Departamento de Ciências Fisiológicas, Instituto de Biologia Roberto Alcântara Gomes, Centro Biomédico, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Neuroscience. 2010 Apr 28;167(1):163-73. doi: 10.1016/j.neuroscience.2010.01.060. Epub 2010 Feb 4.
We have recently identified hippocampal cell death and reduced neuronal and glial cells densities during adolescent nicotine and ethanol exposures and outcomes reduced in severity when nicotine and ethanol are co-administered during this developmental period. In the present study, we investigated the effects of adolescent nicotine and/or ethanol withdrawal on the following regions of the hippocampus: Granular layer of the Dentate Gyrus (GrDG), Molecular layer (Mol), CA1, CA2 and CA3. From the 30th to the 45th postnatal day (PN30-PN45), C57BL/6 male and female mice were exposed to nicotine free base (NIC) and/or ethanol (ETOH). Four groups were analyzed: (1) concomitant NIC (50 microg/ml in 2% saccharin to drink) and ETOH (25%, 2 g/kg i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) vehicle. We evaluated cell degeneration (TUNEL assay), neuronal and glial densities (optical Disector) and region thicknesses two (PN47) and five (PN50) days post-exposure. On PN47, there were increases in the number of TUNEL+ cells in most hippocampal regions of both ETOH and NIC groups. In the NIC+ETOH group there were less severe effects. These results were paralleled by reductions in neuronal and glial cells densities for all treatment groups. In contrast, on PN50, ethanol and/or nicotine withdrawal were associated with compensatory reductions in TUNEL+ cells in all hippocampal regions. These results were paralleled by a reversal of effects on neuronal and glial densities so that there were no longer differences between groups. There were no effects on region thicknesses. These results suggest that deleterious effects of nicotine and/or ethanol are reversed during prolonged withdrawal.
我们最近发现，在青春期暴露于尼古丁和乙醇期间会导致海马体细胞死亡和神经元及神经胶质细胞密度降低，而在这一发育阶段同时给予尼古丁和乙醇时，其结果的严重程度会降低。在本研究中，我们研究了青春期尼古丁和/或乙醇戒断对海马体以下区域的影响：齿状回颗粒层（GrDG）、分子层（Mol）、CA1、CA2 和 CA3。从第 30 到第 45 天（PN30-PN45），C57BL/6 雄性和雌性小鼠暴露于无尼古丁碱（NIC）和/或乙醇（ETOH）中。分析了四个组：（1）同时暴露于 NIC（2%糖精中的 50 μg/ml 用于饮用）和 ETOH（25%，每隔一天 2 g/kg 腹腔注射）；（2）NIC 暴露；（3）ETOH 暴露；（4）载体。我们评估了细胞变性（TUNEL 测定）、神经元和神经胶质细胞密度（光学割面计）以及暴露后两天（PN47）和五天（PN50）的区域厚度。在 PN47 时，大多数海马体区域的 ETOH 和 NIC 组的 TUNEL+细胞数量增加。在 NIC+ETOH 组中，效应较轻。这些结果与所有治疗组神经元和神经胶质细胞密度降低相平行。相比之下，在 PN50 时，乙醇和/或尼古丁戒断与所有海马体区域的 TUNEL+细胞代偿性减少有关。这些结果与神经元和神经胶质细胞密度的逆转效应平行，因此组间不再存在差异。区域厚度没有变化。这些结果表明，尼古丁和/或乙醇的有害作用在长时间戒断期间会逆转。
