1992
DOI: 10.1016/0920-1211(92)90064-z
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Glutamate in the inferior colliculus plays a critical role in audiogenic seizure initiation

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Cited by 70 publications
(17 citation statements)
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“…Excessive excitatory transmission may also char- acterize other models of seizure proclivity with similarities to metaphit. A role for the NMDAIPCP complex has been documented in brainstem seizures of genetic models of the epilepsies (Chapman and Meldrum, 1989;Faingold et al, 1992) and in kindling (Freeman et al, 1982;Glibert, 1988;Leander et al, 1988;McNamara et al, 1988;Morimoto and Sato, 1992). This proposed commonality in excessive excitatory transmission by the NMDA/PCP receptor complex may be responsible for the similar pharmacologic profiles that characterize some of the effects of metaphit and NMDA.…”
Section: Epilepsiamentioning
confidence: 99%
“…Excessive excitatory transmission may also char- acterize other models of seizure proclivity with similarities to metaphit. A role for the NMDAIPCP complex has been documented in brainstem seizures of genetic models of the epilepsies (Chapman and Meldrum, 1989;Faingold et al, 1992) and in kindling (Freeman et al, 1982;Glibert, 1988;Leander et al, 1988;McNamara et al, 1988;Morimoto and Sato, 1992). This proposed commonality in excessive excitatory transmission by the NMDA/PCP receptor complex may be responsible for the similar pharmacologic profiles that characterize some of the effects of metaphit and NMDA.…”
Section: Epilepsiamentioning
confidence: 99%
“…TRPV1 channel is a nonselective cation channel with high Ca 2+ permeability, and its activation results in increased intracellular Ca 2+ and neuronal excitability, leading to enhanced glutamate release . Interestingly, altered intracellular Ca 2+ and glutamate signaling in the IC are known to play important roles in the pathophysiology of seizures in GEPRs . Whether Ca 2+ signaling via TRPV1 channels interacting with glutamate signaling is critical in AGS susceptibility in GEPR‐3s remains unknown.…”
Section: Discussionmentioning
confidence: 99%
“…[23][24][25][26] Interestingly, altered intracellular Ca 2+ and glutamate signaling in the IC are known to play important roles in the pathophysiology of seizures in GEPRs. 27,28 Whether Ca 2+ signaling via TRPV1 channels interacting with glutamate signaling is critical in AGS susceptibility in GEPR-3s remains unknown. Another putative mechanism underlying epileptogenesis is long-term potentiation (LTP), where repeated synaptic stimulation lead to enhancement of synaptic efficiency.…”
Section: Discussionmentioning
confidence: 99%
“…Similarly, administration of AMPA alone increased the frequency of SWD [73], but co-administration of an NMDA receptor-antagonist was sufficient to block this increase. In GEPRs, inhibition of glutamate synthesis, NMDA, or AMPA receptors attenuated seizure severity [74]. Contrary to the pilocarpine-SE model, where decreases in mGluR 2/3 activation increased with seizure sensitivity, mGluR 2/3 antagonists decreased seizure frequency in Wag/Rij rats [75].…”
Section: Potential Mechanisms and Therapeutic Targetsmentioning
confidence: 99%