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.
Highlights
The ability to experience pain possesses a protective role since it warns of imminent or ongoing tissue damage and elicits behavioral responses in order to minimize this damage
This study revealed that the projection from the medial prefrontal cortex (mPFC) to the nucleus accumbens is involved in the anti-nociceptive effects induced by optogenetic activation of the neuronal circuit
Animal models of neuropathic pain are commonly employed in order to screen new compounds for their analgesic activity, as well as to investigate possible novel pathways in pain pathophysiology
Summary
The ability to experience pain possesses a protective role since it warns of imminent or ongoing tissue damage and elicits behavioral responses in order to minimize this damage. Whether tissue harm is inevitable, a plethora of excitability changes in the peripheral or the central nervous system (PNS and CNS, respectively) establish a profound, but reversible pain hypersensitivity in the inflamed tissue. This process assists injury repair because any contact with the damaged part is avoided until healing has occurred. Neuropathic pain can be triggered by injuries affecting the PNS or CNS and is characterized by spontaneous or abnormal pain sensation [2]. The source of neuropathic pain development cannot be always established or reversed, and the available pharmacological tools are unsatisfactory.
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