Ramirez-Castillejo Carmen, Nacher Juan, Molowny Asuncion, Ponsoda Xavier, Lopez-Garcia Carlos
Neurobiologia, Biologia Celular, Facultad de Ciencias Biologicas, Universidad de Valencia, 46100 Burjassot, Spain.
J Comp Neurol. 2002 Nov 11;453(2):145-56. doi: 10.1002/cne.10390.
The lizard medial cortex, a region homologous to the mammalian dentate gyrus, shows postnatal neurogenesis and the surprising ability to replace its neurons after being lesioned specifically with the neurotoxin 3-acetylpyridine. As the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) is expressed during neuronal migration and differentiation, we have studied its distribution in adult lizards and also during the lesion-regeneration process. In the medial cortex of control animals, many labeled fusiform somata, presumably corresponding to migratory neuroblasts, appeared in the inner plexiform layer. There were also scattered immunoreactive granule neurons in the cell layer. Double immunocytochemistry with 5'-bromodeoxyuridine revealed that some of the PSA-NCAM-expressing cells in the inner plexiform and cell layers were generated recently. PSA-NCAM immunoreactivity was also present in the dorsomedial, dorsal, and lateral cortices, as well as in the dorsal ventricular ridge, the nucleus accumbens, and the nucleus sphericus. Twelve hours after the injection of 3-acetylpyridine, some medial cortex granule neurons appeared degenerated, although some of them still expressed PSA-NCAM. One to 2 days after the injection, most granule neurons appeared degenerated and no PSA-NCAM immunoreactivity was detected in the medial cortex cell layer. Four to 7 days after treatment, abundant labeled fusiform cells populated the inner plexiform layer and some immunoreactive somata were seen in the cell layer. Fifteen to 30 days after the neurotoxin injection, the number of PSA-NCAM expressing granule neurons augmented considerably and the level was still above control levels in lizards that survived 42 days. Our results show for the first time the expression of PSA-NCAM in a reptile brain, where it appears to participate in the migration and differentiation of granule neurons during adult neurogenesis and regeneration.
蜥蜴的内侧皮质是与哺乳动物齿状回同源的区域,具有出生后神经发生的现象,并且在被神经毒素3-乙酰吡啶特异性损伤后,展现出令人惊讶的神经元替代能力。由于神经细胞黏附分子的多唾液酸化形式(PSA-NCAM)在神经元迁移和分化过程中表达,我们研究了它在成年蜥蜴以及损伤-再生过程中的分布。在对照动物的内侧皮质中,许多标记为梭形的胞体出现在内丛状层,推测它们对应迁移的成神经细胞。细胞层中也有散在的免疫反应性颗粒神经元。用5'-溴脱氧尿苷进行双重免疫细胞化学显示,内丛状层和细胞层中一些表达PSA-NCAM的细胞是最近产生的。PSA-NCAM免疫反应性也存在于背内侧、背侧和外侧皮质,以及背侧室嵴、伏隔核和球形核中。注射3-乙酰吡啶12小时后,一些内侧皮质颗粒神经元出现退化,尽管其中一些仍表达PSA-NCAM。注射后1至2天,大多数颗粒神经元出现退化,在内侧皮质细胞层未检测到PSA-NCAM免疫反应性。治疗后4至7天,大量标记的梭形细胞聚集在内丛状层,细胞层中可见一些免疫反应性胞体。神经毒素注射后15至30天,表达PSA-NCAM的颗粒神经元数量显著增加,在存活42天的蜥蜴中,该水平仍高于对照水平。我们的结果首次显示了PSA-NCAM在爬行动物大脑中的表达,它似乎在成年神经发生和再生过程中参与颗粒神经元的迁移和分化。