Topic: spared nerve injury

Neuropathic pain (NeuP) is a global health problem, with clinical manifestations including spontaneous (non-evoked) chronic pain (i.e. burning sensation) and altered somatosensory perception. To date, we still lack a detailed understanding of the molecular mechanisms driving NeuP. In preclinical mouse studies of NeuP, the main behaviour endpoints often fail to reflect typically observed patient symptoms, and the routine use of male subjects across diverse age ranges likely masks potential age- and sex-dependent variations. We aim to investigate the impact of age and sex on pain-related behavio

Pain elaboration results from the integration within dorsal spinal cord networks of sensory and nociceptive information conveyed by primary afferents. While many evidence suggest that a major disinhibition of dorsal horn networks may promote enhanced pain transmission in chronic pain pathologies, little is known about inhibitory neurons properties themselves and whether specific inhibitory subpopulations are preferentially altered in chronic pain conditions.We used the Spared Nerve Injury (SNI) neuropathic pain model on Gad67-GFP transgenic mice, which specifically labels dorsal horn inhibitor

microRNAs (miRNAs) are small, non-coding RNAs involved in all processes in health and disease, including neuropathic pain and neuroregeneration. Upon peripheral nerve injury (PNI), dorsal root ganglia (DRG) neurons exhibit increased excitability and altered signaling, leading to dysregulation of their transcriptomic profiles indicative of neuropathic pain and axono-regenerative processes. The complexity of these neuronal responses makes distinguishing between the mechanisms involved in neuroregeneration and neuropathy highly challenging. To elucidate the role of miRNAs in these processes, we u

Recently, research has focused extensively on the peripheral mechanisms that contribute to pain chronification, but our knowledge on the involvement of different brain regions remains limited. The Nucleus Accumbens (NAc) is a central hub for reward-related processes, with its interneurons having significant potential to control NAc output signals. However, their involvement in the chronification of pain has not been investigated until now.In this study, we performed patch-clamp recordings of cholinergic interneurons (ChIs) and GABAergic interneurons positive for parvalbumin (PV-GaIs) and somat

microRNAs (miRNAs) are small non-coding RNAs (ncRNAs) of ~22 nucleotides that regulate gene expression in all biological processes in health and disease, including nerve injury-induced neuronal regeneration and neuropathic pain. Although miRNAs have been under investigation for their potential application as biomarkers or even in novel therapeutic approaches, the signaling pathways involved in their regulation as well as their biological role remains elusive. Mice were subjected to the spared nerve injury model for neuropathic pain and paired-miRNA::mRNA sequencing was performed on dorsal root