Properties of LTD and LTP of retinocollicular synaptic transmission in the developing rat superior colliculus

被引:33
作者
Lo, FS
Mize, RR [1 ]
机构
[1] Louisiana State Univ, Hlth Sci Ctr, Dept Cell Biol & Anat, New Orleans, LA 70112 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Dept Ophthalmol, New Orleans, LA 70112 USA
[3] Louisiana State Univ, Hlth Sci Ctr, Neurosci Ctr Excellence, New Orleans, LA 70112 USA
关键词
calcium channels; NMDA; synaptic plasticity; visual system;
D O I
10.1046/j.1460-9568.2002.01979.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The developing retinocollicular pathway undergoes synaptic refinement in order to form the precise retinotopic pattern seen in adults. To study the mechanisms which underlie refinement, we investigated long-term changes in retinocollicular transmission in rats aged P0-P25. Field potentials (FPs) in the superior colliculus (SC) were evoked by stimulation of optic tract fibers in an in vitro isolated brainstem preparation. High intensity stimulation induced long-term depression (LTD) in the SC after both low (1000 stimuli at 1 Hz) and higher (1000 stimuli at 50 Hz) frequency stimulation. The induction of LTD was independent of activation of NMDA and GABA(A) receptors, because d-APV (100 muM) and bicuculline (10 muM) did not block LTD. Induction of LTD was dependent upon activation of l-type Ca2+ channels as 10 muM nitrendipine, an l-type Ca2+ channel blocker, significantly decreased the magnitude of LTD. LTD was down-regulated during development. LTD magnitude was greatest in rats aged P0-P9 and significantly less in rats aged P10-P25. Long-term potentiation (LTP) was induced by low intensity stimulation and only after high frequency tetanus (1000 stimuli at 50 Hz). LTP was NMDA receptor dependent because d-APV (100 muM) completely abolished it. LTP induction was also blocked by the l-type Ca2+ channel blocker nitrendipine. The magnitude of LTP first increased with age, being significantly greater at P7-P13 than at P0-3 and then decreased at P23-25. In summary, both LTD and LTP are present during retinocollicular pathway refinement, but have different transmitter and ionic mechanisms and time courses of expression.
引用
收藏
页码:1421 / 1432
页数:12
相关论文
共 73 条
[1]   THE ROLE OF NMDA RECEPTORS IN LONG-TERM POTENTIATION (LTP) AND DEPRESSION (LTD) IN RAT VISUAL-CORTEX [J].
ARONIADOU, VA ;
TEYLER, TJ .
BRAIN RESEARCH, 1991, 562 (01) :136-143
[2]   LONG-TERM DEPRESSION OF EXCITATORY SYNAPTIC TRANSMISSION AND ITS RELATIONSHIP TO LONG-TERM POTENTIATION [J].
ARTOLA, A ;
SINGER, W .
TRENDS IN NEUROSCIENCES, 1993, 16 (11) :480-487
[3]   DEVELOPMENTAL SHIFT FROM LONG-TERM DEPRESSION TO LONG-TERM POTENTIATION AT THE MOSSY FIBER SYNAPSES IN THE RAT HIPPOCAMPUS [J].
BATTISTIN, T ;
CHERUBINI, E .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1994, 6 (11) :1750-1755
[4]   LONG-TERM POTENTIATION IN SLICES OF KITTEN VISUAL-CORTEX AND THE EFFECTS OF NMDA RECEPTOR BLOCKADE [J].
BEAR, MF ;
PRESS, WA ;
CONNORS, BW .
JOURNAL OF NEUROPHYSIOLOGY, 1992, 67 (04) :841-851
[5]   A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS [J].
BLISS, TVP ;
COLLINGRIDGE, GL .
NATURE, 1993, 361 (6407) :31-39
[6]   POSTSYNAPTIC INDUCTION AND PRESYNAPTIC EXPRESSION OF HIPPOCAMPAL LONG-TERM DEPRESSION [J].
BOLSHAKOV, VY ;
SIEGELBAUM, SA .
SCIENCE, 1994, 264 (5162) :1148-1152
[7]   INTRACELLULAR INJECTION OF CA2+ CHELATORS BLOCKS INDUCTION OF LONG-TERM DEPRESSION IN RAT VISUAL-CORTEX [J].
BROCHER, S ;
ARTOLA, A ;
SINGER, W .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (01) :123-127
[8]   Glutamate-triggered events inducing corticostriatal long-term depression [J].
Calabresi, P ;
Centonze, D ;
Gubellini, P ;
Marfia, GA ;
Bernardi, G .
JOURNAL OF NEUROSCIENCE, 1999, 19 (14) :6102-6110
[9]  
CALABRESI P, 1992, J NEUROSCI, V12, P4224
[10]   Decreased probability of neurotransmitter release underlies striatal long-term depression and postnatal development of corticostriatal synapses [J].
Choi, S ;
Lovinger, DM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (06) :2665-2670