Two aspects of ASIC function: Synaptic plasticity and neuronal injury

Huang, Yan; Jiang, Nan; Li, Jun; Ji, Yonghua; Xiong, Zhi‐Gang; Zha, Xiang-ming

doi:10.1016/j.neuropharm.2014.12.010

Cited by 62 publications

(59 citation statements)

References 103 publications

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“…Overall, data here presented further confirm that ASICs can mediate proton signaling at synaptic sites [52] and reveal for the first time alink between ASIC1a channels and mGlu receptors. Of note, recent evidence published by Gan and colleagues [19] demonstrated a crosstalk between group I mGlu receptor and ASIC3 in dorsal root ganglion (DRG) neurons.…”

Section: Discussionsupporting

confidence: 80%

“…On the one hand, this study highlights a novel role of ASICs in hippocampal synaptic plasticity and in cellular responses to mGlu receptors activation, opening a stream of investigation on their possible role in regulating cognitive processes; on the other it might shed new light on the possible contribution of these channels to pathological events at the synapse. Accordingly, several reports have previously shown the involvement of ASICs in ischemic neuronal injury, traumatic neuronal multiple sclerosis and Parkinson's disease [52]. Therefore, ASICs are emerging as potential therapeutic targets for the treatment of several brain disorders [53].…”

Section: Discussionmentioning

confidence: 99%

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Acid-sensing ion channel 1a is required for mGlu receptor dependent long-term depression in the hippocampus

Mango

Braksator

Battaglia

et al. 2017

Pharmacological Research

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a b s t r a c tAcid-sensing ion channels (ASICs), members of the degenerin/epithelial Na + channel superfamily, are widely distributed in the mammalian nervous system. ASIC1a is highly permeable to Ca 2+ and are thought to be important in a variety of physiological processes, including synaptic plasticity, learning and memory. To further understand the role of ASIC1a in synaptic transmission and plasticity, we investigated metabotropic glutamate (mGlu) receptor-dependent long-term depression (LTD) in the hippocampus. We found that ASIC1a channels mediate a component of LTD in P30-40 animals, since the ASIC1a selective blocker psalmotoxin-1 (PcTx1) reduced the magnitude of LTD induced by application of the group I mGlu receptor agonist (S)-3,5-Dihydroxyphenylglycine (DHPG) or induced by paired-pulse low frequency stimulation (PP-LFS). Conversely, PcTx1 did not affect LTD in P13-18 animals. We also provide evidence that ASIC1a is involved in group I mGlu receptor-induced increase in action potential firing. However, blockade of ASIC1a did not affect DHPG-induced polyphosphoinositide hydrolysis, suggesting the involvement of some other molecular partners in the functional crosstalk between ASIC1a and group I mGlu receptors. Notably, PcTx1 was able to prevent the increase in GluA1 S845 phosphorylation at the post-synaptic membrane induced by group I mGlu receptor activation. These findings suggest a novel function of ASIC1a channels in the regulation of group I mGlu receptor synaptic plasticity and intrinsic excitability.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Acid-sensing ion channel 1a is required for mGlu receptor dependent long-term depression in the hippocampus

Mango

Braksator

Battaglia

et al. 2017

Pharmacological Research

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“…Synaptic transmission reduces pH at the synaptic cleft, and this acidification contributes to postsynaptic currents and synaptic plasticity (1)(2)(3)(4). Moreover, acidosis is common in neurologic diseases and is a major cause of neuronal injury in diseases, such as ischemia (5,6). These observations indicate that proton-mediated signaling is important for both physiologic and pathophysiological responses.…”

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confidence: 99%

“…The ASIC subunits expressed throughout mouse brain are ASIC1a, -2a, and -2b (8). Electrophysiological studies further showed that ASIC1a and ASIC2 subunits are the main contributor to acidactivated currents in the vast majority of brain neurons (5). ASIC1a is the key determinant of the acid-activated current, whereas ASIC2 plays important modulator roles.…”

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confidence: 99%

Human ASIC1a mediates stronger acid‐induced responses as compared with mouse ASICIa

Jiang

et al. 2018

FASEB j.

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Acid-sensing ion channels (ASICs) are the major proton receptor in the brain and a key mediator of acidosis-induced neuronal injuries in disease. Most of published data on ASIC function came from studies performed in mice, and relatively little is known about potential differences between human and mouse ASICs (hASIC and mASIC, respectively). This information is critical for us to better interpret the functional importance of ASICs in human disease. Here, we examined the expression of ASICs in acutely resected human cortical tissue. Compared with mouse cortex, human cortical tissue showed a similar ratio of ASIC1a:ASIC2a expression, had reduced ASIC2b level, and exhibited a higher membrane:total ratio of ASIC1a. We further investigated the mechanism for higher surface trafficking of hASIC1a in heterologous cells. A single amino acid at position 285 was critical for increased N-glycosylation and surface expression of hASIC1a. Consistent with the changes in trafficking and current, cells expressing hASIC1a or mASIC1a S285P mutant had a higher acid-activated calcium increase and exhibited worsened acidotoxicity. These data suggest that ASICs are likely to have a larger impact on acidosis-induced neuronal injuries in humans than mice, and this effect is, at least in part, a result of more efficient trafficking of hASIC1a.-Xu, Y., Jiang, Y.-Q., Li, C., He, M., Rusyniak, W. G., Annamdevula, N., Ochoa, J., Leavesley, S. J., Xu, J., Rich, T. C., Lin, M. T., Zha, X.-M. Human ASIC1a mediates stronger acid-induced responses as compared with mouse ASIC1a.

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“…The review covers a range of topics from the history of the first electrophysiological observations of these channels (Krishtal et al, 2015) to what we currently know of their structure and biophysical properties (Gründer and Pusch, 2015), their pharmacology (Baron and Lingueglia, 2015), some of the mechanisms by which they are regulated (and especially those by neuropeptides, Vick and Askwith, 2015) and their physiological roles in both the central and the peripheral nervous systems. Brain ASICs have been implicated in functions such as synaptic plasticity and neuronal injury (Huang et al, 2015), but the largest body of data to-date has been obtained on their contribution to sensory function in the peripheral and/or the central nervous systems. This includes nociception, with roles for ASIC channels in pain (Deval and Lingueglia, 2015;Sluka and Gregory, 2015) and migraine (Dussor, 2015), as well as in gastrointestinal function (Holzer, 2015), mechanoreception (Omerbasic at al.…”

mentioning

confidence: 99%