Mature intrastriatal striatal grafts revert the changes in the expression of pallidal and thalamic α1, α2 and β2/3 GABAA receptor subunit induced by ibotenic acid lesions in the rat striatum

被引:4
作者
Caruncho, HJ [1 ]
Rodríguez-Pallares, J [1 ]
Guerra, MJ [1 ]
Labandeira-García, JL [1 ]
机构
[1] Univ Santiago, Fac Med, Dept Morphol Sci, Sch Med, E-15705 Santiago De Compostela, Galicia, Spain
来源
MOLECULAR BRAIN RESEARCH | 1998年 / 57卷 / 02期
关键词
Huntington's disease; GABAergic transmission; basal ganglia;
D O I
10.1016/S0169-328X(98)00101-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A between-side comparison of GABA(A) receptor subunit expression levels in the globus pallidus and anterior-pole motor thalamic nuclei of rats with an ibotenate lesion of the striatum, and rats receiving a fetal striatal graft in the lesioned area was made by using immunocytochemistry with subunit-specific antibodies, at different times post-lesion or different times post-grafting. At 10 days post-lesion, there was already an increase in the labeling of the alpha 1- and beta 2/3-subunits in the globus pallidus, entopeduncular nucleus and ventrolateral nucleus ipsilateral to the lesion when compared with the contralateral side, while there were no significant changes at the level of the ventromedial nucleus. Labeling of the alpha 2-subunit showed a clear increase in the entopeduncular nucleus compared with the contralateral side at 10 days post-lesion. Similar changes were also observed for the different subunits studied at 30 and 120 days after lesioning. Rats with 20-day old transplants of fetal striatal neurons that were implanted in the ibotenate lesioned striatum at 10 days post-lesioning, continued to show changes in the expression of GABA(A) receptor subunits, albeit at a lower level than those of ibotenate lesioned rats at similar age post-lesion. However, when examining rats with 70-day old transplants, the ibotenate-lesion induced between-side changes were almost completely compensated. These findings suggest a correlation between the maturation of the grafts and their capability to function in reestablishing neuronal circuits as shown by the reduction of changes in GABAergic transmission induced by ibotenate lesions, as indicated by the reversal of changes in GABA(A) receptor subunit in several areas of the basal ganglia circuit. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:301 / 309
页数:9
相关论文
共 44 条
[1]   PREFERENTIAL LOSS OF STRIATO-EXTERNAL PALLIDAL PROJECTION NEURONS IN PRESYMPTOMATIC HUNTINGTONS-DISEASE [J].
ALBIN, RL ;
REINER, A ;
ANDERSON, KD ;
DURE, LS ;
HANDELIN, B ;
BALFOUR, R ;
WHETSELL, WO ;
PENNEY, JB ;
YOUNG, AB .
ANNALS OF NEUROLOGY, 1992, 31 (04) :425-430
[2]   THE FUNCTIONAL-ANATOMY OF BASAL GANGLIA DISORDERS [J].
ALBIN, RL ;
YOUNG, AB ;
PENNEY, JB .
TRENDS IN NEUROSCIENCES, 1989, 12 (10) :366-375
[3]   DIFFERENTIAL EXPRESSION OF THE GABA-A RECEPTOR COMPLEX IN THE DORSAL THALAMUS AND RETICULAR NUCLEUS - AN IMMUNOHISTOCHEMICAL STUDY IN THE ADULT AND DEVELOPING RAT [J].
BENTIVOGLIO, M ;
SPREAFICO, R ;
ALVAREZBOLADO, G ;
SANCHEZ, MP ;
FAIREN, A .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1991, 3 (02) :118-125
[4]   CHARACTERIZATION OF GABA RELEASE FROM INTRASTRIATAL STRIATAL TRANSPLANTS - DEPENDENCE ON HOST-DERIVED AFFERENTS [J].
CAMPBELL, K ;
KALEN, P ;
WICTORIN, K ;
LUNDBERG, C ;
MANDEL, RJ ;
BJORKLUND, A .
NEUROSCIENCE, 1993, 53 (02) :403-415
[5]   GABA(A) receptor alpha(1)-subunit-immunopositive neurons in the rat striatum [J].
Caruncho, HJ ;
Liste, I ;
Labandeira-Garcia, JL .
BRAIN RESEARCH, 1996, 722 (1-2) :185-189
[6]  
Caruncho HJ, 1996, RECEPTOR CHANNEL, V4, P85
[7]   THE DENSITY AND DISTRIBUTION OF 6 GABA(A) RECEPTOR SUBUNITS IN PRIMARY CULTURES OF RAT CEREBELLAR GRANULE CELLS [J].
CARUNCHO, HJ ;
PUIA, G ;
MOHLER, H ;
COSTA, E .
NEUROSCIENCE, 1995, 67 (03) :583-593
[8]   Time course of striatal, pallidal and thalamic alpha(1), alpha(2) and beta(2/3) GABA(A) receptor subunit changes induced by unilateral 6-OHDA lesion of the nigrostriatal pathway [J].
Caruncho, HJ ;
Liste, I ;
Rozas, G ;
LopezMartin, E ;
Guerra, MJ ;
Labandeira-Garcia, JL .
MOLECULAR BRAIN RESEARCH, 1997, 48 (02) :243-250
[9]  
CARUNCHO HJ, 1996, EUR J ANAT, V1, P43
[10]  
Chesselet MF, 1996, TRENDS NEUROSCI, V19, P417