Behavioral, Biochemical and Electrophysiological Changes in Spared Nerve Injury Model of Neuropathic Pain

Abstract

Neuropathic pain is a pathological condition induced by a lesion or disease affecting the somatosensory system, with symptoms like allodynia and hyperalgesia. It has a multifaceted pathogenesis as it implicates several molecular signaling pathways involving peripheral and central nervous systems. Affective and cognitive dysfunctions have been reported as comorbidities of neuropathic pain states, supporting the notion that pain and mood disorders share some common pathogenetic mechanisms. The understanding of these pathophysiological mechanisms requires the development of animal models mimicking, as far as possible, clinical neuropathic pain symptoms. Among them, the Spared Nerve Injury (SNI) model has been largely characterized in terms of behavioral and functional alterations. This model is associated with changes in neuronal firing activity at spinal and supraspinal levels, and induces late neuropsychiatric disorders (such as anxious-like and depressive-like behaviors, and cognitive impairments) comparable to an advanced phase of neuropathy. The goal of this review is to summarize current findings in preclinical research, employing the SNI model as a tool for identifying pathophysiological mechanisms of neuropathic pain and testing pharmacological agent.

Cortico-autonomic local arousals and heightened somatosensory arousability during NREM sleep of mice in neuropathic pain

“…We also found no alterations in theta power or for shifts in theta peaks in wakefulness, as reported for other animal models of chronic pain (LeBlanc et al, 2014) or for humans with severe neurogenic pain or arthritis (Sarnthein et al, 2006). Analysis of sleep disruptions at later stages in the disease will help decide whether distinct phases of sleep disruptions mark distinct phases of pain chronicity when anxiety-and depression-related behaviors appear more strongly (Guida et al, 2020).…”

“…The lack of major sleep disruptions in the SNI mouse model was initially unexpected but seemed in line with other studies. We analyzed these animals at a time point when pain from the wound and associated inflammations are largely over (Guida et al, 2020), both of which can strongly disrupt sleep (Landis et al, 1989;Andersen & Tufik, 2003;Silva et al, 2008). Moreover, the animals showed a preserved time spent in REMS, suggesting that they did not suffer from chronic mild stress-inflicted sleep disruptions (Nollet et al, 2019).…”

N-palmitoyl-D-glucosamine, A Natural Monosaccharide-Based Glycolipid, Inhibits TLR4 and Prevents LPS-Induced Inflammation and Neuropathic Pain in Mice

“…The spared nerve injury. Mononeuropathy was induced according to the method of Decosterd and Woolf [ 33 , 41 , 42 ]. Mice were anaesthetized by intraperitoneal injection of ketamine xylazine (60 mg/kg + 10 mg/kg).…”

Neuropathic pain-induced cognitive dysfunction and down-regulation of neuronal pentraxin 2 in the cortex and hippocampus

“…Neuropathic pain is a complex multidimensional insult with marked effects on many aspects of an individual’s daily life beyond physical functioning, especially cognitive components such as attentional capacity, processing speed, and psychomotor speed [ 1 ]. Existing therapeutics for pain are often less effective for neuropathic pain; moreover, effective pain relief with existing analgesics usually do not target improvement of pain-related cognitive dysfunction [ 2 ].…”