Experimental efforts of PAIN LAB are currently directed towards:


  • Impact of exogenous and endogenous anandamide for the treatment of chronic neuropathic pain, as well as the role of TRPV1 receptors in anandamide’s analgesic effects

Chronic pain is a common healthcare problem worldwide that ranks as a predominant reason for consulting a physician, yet effective management of chronic pain remains suboptimal. This results in unnecessary suffering, decreased quality of life, lost productivity and excessive healthcare costs. A novel and effective pain therapy is still a challenge. We suggest that spinal AEA reduces neuropathic pain via CB1 or TRPV1, depending on its local concentration.


  • Determination of the role of endovanilloids and/or endocannabinoids– endogenous TRPV1 and CB1 receptor activators – and identification of their possible use in neuropathic pain treatment.

Considering the fact that anandamide is currently perceived as the ligand for both CB1 and TRPV1 receptors, and that the exogenous TRPV1 ligands have a desensitizing effect, while the endogenous substances, i.e. endovanilloid/endocannabinoids probably do not reach levels required of the TRPV1 channel desensitization, it can be postulated that the interaction between these systems is a new challenge in the search for efficient neuropathic pain treatments. Understanding the relationship between endovanilloid and endocannabinoid systems should help with finding novel, more efficient pharmacotherapeutic methods of pain management, based on amplifying the effects of substances endogenously produced by the system.


  • Investigation of the role of multiple AEA production (both in Ca2+-dependent and Ca2+-independent manners) and degradation pathways as well as the possible consequences of altering its signaling during the development of neuropathic pain.

Endocannabinoids are present in multiple pain-modulating regions throughout the central nervous system (CNS), including the dorsal horn of the spinal cord and the dorsal root ganglia (DRGs), where their levels are modified by acute nociceptive stimuli and stress. Tissue concentrations of AEA in pain pathways become altered as an adaptive response to neuropathic pain, what further confirms the significant role of the AEA in chronic pain development. Alterations in a variety of synthesis and degradation enzymes of AEA illustrate the flexibility of the EC system.


  • Potential new treatments for OA thorough understanding of the molecular mechanisms underlying the degenerative process

Osteoarthritis(OA) is the most common joint pathology, as well as the most common cause of pain and disabilities in the populations of developed countries. Aging of societies in developed countries resulted in the situation that OA has become one of the most important diseases of today’s civilization. Until now, there are no disease modifying drugs for OA or agents which effectively stop its progress. Instead,the treatment involves only ad hoc alleviation of the acute symptoms of the affected joint. In recent years, significant progress has been made in research on the pathogenesis of osteoarthritis. New mediators involved in the pathogenic pathways have been discovered, what’s more a number of clinical and radiological experiments have been made and allowed for a new interpretation of the role of each of the joint tissues in the development of this disease. However, despite the expanding knowledge about pathogenesis of osteoarthritis, as yet, neither an effective causal treatment nor a disease modifying treatment can be successfully implemented.


  • Importance of TRPV1-sensitisation factors for the development of neuropathic pain

A number of modulators regulate TRPV1 activity and promote inflammatory or painful responses. TRPV1 sensitization is associated with phosphorylation controlled by at least four serine/threonine kinases, including protein kinase A (PKA), protein kinase C (PKC), Ca2 +/calmodulin-dependent kinase 2 (CaMK 2), and cyclin-dependent kinase 5 (Cdk5). Among these, PKA- and PKC-mediated phosphorylation has been widely investigated in various pain models. We reported that the maintenance of TRPV1 sensitization in this CCI model of neuropathic pain is mainly due to PKCε-mediated phosphorylation. Moreover, we identified TNFα and NGF as factors that might be responsible for the acute-to-chronic transition and for maintenance of pain, thus we suggest them as targets for the therapy of neuropathic pain.


  • Investigation of the cytoprotective action of (endo)cannabinoids on osteoblasts and their role in bone mineral density regulation.

As no data are available on the possible protective and regenerative properties of EC system in OA, further studies may address this issue in in vitro studies. EC system cytotoxicity (MTT and/or LDH test) and proliferation capability (BrdU test) and their effects on wound-healing are currently under investigation.