Effects of alcohol and nicotine on developing olfactory bulb: Loss of mitral cells and alterations in neurotransmitter levels
Effects of alcohol and nicotine on developing olfactory bulb: Loss of mitral cells and alterations in neurotransmitter levels
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DOI：
10.1111/j.1530-0277.1999.tb04019.x
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发表时间：
1999-01-01
影响因子：
3.2
通讯作者：
West, JR
中科院分区：
文献类型：
--
作者：
Chen, WJA;Parnell, SE;West, JR
我们实验室之前的研究表明，大脑快速生长期间接触[乙醇 (EtOH)] 不利于嗅球发育。这项研究通过检查乙醇、尼古丁 (NIC) 以及这些药物的组合 (EtOH/NIC) 对新生大鼠嗅球二尖瓣细胞数量以及各种主要神经递质水平的影响，扩展了这些发现。本研究中使用了人工饲养范例。这些人工饲养的幼崽在出生后第 4 天至第 9 天被给予 4 g/kg/天的 EtOH 和/或 6 mg/kg/天的 NIC，但在急性神经化学研究中，幼崽仅在 PD 9 天接受治疗。包括人工饲养的胃造口对照组（GC）和哺乳对照组。 EtOH 组和 NIC 组的二尖瓣细胞平均总数较 GC 组显着减少，左主嗅球体积也显着减少。任何组间二尖瓣细胞密度均无差异。至于神经化学数据，重复暴露方案中任何组之间的神经递质水平没有差异。然而，急性暴露后发生了变化（仅在 PC 9 上暴露）。仅在暴露于 NIC 后，血清素和 GABA 水平才会显着增加。然而，与对照组相比，所有三个药物治疗组在急性暴露后去甲肾上腺素水平均显着降低。除 GC 对照组外，急性暴露于 EtOH、NIC 或 EtOH/NIC 后，多巴胺水平检测结果不一致。总的来说，这些发现表明，在大脑生长突增期间单独接触 EtOH 或 NIC 会导致嗅球发育缺陷，这表明 EtOH 和 NIC 都是神经致畸剂。此外，这项研究证明了 NIC 能够对抗（保护）乙醇诱导的嗅球发育中二尖瓣细胞损失。
Previous research from our laboratory has shown that [ethanol (EtOH)] exposure during the brain growth spurt is detrimental to olfactory bulb development This study extends those findings by examining the effects of EtOH, nicotine (NIC), and the combination of these drugs (EtOH/NIC) on olfactory bulb mitral cell numbers, as well as on various major neurotransmitter levels in neonatal rats. An artificial rearing paradigm was used in the present studies. These artificially reared pups were given 4 g/kg/day of EtOH and/or 6 mg/kg/ day of NIC on postnatal day (PD) 4 to PD 9, except in the case of the acute neurochemistry study, in which the pups received treatment on PD 9 only. An artificially reared gastrostomy control group (GC) and a suckle control group were included. The mean total numbers of mitral cells in the EtOH and NIC groups were significantly reduced from that of the GC, as well as the volume of the left main olfactory bulb. There was no difference among any of the groups in mitral cell density. As for neurochemistry data, there was no difference in neurotransmitter levels among any of the groups in the repeat exposure regimen. There were, however, changes after the acute exposure (exposure on PC 9 only). Both serotonin and GABA levels were significantly increased only after NIC exposure. However, norepinephrine levels were significantly decreased after acute exposure in all three drug treatment groups, compared with that of the control group. Except for the GC control group, dopamine levels were not detected consistently after acute exposure to EtOH, NIC, or EtOH/ NIC. Collectively, these findings demonstrate that exposure to EtOH or NIC individually during the brain growth spurt results in developmental deficits in the olfactory bulb, suggesting that both EtOH and NIC are neuroteratogens. Furthermore, this study demonstrated the capability of NIC to antagonize (protect) EtOH-induced mitral cell loss in the developing olfactory bulb.