The Local Peripheral Antihyperalgesic Effect of Levetiracetam and Its Mechanism of Action in an Inflammatory Pain Model

Abstract

Our results show that levetiracetam produces local peripheral antihyperalgesic and anti-edematous effects in a rat model of localized inflammation. Antihyperalgesia is at least in part mediated by peripheral μ-opioid, α2A,C-adrenergic, A1 adenosine, and 5-HT1B/1D receptors, but not by GABAA receptors. These findings could contribute toward a better understanding of the analgesic effects of levetiracetam, and improved treatments of inflammatory pain with a lower incidence of systemic side effects and drug interactions of levetiracetam.

Acid‐sensing ion channels in trigeminal ganglion neurons innervating the orofacial region contribute to orofacial inflammatory pain

“…However, the role of ASICs in orofacial inflammatory pain processing is still not well defined. A variety of inflammatory pain animal models have been established by mimicking orofacial injury, such as capsaicin model, formalin test, carrageenan model, mustard oil model and complete Freund's adjuvant (CFA)‐induced chronic inflammation model . It is generally accepted that the orofacial formalin test is used to investigate the pathophysiology of acute orofacial inflammatory pain.…”

Levetiracetam synergises with common analgesics in producing antinociception in a mouse model of painful diabetic neuropathy

“…-Opioid receptors are integral part of this circuity too [62]. In our previous studies, we have shown that levetiracetam's antihyperalgesia in an inflammatory pain model involves indirect activation of central and/or peripheral GABA A , ␣ 2 -adrenergic, 5-HT-ergic and -opioidergic receptors [8,9]. Since inflammatory component contributes to the pathogenesis and/or maintenance of painful diabetic neuropathy [2,3,62] and both central and peripheral changes accompany neuropathy, it could be assumed that these mechanisms of levetiracetam-induced analgesia in an inflammatory pain model may also be relevant for its antinociception in diabetic neuropathic pain.…”

Increased neurogenesis after ACEA and levetiracetam treatment in mouse pilocarpine model of epilepsy

“…Additionally, results from different experimental research suggests that LEV provides antihyperalgesic effects in inflammatory pain [45][46][47], chronic pain [48] and neuropathic pain [49][50][51] models. Several studies have proposed that LEV possesses considerable neuroprotective properties in both epileptic and non-epileptic disorders [42].…”