Aquaporin-4 Deficiency Impairs Synaptic Plasticity and Associative Fear Memory in the Lateral Amygdala: Involvement of Downregulation of Glutamate Transporter-1 Expression

Li, Yan-Kun; Wang, Fang; Wang, Wei; Luo, Yi; Wu, Pengfei; Xiao, Jun-Li; Hu, Zhuang-Li; You, Jing; Hu, Gang; Chen, Jianguo

doi:10.1038/npp.2012.34

Cited by 101 publications

(111 citation statements)

References 59 publications

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“…However, certain investigators have reported that the effect of BYHWD on decreasing glutamate peaked at 3 h after administration (6,7), but there should be other mechanisms, as BYHWD absorption and changes of protein expression possibly require a longer period of time. Although upregulation of GLT-1 and GS in the present study did not appear earlier to prevent ischemic injury efficiently, they could be beneficial for subsequent strokes, later regeneration and functional restoration, as GLT-1 was reported to be involved in synaptic plasticity and associative fear memory (23). Recently, PACAP-38, which reduced infarct volume and attenuated the neuronal injury (16), has been found to be involved in GLT-1 and GS expression.…”

Section: Discussioncontrasting

confidence: 58%

Buyang Huanwu decoction increases the expression of glutamate transporter-1 and glutamate synthetase in association with PACAP-38 following focal ischemia

Ding

Liu

et al. 2015

Biomedical Reports

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Abstract. The neuroprotective role of Buyang Huanwu decoction (BYHWD) in focal ischemia is associated with decreasing glutamate concentration. However, the mechanisms are not fully understood. The present study aimed to explore whether glutamate transporter-1 (GLT-1) and glutamine synthetase (GS) participated in the decreased level of glutamate and whether pituitary adenylate cyclase-activating polypeptide-38 (PACAP-38) was involved in this process. BYHWD was found to significantly upregulate the expression of GLT-1 and GS in the hippocampal CA1 area compared to the ischemia group, with the difference on day 3 being most significant. BYHWD increased the level of PACAP-38, and PACAP-(6-38) (PACAP receptor antagonist) significantly attenuated the effect of BYHWD on GLT-1 and GS, suggesting that PACAP-38 was involved in the upregulation of GLT-1 and GS induced by BYHWD. In addition, as GLT-1 and GS are mainly located in astrocytes, the changes of astrocytes were detected by glial fibrillary acidic protein (GFAP; an astrocytic marker) immunostaining. The results showed that BYHWD inhibited the expression of GFAP compared with the ischemia group, however, co-administration with PACAP-(6-38), which inhibited the effect of BYHWD on GLT-1 and GS in astrocytes, attenuated this effect, indicating that astrocytes participated in the protective role of BYHWD following focal ischemia. These results provided the evidence for the first time that not only neurons but also astrocytes contribute to the protective role of BYHWD, which opposes previous studies and may be a starting point for traditional medicine.

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Section: Discussioncontrasting

confidence: 58%

Buyang Huanwu decoction increases the expression of glutamate transporter-1 and glutamate synthetase in association with PACAP-38 following focal ischemia

Ding

Liu

et al. 2015

Biomedical Reports

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“…It is also possible that dynamical coupling in the morphology of microstructures allows the formation of networks to represent the plasticity-related morphological changes following brain stimulation protocols. The morphology of dendritic spines can modulate synaptic efficacy and plasticity (3,4,38); therefore, it is possible that the nodes in the identified networks can indirectly achieve long-distance coupling with each other by modulating synaptic plasticity or efficacy of the transsynaptic signaling (39).…”

Section: Discussionmentioning

confidence: 99%

“…R epetitive electrical brain stimulation induces long-term potentiation (LTP) or depression (LTD) at the stimulated neurons (1)(2)(3)(4). In humans, repetitive transcranial magnetic stimulation (rTMS) alters cortical excitability at the stimulated site that outlasts the end of the stimulation, analogous to LTP or LTD in animal models (5,6), but also affects remote regions, possibly through transsynaptic pathways (7,8).…”

mentioning

confidence: 99%

Water diffusion reveals networks that modulate multiregional morphological plasticity after repetitive brain stimulation

Abe

Fukuyama

Mima

2014

Proc. Natl. Acad. Sci. U.S.A.

