RESUMEN
Itch and pain are distinct sensations that share anatomically similar pathways: from the periphery to the brain. Over the last decades, several itch-specific neural pathways and molecular markers have been identified at the peripheral and spinal cord levels. Although the perception of sensation is ultimately generated at the brain level, how the brain separately processes the signals is unclear. The primary somatosensory cortex (S1) plays a crucial role in the perception of somatosensory information, including touch, itch, and pain. In this study, we investigated how S1 neurons represent itch and pain differently. First, we established a spontaneous itch and pain mouse model. Spontaneous itch or pain was induced by intradermal treatment with 5-HT or capsaicin on the lateral neck and confirmed by a selective increase in scratching or wiping-like behavior, respectively. Next, in vivo two-photon calcium imaging was performed in awake mice after four different treatments, including 5-HT, capsaicin, and each vehicle. By comparing the calcium activity acquired during different sessions, we distinguished the cells responsive to itch or pain sensations. Of the total responsive cells, 11% were both responsive, and their activity in the pain session was slightly higher than that in the itch session. Itch- and painpreferred cells accounted for 28.4% and 60.6%, respectively, and the preferred cells showed the lowest activity in their counter sessions. Therefore, our results suggest that S1 uses a multiplexed coding strategy to encode itch and pain, and S1 neurons represent the interaction between itch and pain.
RESUMEN
Electrical conductivity, mechanical flexibility, and large electroactive surface areas are the most important factors in determining the performance of various flexible electrodes in energy storage devices. Herein, a layer-by-layer (LbL) assembly-induced metal electrodeposition approach is introduced to prepare a variety of highly porous 3D-current collectors with high flexibility, metallic conductivity, and large surface area. In this study, a few metal nanoparticle (NP) layers are LbL-assembled onto insulating paper for the preparation of conductive paper. Subsequent Ni electroplating of the metal NP-coated substrates reduces the sheet resistance from ≈103 to <0.1 Ω sq-1 while maintaining the porous structure of the pristine paper. Particularly, this approach is completely compatible with commercial electroplating processes, and thus can be directly extended to electroplating applications using a variety of other metals in addition to Ni. After depositing high-energy MnO NPs onto Ni-electroplated papers, the areal capacitance increases from 68 to 811 mF cm-2 as the mass loading of MnO NPs increases from 0.16 to 4.31 mg cm-2 . When metal NPs are periodically LbL-assembled with the MnO NPs, the areal capacitance increases to 1710 mF cm-2 .
RESUMEN
Bee venom (BV) has a long history of being used in traditional Korean medicine to relieve pain. Here, we investigated the effect of BV-derived phospholipase A2 (bvPLA2), a major component of BV, on peripheral nerve injury-induced neuropathic pain in rats. Spinal nerve ligation (SNL) was performed in Sprague Dawley rats to induce neuropathic pain, and paw withdrawal thresholds were measured using von Frey test. Mechanical allodynia, the representative symptom of neuropathic pain, was manifested following SNL and persisted for several weeks. The repetitive bvPLA2 treatment (0.2 mg/kg/day, i.p.) for two days significantly relieved the SNL-induced mechanical allodynia. The antiallodynic effect of bvPLA2 was blocked by spinal pretreatment with α1-adrenergic antagonist prazosin (30 µg, i.t.) but not with α2-adrenergic antagonist idazoxan (50 µg, i.t.). Also, the spinal application of α1-adrenergic agonist phenylephrine (50 µg, i.t.) reduced mechanical allodynia. These results indicate that bvPLA2 could relieve nerve injury-induced neuropathic mechanical allodynia through the activation of spinal α1-adrenergic receptors.