Postnatal development of zinc-rich terminal fields in the brain of the rat

被引:35
作者
Valente, T [1 ]
Auladell, C [1 ]
Pérez-Clausell, J [1 ]
机构
[1] Univ Barcelona, Dept Cellular Biol, E-08071 Barcelona, Spain
关键词
development; histochemistry; mammals; neuroanatomy; selenium; trace elements; zinc;
D O I
10.1006/exnr.2002.7876
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The appearance and distribution of zinc-rich terminal fields in the rat forebrain was analyzed at 12 stages of postnatal development using the selenium method. Zinc stain was detected in neonates in piriform, cingulate, and motor cortices, septal area, and hippocampal formation. In the neocortex, a laminar pattern appeared progressively following an inside-out gradient: layer VI at postnatal day 0 (PO), layer V at P1, layers Va and Vb at P5, layer II-III at P9, and layer IV at P12. In the hippocampal formation the layered pattern in the dentate molecular layer appeared at P1-P3, and in the hilus and mossy fibers the stain was observed at P5. Patches in the caudate-putamen were sharply delimited at P1-P3. At these ages, staining was observed in the amygdaloid complex. In the thalamic and hypothalamic nuclei, stain appeared at P5-P7. Thus, a general increase in vesicular zinc over different telencephalic areas was determined until P15-P21, which was followed by a slight decrease thereafter (at P41). The increased stain in zinc-rich terminal fields is consistent with the development of telencephalic circuits. The rise in zinc might be relevant for the establishment and maturation of these circuits. On the other hand, the decrease in staining for zinc at later stages might be due to methodological problems but it might also reflect pruning of supernumerary connections and programmed cell death affecting zinc-rich circuits. (C) 2002 Elsevier Science (USA).
引用
收藏
页码:215 / 229
页数:15
相关论文
共 79 条
[21]   A SILVER METHOD FOR COUNTERSTAINING PLASTIC EMBEDDED TISSUE [J].
DANSCHER, G .
STAIN TECHNOLOGY, 1983, 58 (06) :365-372
[22]   ALTERATIONS IN THE POSTNATAL-DEVELOPMENT OF THE CEREBELLAR CORTEX DUE TO ZINC-DEFICIENCY .1. IMPAIRED ACQUISITION OF GRANULE CELLS [J].
DVERGSTEN, CL ;
FOSMIRE, GJ ;
OLLERICH, DA ;
SANDSTEAD, HH .
BRAIN RESEARCH, 1983, 271 (02) :217-226
[23]   HISTOCHEMICAL-LOCALIZATION OF SYNAPTIC ZINC IN THE DEVELOPING CAT VISUAL-CORTEX [J].
DYCK, R ;
BEAULIEU, C ;
CYNADER, M .
JOURNAL OF COMPARATIVE NEUROLOGY, 1993, 329 (01) :53-67
[24]  
FINK ROBERT P., 1967, BRAIN RES, V4, P369, DOI 10.1016/0006-8993(67)90166-7
[25]  
Frederickson C. J., 1994, Biological Signals, V3, P127
[26]   ZINC-CONTAINING 7S-NGF COMPLEX - EVIDENCE FROM ZINC HISTOCHEMISTRY FOR LOCALIZATION IN SALIVARY SECRETORY GRANULES [J].
FREDERICKSON, CJ ;
PEREZCLAUSELL, J ;
DANSCHER, G .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1987, 35 (05) :579-583
[27]   Importance of zinc in the central nervous system: The zinc-containing neuron [J].
Frederickson, CJ ;
Suh, SW ;
Silva, D ;
Frederickson, CJ ;
Thompson, RB .
JOURNAL OF NUTRITION, 2000, 130 (05) :1471S-1483S
[28]   A QUINOLINE FLUORESCENCE METHOD FOR VISUALIZING AND ASSAYING THE HISTOCHEMICALLY REACTIVE ZINC (BOUTON ZINC) IN THE BRAIN [J].
FREDERICKSON, CJ ;
KASARSKIS, EJ ;
RINGO, D ;
FREDERICKSON, RE .
JOURNAL OF NEUROSCIENCE METHODS, 1987, 20 (02) :91-103
[29]   TRANSLOCATION OF ZINC MAY CONTRIBUTE TO SEIZURE-INDUCED DEATH OF NEURONS [J].
FREDERICKSON, CJ ;
HERNANDEZ, MD ;
MCGINTY, JF .
BRAIN RESEARCH, 1989, 480 (1-2) :317-321
[30]  
FREDERICKSON CJ, 1991, SOC NEUR ABSTR, V17