Wofchuk S T, Rodnight R
Departmento de Bioquímica, Instituto de Biociências UFRGS, Porto Alegre, RS Brazil.
Brain Res Dev Brain Res. 1995 Apr 18;85(2):181-6. doi: 10.1016/0165-3806(94)00208-h.
We studied the effect of external Ca2+ on the incorporation of [32P]phosphate into the astrocytic marker protein, glial fibrillary acidic protein (GFAP), in hippocampal slices from rats in the postnatal age range 12-16 days to +60 days (P12-P16 to +P60). At age P12-P16 the presence of Ca2+ in the incubation medium inhibited the incorporation of 32P into GFAP; this inhibition declined to near zero by P21 and subsequently 32P-incorporation became progressively more dependent on Ca2+ until by P60 no GFAP phosphorylation was observed in the absence of Ca2+. With tissue from immature rats inhibition of 32P-incorporation into GFAP started at a medium concentration of 7.5 microM Ca2+, reached 50% at 100 microM and then remained constant up to 1 mM; with adults maximal phosphorylation required 1 mM Ca2+ in the medium. The inorganic Ca(2+)-channel blockers, Co2+ and Ni2+, and a high concentration of the L-type blocker, nifedipine, reversed the effects of external Ca2+ on GFAP phosphorylation. The results suggest a late developmental change in the compartmental disposition of Ca2+ in astrocytes.
我们研究了细胞外钙离子(Ca2+)对出生后12至16天到60天(P12 - P16至+P60)大鼠海马切片中[32P]磷酸盐掺入星形胶质细胞标志物蛋白——胶质纤维酸性蛋白(GFAP)的影响。在P12 - P16时,孵育培养基中Ca2+的存在抑制了32P掺入GFAP;到P21时这种抑制作用降至接近零,随后32P掺入逐渐变得更依赖Ca2+,直到P60时,在无Ca2+的情况下未观察到GFAP磷酸化。对于未成熟大鼠的组织,32P掺入GFAP的抑制作用在Ca2+浓度为7.5微摩尔时开始,在100微摩尔时达到50%,然后在1毫摩尔时保持恒定;对于成年大鼠,培养基中最大磷酸化需要1毫摩尔Ca2+。无机Ca(2+)通道阻滞剂Co2+和Ni2+以及高浓度的L型阻滞剂硝苯地平可逆转细胞外Ca2+对GFAP磷酸化的影响。结果表明星形胶质细胞中Ca2+的区室分布存在后期发育变化。