000			02080na a2200229 4500
003			H12O
005			20180417112606.0
008			130622s2011 xxx||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_9730 _aMolina Arjona, José Antonio _eNeurología
245	0	0	_aIncreased vulnerability to 6-hydroxydopamine lesion and reduced development of dyskinesias in mice lacking CB1 cannabinoid receptors _h[artículo]
260			_bNeurobiology of Aging, _c2011
300			_a32(4):631-645.
500			_aFormato Vancouver: Pérez-Rial S, García-Gutiérrez MS, Molina JA, Pérez-Nievas BG, Ledent C, Leiva C, et al. Increased vulnerability to 6-hydroxydopamine lesion and reduced development of dyskinesias in mice lacking CB1 cannabinoid receptors. Neurobiol Aging. 2011 Apr;32(4):631-45.
501			_aPMID: 19419794
504			_aContiene 95 referencias
520			_2Motor impairment, dopamine (DA) neuronal activity and proenkephalin (PENK) gene expression in the caudate-putamen (CPu) were measured in 6-OHDA-lesioned and treated (L-DOPA+benserazide) CB1 KO and WT mice. A lesion induced by 6-OHDA produced more severe motor deterioration in CB1 KO mice accompanied by more loss of DA neurons and increased PENK gene expression in the CPu. Oxidative/nitrosative and neuroinflammatory parameters were estimated in the CPu and cingulate cortex (Cg). CB1 KO mice exhibited higher MDA levels and iNOS protein expression in the CPu and Cg compared to WT mice. Treatment with L-DOPA+benserazide (12 weeks) resulted in less severe dyskinesias in CB1 KO than in WT mice. The results revealed that the lack of cannabinoid CB1 receptors increased the severity of motor impairment and DA lesion, and reduced L-DOPA-induced dyskinesias. These results suggest that activation of CB1 receptors offers neuroprotection against dopaminergic lesion and the development of L-DOPA-induced dyskinesias.
710			_9267 _aServicio de Neurología-Neurofisiología
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/5/pc5473.pdf _ySolicitar documento
942			_n0 _2ddc _cART
999			_c5473 _d5473