98%
921
2 minutes
20
Adenosine and excitatory amino acids have been known to be involved in modulating nociceptive transmission at the spinal level. The authors assessed the characteristics of the interaction of the adenosine-excitatory amino acid antagonist combinations in the spinal cord of rats on the formalin-induced nociception. Intrathecal NMDA antagonist ((5R, 10S)-(+)-5-methyl-10,11-dihydro-(5)H-dibenzo[a[,]d]cyclohepten-5,10-imine hydrogen maleate, MK801, 30 microg) and AMPA antagonist (2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[F]quinoxaline-7-sulfonamide, NBQX, 3 microg) decreased the total number of flinches during both phases in the formalin test. Intrathecal adenosine (300 microg) had little effect on the phase 1 flinching response, but decreased the phase 2 response. The fixed dose analysis and the isobolographic analysis revealed that adenosine interacts additively with MK801 and NBQX in the spinal cord.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1159/000088345 | DOI Listing |
ACS Chem Neurosci
July 2025
Department of Pain Management, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan 250021 Shandong, China.
Spinal cord injury (SCI) is a severe clinical condition often accompanied by multiple complications, with neuropathic pain (NP) being one of the most persistent and difficult conditions to treat. The underlying mechanisms of NP remain unclear, and effective clinical treatments are lacking. Some studies suggest that phosphodiesterase 2A (PDE2A) may contribute to the development of NP.
View Article and Find Full Text PDFNeurochem Int
September 2025
Division of Pain Management, Department of Anesthesiology, Taipei Veterans General Hospital, Taipei, 112201, Taiwan; School of Medicine, National Yang-Ming Chiao Tung University, Taipei, 112304, Taiwan. Electronic address:
Neuropathic pain has multiple etiologies, and many patients remain inadequately treated. The cyclic adenosine monophosphate (cAMP) signaling pathway plays a critical role in inflammatory responses, particularly through the upregulation of proinflammatory cytokines. This study aimed to investigate the anti-inflammatory and analgesic properties of the marine-derived antimicrobial peptide Tilapia Piscidin 3 (TP3), using a chronic constriction injury (CCI) model to simulate neuropathic pain.
View Article and Find Full Text PDFCell Mol Biol Lett
January 2025
Department of Anesthesiology, The First Hospital of China Medical University, NO.155, North Nanjing Street, Heping District, Shenyang, 110001, Liaoning, China.
Background: Neuropathic pain (NP) represents a debilitating and refractory condition. However, the understanding of NP and the current treatment approaches available for its management are limited. Therefore, there is a significant need to address the dearth of effective therapeutic interventions.
View Article and Find Full Text PDFBiomed Pharmacother
February 2025
College of Veterinary Medicine, Konkuk University, 120, Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address:
Rett syndrome (RTT) is a neurological disorder caused by a mutation in the X-linked methyl-CpG binding protein 2 (MECP2), leading to cognitive and motor skill regression. Therapeutic strategies aimed at increasing brain-derived neurotrophic factor (BDNF) levels have been reported; however, BDNF treatment has limitations, including the inability to penetrate the blood-brain barrier, a short half-life, and potential for adverse effects when administered via intrathecal injection, necessitating novel therapeutic approaches. In this study, we focused on the adenosine A receptor (AR), which modulates BDNF and its downstream pathways, and investigated the therapeutic potential of CGS21680, an AR agonist, through in vitro and in vivo studies using R106W RTT model.
View Article and Find Full Text PDFNat Commun
December 2024
Department of Biochemistry, Duke University School of Medicine, Durham, NC, 27710, USA.
The current opioid crisis urgently calls for developing non-addictive pain medications. Progress has been slow, highlighting the need to uncover targets with unique mechanisms of action. Extracellular adenosine alleviates pain by activating the adenosine A1 receptor (A1R).
View Article and Find Full Text PDF