Article

Long-term plasticity of endocannabinoid signaling induced by developmental febrile seizures.

Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, CA 92697, USA.
Neuron (impact factor: 14.74). 09/2003; 39(4):599-611. pp.599-611
Source: PubMed

ABSTRACT 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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Keywords

activity-dependent
 
cholecystokinin-containing perisomatic inhibitory inputs
 
common form
 
endocannabinoid signaling results
 
endocannabinoid-mediated inhibition
 
endocannabinoid-mediated retrograde signaling
 
endogenous cannabinoids
 
Febrile
 
febrile seizures
 
GABAergic synapses
 
human neurological disease
 
long-term increase
 
postnatal development
 
potentiation
 
presynaptic cannabinoid type 1 receptors
 
rat hippocampus
 
retrograde inhibition
 
single episode