Abstract:
:The N-type voltage-gated calcium channel (CaV2.2) is a clinically endorsed target in chronic pain treatments. As directly targeting the channel can lead to multiple adverse side effects, targeting modulators of CaV2.2 may prove better. We previously identified ST1-104, a short peptide from the collapsin response mediator protein 2 (CRMP2), which disrupted the CaV2.2-CRMP2 interaction and suppressed a model of HIV-related neuropathy induced by anti-retroviral therapy but not traumatic neuropathy. Here, we report ST2-104 -a peptide wherein the cell-penetrating TAT motif has been supplanted with a homopolyarginine motif, which dose-dependently inhibits the CaV2.2-CRMP2 interaction and inhibits depolarization-evoked Ca(2+) influx in sensory neurons. Ca(2+) influx via activation of vanilloid receptors is not affected by either peptide. Systemic administration of ST2-104 does not affect thermal or tactile nociceptive behavioral changes. Importantly, ST2-104 transiently reduces persistent mechanical hypersensitivity induced by systemic administration of the anti-retroviral drug 2',3'-dideoxycytidine (ddC) and following tibial nerve injury (TNI). Possible mechanistic explanations for the broader efficacy of ST2-104 are discussed.
journal_name
J Neurochemjournal_title
Journal of neurochemistryauthors
Ju W,Li Q,Allette YM,Ripsch MS,White FA,Khanna Rdoi
10.1111/jnc.12070subject
Has Abstractpub_date
2013-03-01 00:00:00pages
869-79issue
6eissn
0022-3042issn
1471-4159journal_volume
124pub_type
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journal_title:Journal of neurochemistry
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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doi:10.1046/j.1471-4159.2003.01571.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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更新日期:1986-01-01 00:00:00
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journal_title:Journal of neurochemistry
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doi:10.1046/j.1471-4159.1996.67020717.x
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journal_title:Journal of neurochemistry
pub_type: 杂志文章
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journal_title:Journal of neurochemistry
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