Joseph and Levine showed that caspase signaling pathway contributed to the pain induced in two models of painful peripheral neuropathy [ 16].
A recent study demonstrated that pre-emptive chronic zoledronate (a nitrogenous BP) treatment increases bone mineral density, and is chondroprotective and analgesic in both chemical (mono-iodo-acetate, MIA) and surgical experimental models of painful joint degeneration in the rat [ 12].
For example, GABAA agonists, such as muscimol and THIP (4,5,6,7-tetrahydroisoxazolo[5,4 c]pyridin-3-ol hydrochloride), have been shown to alleviate both thermal and mechanical hyperalgesia in rat models of painful neuropathy after peripheral nerve injury, whereas application of GABAA antagonists such as bicuculline and picrotoxin led to more pronounced hyperalgesia [ 37].
Nociceptin/orphanin FQ (N/OFQ) acts through the N/OFQ peptide receptor (NOP) [ 3] and can change responsiveness to painful stimuli in several models of pain [ 4– 6].
In this review, the features of animal models of chemotherapy-induced painful neuropathy developed for 20 years, due to the administration of the most widely used drugs, such as platinum drugs, taxanes, and vinca alkaloids, will be discussed.
Behavioral changes observed in pre-clinical models of lumbar radicular pain may relate to painful symptoms observed in human subjects.
According to cognitive-behavioral models, such as the fear-avoidance models [ 4, 5] or the avoidance-endurance model of chronic pain [ 6], painful experiences will elicit a fear of movement/(re)injury in certain individuals, which often leads to behavioral avoidance and, in the long run, disuse, depression and increased disability.
We introduce a new conceptual model of maturation and painful IVD degeneration in which dynamic pressurization induces maturation of NP tissue, differentiation of NCs to SNPCs, and maintenance of developmental patterning and neurovascular inhibiting factors (SHH, Sema3A and Noggin).
We have recently developed and characterized an in vivo rat model of BTZ-induced painful sensory neurotoxicity designed to mimic the typical long-term clinical use of the drug [ 27– 29].
Patient also complains of painful menses (dysmenorrhea), painful urination (dysuria), painful sex (dyspareunia) and severe pain in the legs.
The mechanism by which gabapentin exerts its analgesic action is unknown, but in animal models of analgesia, gabapentin prevents allodynia (pain related behavior in response to a normally innocuous stimulus) and hyperalgesia (exaggerated response to painful stimuli).
