Journal
NEURON
Volume 39, Issue 4, Pages 599-611Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(03)00499-9
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Funding
- NIDA NIH HHS [DA00286, DA11322, DA3412, DA12447] Funding Source: Medline
- NINDS NIH HHS [NS33213, NS38580] Funding Source: Medline
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Febrile (fever-induced) seizures are the most common form of childhood seizures, affecting 3%-5% of infants and young children. Here we show that the activity-dependent, retrograde inhibition of GABA release by endogenous cannabinoids is persistently enhanced in the rat hippocampus following a single episode of experimental prolonged febrile seizures during early postnatal development. The potentiation of endocannabinoid signaling results from an increase in the number of presynaptic cannabinoid type 1 receptors associated with cholecystokinin-containing perisomatic inhibitory inputs, without an effect on the endocannabinoid-mediated inhibition of glutamate release. These results demonstrate a selective, long-term increase in the gain of endocannabinoid-mediated retrograde signaling at GABAergic synapses in a model of a human neurological disease.
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