WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges

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	WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges
	van Rijn, Clementina M. ; Gaetani, Silvana ; Santolini, Ines ; Badura, Aleksandra ; Gabova, Aleksandra ; Fu, Jin ; Watanabe, Masashiko ; Cuomo, Vincenzo ; van Luijtelaar, Gilles ; Nicoletti, Ferdinando ; Ngomba, Richard T. ; Fu J(傅瑾)
刊名	http://dx.doi.org/10.1111/j.1528-1167.2009.02510.x
	2010-08
关键词	DEPOLARIZATION-INDUCED SUPPRESSION TEMPORAL-LOBE EPILEPSY CANNABINOID RECEPTOR ABSENCE EPILEPSY ENDOGENOUS CANNABINOIDS GABAERGIC INHIBITION HIPPOCAMPAL SYNAPSES PILOCARPINE MODEL GENETIC MODEL SEIZURES
英文摘要	P>Purpose: Genetically epileptic WAG/Rij rats develop spontaneous absence-like seizures after 3 months of age. We used WAG/Rij rats to examine whether absence seizures are associated with changes in the expression of type-1 cannabinoid (CB1) receptors. Methods: Receptor expression was examined by in situ hybridization and western blot analysis in various brain regions of "presymptomatic" 2-month old and "symptomatic" 8-month-old WAG/Rij rats relative to age-matched nonepileptic control rats. Furthermore, we examined whether pharmacologic activation of CB1 receptor affects absence seizures. We recorded spontaneous spike-wave discharges (SWDs) in 8-month old WAG/Rij rats systemically injected with the potent CB1 receptor agonist, R(+)WIN55,212-2 (3-12 mg/kg, s.c.), given alone or combined with the CB1 receptor antagonist/inverse agonist, AM251 (12 mg/kg, s.c.). Results: Data showed a reduction of CB1 receptor mRNA and protein levels in the reticular thalamic nucleus, and a reduction in CB1 receptor protein levels in ventral basal thalamic nuclei of 8-month-old WAG/Rij rats, as compared with age-matched ACI control rats. In vivo, R(+)WIN55,212-2 caused a dose-dependent reduction in the frequency of SWDs in the first 3 h after the injection. This was followed by a late increase in the mean SWD duration, which suggests a biphasic modulation of SWDs by CB1 receptor agonists. Both effects were reversed or attenuated when R(+)WIN55,212-2 was combined with AM251. Discussion: These data indicate that the development of absence seizures is associated with plastic modifications of CB1 receptors within the thalamic-cortical-thalamic network, and raise the interesting possibility that CB1 receptors are targeted by novel antiabsence drugs.
语种	英语
出版者	EPILEPSIA
内容类型	期刊论文
源URL	[http://dspace.xmu.edu.cn/handle/2288/93204]
专题	医学院－已发表论文
推荐引用方式 GB/T 7714	van Rijn, Clementina M.,Gaetani, Silvana,Santolini, Ines,et al. WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges[J]. http://dx.doi.org/10.1111/j.1528-1167.2009.02510.x,2010.
APA	van Rijn, Clementina M..,Gaetani, Silvana.,Santolini, Ines.,Badura, Aleksandra.,Gabova, Aleksandra.,...&傅瑾.(2010).WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges.http://dx.doi.org/10.1111/j.1528-1167.2009.02510.x.
MLA	van Rijn, Clementina M.,et al."WAG/Rij rats show a reduced expression of CB1 receptors in thalamic nuclei and respond to the CB1 receptor agonist, R(+)WIN55,212-2, with a reduced incidence of spike-wave discharges".http://dx.doi.org/10.1111/j.1528-1167.2009.02510.x (2010).