Journal Article10.1016/J.BRAINRESBULL.2020.03.008
HCN2 contributes to oxaliplatin-induced neuropathic pain by inducing spinal long-term potentiation via activation of NMDA receptor-mediated CaMKII signaling.
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TL;DR: Rat HCN2 levels significantly increased after high-frequency stimulation-induced long-term potentiation (LTP), and administration of oxaliplatin significantly increased the amplitude of excitatory postsynaptic currents and the number of action potentials, but these effects were attenuated by pretreatment with either CaMKII inhibitor KN-93 or NR2B antagonist Ro 25-6981.
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About: This article is published in Brain Research Bulletin. The article was published on 01 Jun 2020. The article focuses on the topics: LTP induction & Long-term potentiation.
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Citations
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TL;DR: A synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers is identified and this model integrates known signal transduction pathways of hyperalgesia without contradiction.
HCN2 Ion Channels Play a Central Role in Inflammatory and Neuropathic Pain
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TL;DR: It is found that genetic deletion of HCN2 removed the cyclic adenosine monophosphate (cAMP)–sensitive component of Ih and abolished action potential firing caused by an elevation of cAMP in nociceptors.
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Calcium Signaling in Neuronal Development
TL;DR: The development of the nervous system involves the generation of a stunningly diverse array of neuronal subtypes that enable complex information processing and behavioral outputs that will be greatly enhanced by the identification of distinct neuronal circuits and by an understanding of how these circuits are formed, changed, and/or maintained over time.