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Repetitive brain stimulation protocols induce plasticity in the stimulated site in brain slice models. Recent evidence from network models has indicated that additional plasticity-related changes occur in nonstimulated remote regions. Despite increasing use of brain stimulation protocols in experimental and clinical settings, the neural substrates underlying the additional effects in remote regions are unknown. Diffusion-weighted MRI (DWI) probes water diffusion and can be used to estimate morphological changes in cortical tissue that occur with the induction of plasticity. Using DWI techniques, we estimated morphological changes induced by application of repetitive transcranial magnetic stimulation (rTMS) over the left primary motor cortex (M1). We found that rTMS altered water diffusion in multiple regions including the left M1. Notably, the change in water diffusion was retained longest in the left M1 and remote regions that had a correlation of baseline fluctuations in water diffusion before rTMS. We conclude that synchronization of water diffusion at rest between stimulated and remote regions ensures retention of rTMS-induced changes in water diffusion in remote regions. Synchronized fluctuations in the morphology of cortical microstructures between stimulated and remote regions might identify networks that allow retention of plasticityrelated morphological changes in multiple regions after brain stimulation protocols. These results increase our understanding of the effects of brain stimulation-induced plasticity on multiregional brain networks. DWI techniques could provide a tool to evaluate treatment effects of brain stimulation protocols in patients with brain disorders.R epetitive electrical brain stimulation induces long-term potentiation (LTP) or depression (LTD) at the stimulated neurons (1-4). In humans, repetitive transcranial magnetic stimulation (rTMS) alters cortical excitability at the stimulated site that outlasts the end of the stimulation, analogous to LTP or LTD in animal models (5, 6), but also affects remote regions, possibly through transsynaptic pathways (7,8). Although rTMS has been proposed as a potential treatment for neurological and psychiatric disorders (9, 10) and as a method to facilitate learning (11), the neural substrates underlying the effects of rTMS on remote regions of the brain remain poorly understood.Diffusion-weighted MRI (DWI) probes water diffusion, a thermal physical phenomena that is characterized by random motion of water molecules (12). Water diffusion is altered by the structures of gray matter (12). DWI can be used to evaluate morphological changes in cortical microstructures (13)(14)(15)(16)(17)(18)(19) and can function as a probe to estimate immediate and transient changes in water diffusion that are associated with ischemia (17) or neuronal firing (13,16,19) and delayed and persistent changes that are associated with long-term plasticity in experimental settings (20) or pathological conditions (15,18,21). Here, using DWI techniques, we examined whether subt...

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“…So far the results have been negative. Specifically, deletion of Aqp4 did not affect key parameters of synaptic transmission including excitability (53,88,171). Also, paired pulse facilitation, a form of short time plasticity, was not changed in Aqp4 Ϫ/Ϫ animals (53, 88, 171).…”

Section: Synaptic Plasticity and Behaviormentioning

confidence: 94%

Physiological Roles of Aquaporin-4 in Brain

Nagelhus

Ottersen

2013

Physiological Reviews

592

520

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(AQP4) is one of the most abundant molecules in the brain and is particularly prevalent in astrocytic membranes at the blood-brain and brain-liquor interfaces. While AQP4 has been implicated in a number of pathophysiological processes, its role in brain physiology has remained elusive. Only recently has evidence accumulated to suggest that AQP4 is involved in such diverse functions as regulation of extracellular space volume, potassium buffering, cerebrospinal fluid circulation, interstitial fluid resorption, waste clearance, neuroinflammation, osmosensation, cell migration, and Ca 2ϩ signaling. AQP4 is also required for normal function of the retina, inner ear, and olfactory system. A review will be provided of the physiological roles of AQP4 in brain and of the growing list of data that emphasize the polarized nature of astrocytes.

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Aquaporin-4 Deficiency Impairs Synaptic Plasticity and Associative Fear Memory in the Lateral Amygdala: Involvement of Downregulation of Glutamate Transporter-1 Expression

Cited by 101 publications

References 59 publications

Buyang Huanwu decoction increases the expression of glutamate transporter-1 and glutamate synthetase in association with PACAP-38 following focal ischemia

Buyang Huanwu decoction increases the expression of glutamate transporter-1 and glutamate synthetase in association with PACAP-38 following focal ischemia

Water diffusion reveals networks that modulate multiregional morphological plasticity after repetitive brain stimulation

Physiological Roles of Aquaporin-4 in Brain

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