Sucrose ingestion induces glutamate AMPA receptor phosphorylation in dorsal hippocampal neurons: Increased sucrose experience prevents this effect.
Sucrose ingestion induces glutamate AMPA receptor phosphorylation in dorsal hippocampal neurons: Increased sucrose experience prevents this effect.
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DOI：
10.1016/j.bbr.2018.07.031
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发表时间：
2019-02-01
影响因子：
2.7
通讯作者：
Parent MB
中科院分区：
文献类型：
--
作者：
Ross A;Barnett N;Faulkner A;Hannapel R;Parent MB
有证据表明，与进餐有关的记忆会影响以后的进食行为。记忆可以作为控制进食行为的强大机制，因为它提供了最近摄取的记录，可能比摄取产生的大多数生理信号持续时间更长。背侧(DHC)和腹侧海马区(VHC)神经元对记忆至关重要，我们之前已经证明，它们限制了餐后时期的能量摄入。如果DHC或VHC神经元通过需要记忆的过程来控制摄入，那么摄入应该会增加DHC和VHC在餐后期间突触可塑性所必需的事件。为了测试这一点，我们确定了摄入蔗糖溶液是否诱导了对海马突触可塑性至关重要的翻译后事件：1)丝氨酸831(PSer831)和2)丝氨酸845(PSer845)的AMPAR GluA1亚基的磷酸化。我们还研究了增加先前使用蔗糖溶液的量是否也会减弱蔗糖诱导的磷酸化，预计蔗糖溶液将减少摄取回合中涉及的助记需求。DHC和VHC膜组分的定量免疫印迹显示，摄入蔗糖增加了DHC餐后pSer831的表达，但不增加VHC的表达。增加先前的蔗糖经验可防止蔗糖诱导的DHC pSer831。摄入蔗糖对DHC和VHC中的pSer845均无影响。因此，目前的发现表明，摄入以经验依赖的方式激活了突触可塑性所需的翻译后事件，这与DHC神经元在餐后时期形成对食物的记忆的假设是一致的。
Evidence suggests that meal-related memory influences later eating behavior. Memory can serve as a powerful mechanism for controlling eating behavior because it provides a record of recent intake that likely outlasts most physiological signals generated by ingestion. Dorsal (dHC) and ventral hippocampal (vHC) neurons are critical for memory, and we demonstrated previously that they limit energy intake during the postprandial period. If dHC or vHC neurons control intake through a process that requires memory, then ingestion should increase events necessary for synaptic plasticity in dHC and vHC during the postprandial period. To test this, we determined whether ingesting a sucrose solution induced posttranslational events critical for hippocampal synaptic plasticity: phosphorylation of AMPAR GluA1 subunits at 1) serine 831 (pSer831) and 2) serine 845 (pSer845). We also examined whether increasing the amount of previous experience with the sucrose solution, which would be expected to decrease the mnemonic demand involved in an ingestion bout, would also attenuate sucrose-induced phosphorylation. Quantitative immunoblotting of dHC and vHC membrane fractions demonstrated that sucrose ingestion increased postprandial pSer831 in dHC but not vHC. Increased previous sucrose experience prevented sucrose-induced dHC pSer831. Sucrose ingestion did not affect pSer845 in either dHC or vHC. Thus, the present findings show that ingestion activates a postranslational event necessary for synaptic plasticity in an experience-dependent manner, which is consistent with the hypothesis that dHC neurons form a memory of a meal during the postprandial period.
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影响因子：
2.7
作者：
Clark JK;Furgerson M;Crystal JD;Fechheimer M;Furukawa R;Wagner JJ
通讯作者：
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影响因子：
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影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
1.9
作者：
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通讯作者：
Somerville, EM