Dose- and age-dependent effects of prenatal ethanol exposure on hippocampal metabotropic-glutamate receptor-stimulated phosphoinositide hydrolysis.
Dose- and age-dependent effects of prenatal ethanol exposure on hippocampal metabotropic-glutamate receptor-stimulated phosphoinositide hydrolysis.
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产前乙醇暴露对海马代谢型谷氨酸受体刺激的磷酸肌醇水解的剂量和年龄依赖性影响。
DOI：
10.1111/j.1530-0277.1993.tb00859.x
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Savage,DD
中科院分区：
文献类型：
--
作者：
Queen,SA;Sanchez,CF;Lopez,SR;Paxton,LL;Savage,DD
产前乙醇暴露降低了N-甲基-D-天冬氨酸（NMDA）受体激动剂结合位点的密度，并降低了45日龄大鼠后代海马变形中引起长时程增强（LTP）的能力。我们假设产前乙醇暴露也会减少代谢型谷氨酸受体（mGluR）激活的磷酸肌醇水解。在整个妊娠期间，Sprague-道利大鼠母鼠喂食含3.35%（v/v）乙醇或5.0%乙醇的流质饲料。对照组成对喂食等热量匹配的0%乙醇液体饲料或实验室饲料，自由采食。(1S 3R）-1-氨基环戊烷-1，3-二羧酸（trans-ACPD）通过激活mGluR而刺激摄入3.35%乙醇液体饲料的子代中肌醇-1-磷酸（IP 1）的积累，与对照组相比没有差异。此外，与对照组相比，trans-ACPD刺激的5.0%乙醇饮食组10至13日龄后代中的IP 1积累没有差异。然而，与对照组相比，在饲喂5.0%乙醇液体饲料的母鼠的56 - 82日龄后代中，反式ACPD刺激的IP 1蓄积显著降低。相反，氨甲酰胆碱通过激活毒蕈碱胆碱能受体介导的IP 1积累，不受母亲摄入乙醇液体饮食的影响。这些结果表明，产前乙醇暴露对海马对反式ACPD激活的磷酸肌醇水解的反应性具有剂量和年龄依赖性影响。此外，3.35%乙醇饮食改变海马NMDA受体而不改变mGluR反应的能力表明，海马谷氨酸受体亚型对子宫内乙醇暴露的影响具有不同的敏感性。最近的研究表明，mGluRs的激活促进NMDA受体依赖性LTP。因此，通过消耗5.0%乙醇液体饮食获得的较高血液乙醇浓度对与LTP相关的额外谷氨酸受体机制产生不利影响。这种额外的影响可能会导致更大的影响，产前乙醇暴露对LTP比发生时，NMDA受体功能单独受到影响的母亲消费更温和的量的乙醇。
Prenatal ethanol exposure reduces the density of theN‐methyl‐D‐aspartate (NMDA) receptor agonist binding sites and decreases the capacity to elicit long‐term potentiation (LTP) in hippocampal tormation of 45‐day‐old rat offspring. We hypothesized that prenatal ethanol exposure would reduce metabotropic‐glutamate receptor (mGluR)‐activated phosphoinositide hydrolysis also. Sprague‐Dawley rat dams were fed a liquid diet containing either 3.35% (v/v) ethanol or 5.0% ethanol throughout gestation. Control groups were pair‐fed either isocalorically matched 0% ethanol liquid diets or lab chow ad libitum. (1S,3R)‐1‐aminocyclopentane‐1,3‐dicarboxylic acid (trans‐ACPD) stimulated inositol‐1‐phosphate (IP1) accumulation via activation of the mGluR in offspring whose mothers consumed the 3.35% ethanol liquid diet was not different compared with the control groups. Furthermore, trans‐ACPD stimulated IP1accumulation in 10 to 13‐day‐old offspring of the 5.0% ethanol diet group was not different compared with the control groups. However, trans‐ACPD stimulated IP1accumulation was reduced significantly in 56‐ to 82‐day‐old offspring of dams fed the 5.0% ethanol liquid diet compared with the control groups. In contrast, bethanechol stimulated IP1accumulation, mediated via activation of muscarinic cholinergic receptors, was not affected by maternal consumption of either ethanol liquid diet.These results suggest both dose‐ and age‐dependent effects of prenatal ethanol exposure on hippocampal responsiveness to trans‐ACPD‐activated phosphoinositide hydrolysis. Furthermore, the ability of the 3.35% ethanol diet to alter hippocampal NMDA receptors without altering the mGluR response suggests a differential sensitivity to the effects of ethanol exposure in utero among hippocampal glutamate receptor subtypes. Recent studies indicate that activation of mGluRs facilitates NMDA receptor‐dependent LTP. Thus, higher blood ethanol concentrations achieved by consumption of the 5.0% ethanol liquid diet adversely affects an additional glutamate receptor mechanism associated with LTP. This additional effect may lead to an even greater impact of prenatal ethanol exposure on LTP than occurs when NMDA receptor function alone is affected by maternal consumption of more moderate quantities of ethanol.
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作者：
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影响因子：
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作者：
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DOI：
10.1016/s0006-291x(88)81060-x
发表时间：
1988-08-30
影响因子：
3.1
作者：
CHARNESS, ME;QUERIMIT, LA;HENTELEFF, M
通讯作者：
HENTELEFF, M