Ghrelin对海马学习与记忆的影响及其作用机制的研究
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摘要
Ghrelin,一种促食欲激素,主要由胃产生,并释放到血液循环。Ghrelin受体(GHSR-1a)广泛地分布在大脑皮层、海马和下丘脑等部位。Ghrelin受体的激活能够易化离体高频刺激诱导的LTP的表达,并提高了学习和记忆能力。
本文研究了Ghrelin对海马学习与记忆功能的影响及其作用机制。结果表明:(1)单次脑内注射ghrelin不仅延长了LTP的表达,而且活体诱导了DG区的一种类似于LTP的长期持续的增强。有趣的是,这种增强并不依赖于NMDA受体的激活,而是被PI3K抑制剂所阻断; (2)ghrelin显著性地增加了Akt-Ser473的表达,Akt-Ser473可能是PI3K的下游信号分子;(3)ghrelin也提高了大鼠在水迷宫实验中的记忆能力。结论:ghrelin通过激活了PI3K通路,提高了突触可塑性和空间记忆。(1)单次注射ghrelin可能通过PI3K信号通路诱导一种新的突触可塑性形式,并且不需要高频刺激和NMDA受体的激活; (2)单次注射ghrelin也能够通过激活ERK来维持高频诱导的LTP;(3)重复注射ghrelin可以激活PI3K信号通路,显著性地提高了空间记忆能力。
因此,通过对ghrelin信号通路的研究,可能对学习记忆等某些认知功能的损伤会缺失的治疗具有一定的科学意义和应用价值。
Ghrelin, an orexigenic hormone, is mainly produced by stomach and released to circulation. Ghrelin receptors (GHS-R) are expressed throughout the brain, including hippocampus. The activation of GHS-R facilitates high-frequency stimulation (HFS)-induced long term potentiation (LTP) in vitro, and also improves learning and memory.
In this paper, we investigated the effect and mechanism of ghrelin on hippocampal learning and memory. The results showed that: (1) Single infusion of ghrelin in hippocampus led to long-lasting potentiation of excitatory postsynaptic potential (EPSP) and population spike (PS) in the dentate gyrus (DG) of anesthetized rats. This potentiation was accompanied with a reduction of paired-pulse depression (PPD) of EPSP slope, an increase of paired-pulse facilitation (PPF) of PS amplitude and an enhancement of EPSP-spike coupling, suggesting the involvement of both pre- and post-synaptic mechanisms. (2) Ghrelin infusion time-dependently increased the phosphorylation of Akt-Ser473, a downstream molecule of PI3K. Interestingly, PI3K inhibitors, but not NMDA receptor antagonist, inhibited ghrelin-induced potentiation. Although ghrelin had no effect on the induction of HFS-induced LTP, it prolonged the expression of HFS-induced LTP through ERK1/2 signal molecular. (3) Morris water maze test showed that ghrelin enhanced spatial memory, which was prevented by pretreatment with PI3K inhibitor. Taken together, 1) a single infusion of ghrelin could induce a new form of synaptic plasticity through activating PI3K signal pathway, without HFS and NMDA receptor activation; 2) a single infusion of ghrelin could also enhance the maintenance of HFS-induced LTP through ERK activation; 3) repetitive infusion of ghrelin could enhance spatial memory through activating PI3K signal pathway.
Thus, we propose that ghrelin signaling pathway could have therapeutic values for cognitive deficits.
本文研究了Ghrelin对海马学习与记忆功能的影响及其作用机制。结果表明:(1)单次脑内注射ghrelin不仅延长了LTP的表达,而且活体诱导了DG区的一种类似于LTP的长期持续的增强。有趣的是,这种增强并不依赖于NMDA受体的激活,而是被PI3K抑制剂所阻断; (2)ghrelin显著性地增加了Akt-Ser473的表达,Akt-Ser473可能是PI3K的下游信号分子;(3)ghrelin也提高了大鼠在水迷宫实验中的记忆能力。结论:ghrelin通过激活了PI3K通路,提高了突触可塑性和空间记忆。(1)单次注射ghrelin可能通过PI3K信号通路诱导一种新的突触可塑性形式,并且不需要高频刺激和NMDA受体的激活; (2)单次注射ghrelin也能够通过激活ERK来维持高频诱导的LTP;(3)重复注射ghrelin可以激活PI3K信号通路,显著性地提高了空间记忆能力。
因此,通过对ghrelin信号通路的研究,可能对学习记忆等某些认知功能的损伤会缺失的治疗具有一定的科学意义和应用价值。
Ghrelin, an orexigenic hormone, is mainly produced by stomach and released to circulation. Ghrelin receptors (GHS-R) are expressed throughout the brain, including hippocampus. The activation of GHS-R facilitates high-frequency stimulation (HFS)-induced long term potentiation (LTP) in vitro, and also improves learning and memory.
In this paper, we investigated the effect and mechanism of ghrelin on hippocampal learning and memory. The results showed that: (1) Single infusion of ghrelin in hippocampus led to long-lasting potentiation of excitatory postsynaptic potential (EPSP) and population spike (PS) in the dentate gyrus (DG) of anesthetized rats. This potentiation was accompanied with a reduction of paired-pulse depression (PPD) of EPSP slope, an increase of paired-pulse facilitation (PPF) of PS amplitude and an enhancement of EPSP-spike coupling, suggesting the involvement of both pre- and post-synaptic mechanisms. (2) Ghrelin infusion time-dependently increased the phosphorylation of Akt-Ser473, a downstream molecule of PI3K. Interestingly, PI3K inhibitors, but not NMDA receptor antagonist, inhibited ghrelin-induced potentiation. Although ghrelin had no effect on the induction of HFS-induced LTP, it prolonged the expression of HFS-induced LTP through ERK1/2 signal molecular. (3) Morris water maze test showed that ghrelin enhanced spatial memory, which was prevented by pretreatment with PI3K inhibitor. Taken together, 1) a single infusion of ghrelin could induce a new form of synaptic plasticity through activating PI3K signal pathway, without HFS and NMDA receptor activation; 2) a single infusion of ghrelin could also enhance the maintenance of HFS-induced LTP through ERK activation; 3) repetitive infusion of ghrelin could enhance spatial memory through activating PI3K signal pathway.
Thus, we propose that ghrelin signaling pathway could have therapeutic values for cognitive deficits.
引文
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