Gta Eflc Offline Activation 14 Ⓜ
Gta Eflc Offline Activation 14 Ⓜ
Gta Eflc Offline Activation 14
activation of mglur5 has been reported in a number of seizure models. in the 3-hz stimulation model of prolonged seizures, the activation of mglur5 and ampa receptors has been shown to contribute to the development of epileptiform activity ( yamamoto et al. 1999 ). in the pilocarpine model of epilepsy, the activation of mglur5 has been reported to attenuate spontaneous seizures ( zheng et al. 2007 ). although we report that mglur5 activation attenuates epileptiform bursting induced by 4-ap, it is not yet clear how the mglur5 signaling pathway contributes to the development of epilepsy. however, the role of mglur5 activation has been reported to regulate seizure-induced neuronal changes. increased mglur5 expression in the dentate gyrus and ca1 of the hippocampus has been shown to attenuate seizures induced by kainic acid or electroconvulsive shock ( makino et al. 2004 ).
the glur5 blocker mpep also inhibited bursting, as determined by preincubation for 1 hour and washout of culture medium for 10 min. four-hour treatment of the cultures with bic+4-ap in the presence of mpep completely blocked bursting activity, at bic+4-ap concentrations that completely block bic+4-ap-induced synapse loss ( fig. 5 ) ( n = 9, 5.6 0.8 bursts/min before mpep treatment, 0 bursts/min after mpep treatment; fig. 5d ). these results indicate that blocking mglur5 produces a similar effect as bic+4-ap treatment in our assay. treatment with 2k-1c for 4 h resulted in a massive burst firing ( ma et al. 2004 ) that was abolished by co-treatment with mpep (n = 15; 0.05 0.05 bursts/min before mpep treatment, 0.0 0.1 bursts/min after mpep treatment; fig. 5a, b, and d ). the 4-h-induced bursting was completely blocked by co-treatment with mpep (n = 7; 0.25 0.25 bursts/min before mpep treatment, 0.02 0.03 bursts/min after mpep treatment) ( fig. these results indicate that mglur5 activation by mglur5 agonism is toxic, as determined by the other assay, and by the 4-h-induced synaptic loss assay, which required mglur5 blockade by mpep. blocking mglur5 inhibits the 4-h-induced synaptic loss. the antagonist reduces the effective agonist concentration, since bic+4-ap induces mglur5 activation, pro-epileptiform activity, and synapse loss. thus mglur5-blocking drugs may be effective against the treatment-induced effects. for example, the mpep effect on ap is shown here (anova; p = 0.001). the effect of bic+4-ap on ap is shown here (anova; p = 0.05). similarly, the effect of 2k-1c ap change on ap is shown here (anova; p = 0. in 2k-1c treatment, n = 14 and n = 14 for bic+4-ap and 2k-1c treatment, respectively. #p < 0.05, ***p < 0.001 relative to the control student's t-test; #p < 0.05 relative to the untreated bic+4-ap. anova with the tukey posttest. error bars indicate se.
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