HCN2 contributes to oxaliplatin-induced neuropathic pain by inducing spinal long-term potentiation via activation of NMDA receptor-mediated CaMKII signaling

Thalamocortical Circuit Controls Neuropathic Pain via Up-regulation of HCN2 in the Ventral Posterolateral Thalamus

“…We have not determined here why the expression and function of HCN2 in TC neurons are up-regulated following peripheral nerve injury. Several underlying mechanisms are possible, such as the enhanced activity of p38 mitogen-activated protein kinase [ 53 ] and calmodulin-dependent protein kinase II [ 54 ]. However, the detailed mechanisms need to be further investigated.…”

N-Methyl D-aspartate receptor subtype 2B/Ca2+/calmodulin-dependent protein kinase II signaling in the lateral habenula regulates orofacial allodynia and anxiety-like behaviors in a mouse model of trigeminal neuralgia

“…Ketamine, an NMDAR antagonist, can rapidly relieve symptoms of depression by blocking the bursting activity of LHb neurons ( Yang et al, 2018 ). NR2B is a key functional subunit of NMDARs, and its activation triggers NMDA channel opening, mediates inward calcium flow, and activates downstream Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) ( Bayer et al, 2001 ; Liu et al, 2020 ). This signaling cascade is an essential pathway involved in neuronal activation.…”

Angiotensin (1–7) Attenuates the Nociceptive Behavior Induced by Substance P and NMDA <i>via</i> Spinal MAS1

“…In the spinal cord, NK1-positive projections mediate spinal nerve ligation (SNL)-induced neuropathic pain 1) as well as facet joint injury induced nociception. 2) In addition, the activation of spinal NMDA receptors was shown to be involved in chemotherapy- 3) and SNL-induced neuropathic pain. 4) Substance P (SP) and NMDA act as full agonists at NK1 receptors and NMDA receptors, respectively, and the intrathecal (i.t.)…”

“…injection of these agonists has been shown to induce nociceptive behavior. 5,6) Angiotensin (Ang) (1)(2)(3)(4)(5)(6)(7), an N-terminal fragment of Ang II, is mainly formed from Ang II by the action of Ang-converting enzyme (ACE) 2. By acting on the G protein-coupled receptor MAS1, Ang (1-7) exerts a counter-regulatory effect towards the Ang II/AT1 receptor axis.…”