产前热应激对仔鼠生殖腺GABA能神经元受体发育的影响

Impact of prenatal heat stress on the development of GABA receptors in the genital gland of newborn mice

12只13d孕龄的母鼠随机被分为2组,每组6只,以探讨产前热应激对新生仔鼠生殖腺GABA能神经元受体发育的影响。试验组(热应激组)孕鼠置于42℃±0.31℃、相对湿度为36.7%±1.42%的热应激箱中至肛温达到41℃;对照组孕鼠置于常温对照箱里。之后放回笼中分笼饲养。在仔鼠出生后第1、3、5、7天分别剖取睾丸和卵巢进行Zamboni’s固定,常规石蜡切片及SABC免疫组织化学染色,在光学显微镜下用MiPrd软件检测各组织区域GABA受体免疫细胞阳性率和阳性灰度。结果显示,热应激组的GABAA受体免疫细胞阳性率与对照组无显著差异,但在新生1d的生殖腺区阳性灰度极显著增加;热应激组GABAB受体免疫细胞阳性率只在7d睾丸和5d卵巢显著增加,但其阳性灰度除7d卵巢外均显著增加。结果表明,产前热应激可能通过代偿机制显著增加仔鼠生殖腺GABA受体在细胞膜的密度,从而增强抑制性神经递质在发育中的作用,进一步阻碍新生仔鼠生殖腺的正常发育。

12 pregnant mice of 13 gestational days were randomly divided into 2 groups,each with 6 mice,to study the impact of prenatal heat stress on the development of GABA receptors in the genital gland of newborn mice.The pregnant mice in heat stress group were fastened in a cabin（ambient temperature 42 ℃±0.31 ℃,relative humidity of 34.5%±1.35%） until the rectal temperature reached 41 ℃,while those in the control group were placed in a cabin of room temperature.Then these mice were fed in separate cages.On day 1,3,5 and 7 post-birth,the testicle and the ovary of each mouse were obtained and fixed in Zambon＇s solution,and treated with the conventional paraffin sections and examined by immunohistochemistry technique,and the percentage of immunoreactive cells and the average value of gray-scale were counted with optical microscope using MiPrd software,finally the data were recorded and analyzed.In result,the percentage of GABAA receptor immunoreactive cells had no significant difference,whereas the average value of gray-scale increased significantly in the genital gland of 1 d newborn mice.Meanwhile,the percentage of GABAB receptor immunoreactive cells significantly increased only in 7 d testicle and 5 d ovary,while the average value of gray-scale had significant increase except in 7 d ovary.In conclusion,prenatal heat stress may significantly increase the GABA receptor density in the gonad neurons membrane through compensatory mechanisms,thus enhancing the inhibitory neurotransmitter＇s role in the growth of mice and further impeding the normal development in the genital gland of newborn mice.