A dorsal root ganglia cell line derived from trisomy 16 fetal mice, a model for Down syndrome

被引:5
作者
Allen, DD
Cárdenas, AM
Arriagada, C
Bennett, LB
García, CJ
Caviedes, R
Rapoport, SI
Caviedes, P
机构
[1] Univ Chile, Fac Med, ICBM, Program Mol & Clin Pharmacol, Santiago 7, Chile
[2] Texas Tech Univ, Hlth Sci Ctr, Dept Pharmaceut Sci, Amarillo, TX USA
[3] Univ Valparaiso, Sch Med, Pharmacol Lab, Valparaiso, Chile
[4] Univ Valparaiso, Valparaiso Ctr Cellular & Mol Neurosci, Valparaiso, Chile
[5] Univ Chile, Fac Med, ICBM, Morphol Program, Santiago 7, Chile
[6] NIA, Sect Brain Physiol & Metab, NIH, Bethesda, MD 20892 USA
[7] Sansum Med Res Inst, Santa Barbara, CA USA
关键词
calcium signaling; choline uptake; Down syndrome; murine trisomy 16;
D O I
10.1097/00001756-200203250-00027
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We have established two immortalized cell lines from dorsal root ganglia of normal (G4b) and trisomy 16 mice (GTI), a model for Down syndrome. By immunohistochemistry, both cell lines exhibit neuronal traits and lack glial markers. GTI cells exhibited greater [H-3]choline uptake than G4b cells. K+ and nicotine-mediated acetylcholine release was greater in GTI cells. Basal intracellular Ca2+ concentration ([Ca2+](i)) was significantly lower in GTI cells. More GTI cells responded to neurotransmitters with a transient [Ca2+](i) increase compared to G4b cells, but both cell types showed similar amplitudes of [Ca2+](i) responses. The results show that both cell lines retain neuronal characteristics and respond to specific neurotransmitter stimuli. Altered GTI cell responses could be related to neuronal pathophysiology in Down's syndrome.
引用
收藏
页码:491 / 496
页数:6
相关论文
共 25 条
[1]
Impaired cholinergic function in cell lines derived from the cerebral cortex of normal and trisomy 16 mice [J].
Allen, DD ;
Martin, J ;
Arriagada, C ;
Cárdenas, AM ;
Rapoport, SI ;
Caviedes, R ;
Caviedes, P .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2000, 12 (09) :3259-3264
[2]
Excessive glutamate receptor 1 immunoreactivity in adult down syndrome brains [J].
Arai, Y ;
Mizuguchi, M ;
Takashima, S .
PEDIATRIC NEUROLOGY, 1996, 15 (03) :203-206
[3]
NEUROPHYSIOLOGICAL ABNORMALITIES IN CULTURED DORSAL-ROOT GANGLION NEURONS FROM THE TRISOMY-16 MOUSE FETUS, A MODEL FOR DOWN SYNDROME [J].
AULT, B ;
CAVIEDES, P ;
RAPOPORT, SI .
BRAIN RESEARCH, 1989, 485 (01) :165-170
[4]
Calcium signals in cell lines derived from the cerebral cortex of normal and trisomy 16 mice [J].
Cárdenas, AM ;
Rodríguez, MP ;
Cortés, MP ;
Alvarez, RM ;
Wei, WZ ;
Rapoport, SI ;
Shimahara, T ;
Caviedes, R ;
Caviedes, P .
NEUROREPORT, 1999, 10 (02) :363-369
[5]
THE ROLE OF ALTERED SODIUM CURRENTS IN ACTION-POTENTIAL ABNORMALITIES OF CULTURED DORSAL-ROOT GANGLION NEURONS FROM TRISOMY-21 (DOWN SYNDROME) HUMAN FETUSES [J].
CAVIEDES, P ;
AULT, B ;
RAPOPORT, SI .
BRAIN RESEARCH, 1990, 510 (02) :229-236
[6]
CALCIUM FLUXES, ION CURRENTS AND DIHYDROPYRIDINE RECEPTORS IN A NEW IMMORTAL CELL-LINE FROM RAT-HEART MUSCLE [J].
CAVIEDES, P ;
OLIVARES, E ;
SALAS, K ;
CAVIEDES, R ;
JAIMOVICH, E .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1993, 25 (07) :829-845
[7]
MOUSE TRISOMY-16 - AN ANIMAL-MODEL OF HUMAN TRISOMY-21 (DOWN SYNDROME) [J].
EPSTEIN, CJ ;
COX, DR ;
EPSTEIN, LB .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1985, 450 (JUN) :157-168
[8]
EPSTEIN CJ, 1986, NEUROBIOLOGY DOWN SY, P1
[9]
REGIONAL ALTERATION OF CHOLINERGIC FUNCTION IN CENTRAL NEURONS OF TRISOMY-16 MOUSE FETUSES, AN ANIMAL-MODEL OF HUMAN TRISOMY-21 (DOWN-SYNDROME) [J].
FIEDLER, JL ;
EPSTEIN, CJ ;
RAPOPORT, SI ;
CAVIEDES, R ;
CAVIEDES, P .
BRAIN RESEARCH, 1994, 658 (1-2) :27-32
[10]
Multiple calcium pathways induce the expression of SNAP-25 protein in chromaffin cells [J].
García-Palomero, E ;
Montiel, C ;
Herrero, CJ ;
García, AG ;
Alvarez, RM ;
Arnalich, FM ;
Renart, J ;
Lara, H ;
Cárdenas, AM .
JOURNAL OF NEUROCHEMISTRY, 2000, 74 (03) :1049-1058