid Signaling and Febrile Seizures

(No Ratings Yet)

Loading ...

November 30, 2007

Although febrile seizures are common in childhood and often benign, prolonged febrile seizures can have long-term consequences.

Prolonged febrile seizures paradoxically increase hippocampal GABA release and decrease seizure threshold. In this week’s Journal, Chen et al. strengthen the case for depolarization-induced suppression of inhibition (DSI) as the underlying mechanism for these changes. DSI occurs when increases in postsynaptic calcium trigger production and release of endocannabinoids, which then bind at presynaptic CB1 receptors. The end result is reduced GABA release and heightened network excitability. In hippocampal slices from seizure-naive rats, tetanic stimulation potentiated DSI in a CB1 receptor-dependent manner. However, tetanization did not potentiate DSI in slices from animals that had experienced in vivo hypothermia-induced febrile seizures, in which DSI was already elevated. In vivo, a CB1 antagonist blocked the seizure-induced DSI potentiation, the associated upregulation of CB1 receptors, and diminished long-term hippocampal excitability.

By Society for Neuroscience

Share and Enjoy: These icons link to social bookmarking sites where readers can share and discover new web pages.