The genetic influence of the brain-derived neurotrophic factor Val66Met polymorphism in chronic low back pain.

BACKGROUND: The Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene is a potential biomarker of vulnerability to pain. Thus, the present study aimed to investigate the association of this polymorphism with clinical and biopsychosocial factors in patients with chronic low back pain (CLBP). METHODS: A total of 107 individuals with CLBP answered questionnaires that were validated and adapted for the Brazilian population, including the Brief Inventory of Pain, the Central Sensitization Inventory, the Roland Morris Disability Questionnaire, the Tampa Scale for Kinesiophobia, the Pain Catastrophizing Scale, the Survey of Pain Attitude-Brief, and the Hospital Anxiety and Depression Scale. All of the subjects were genotyped for the BDNF Val66Met polymorphism. RESULTS: The sample showed moderate scores of disability, central sensitization, and kinesiophobia, in addition to mild anxiety, hopelessness, and ruminant thoughts. No significant association was observed between the Val66Met polymorphism and the variables analyzed. Besides, there was no relationship between the BDNF Val66Met polymorphism with CSI, catastrophization, or disabilities that were generated by CLBP. CONCLUSION: The results showed that the Val66Met polymorphism of the BDNF gene was not associated with clinical and biopsychosocial characteristics of CLBP in the sample studied.

Behavioral, Oxidative, and Biochemical Effects of Omega-3 on an Ovariectomized Rat Model of Menopause.

OBJECTIVES: Menopause induces changes in neuronal transmission, leading to anxiety and depression. Changes in the brain's glutamate levels cause psychological behavior in postmenopausal women. Omega-3 has been studied to improve some of these behaviors. METHODS: Twenty-four female Wistar rats were divided into four groups: sham-operated treated with water (SO-W), sham-operated treated with omega-3 (SO-O), ovariectomized (OVX) treated with water (OVX-W), and bilateral OVX treated with omega-3 (OVX-O). These treatments were performed for 20 days via gavage, before and after surgery, totaling 40 days. RESULTS: In the forced swimming, elevated plus-maze, and open field tests to assess behaviors, such as depression and anxiety, omega-3 improved these behaviors in both treated groups. The levels of thiobarbituric acid reactive substances (TBARS) in the brain were not different between the groups; however, there was a significant decrease in the catalase activity in the SO-O group compared with the SO-W group (P < 0.05). The glutamate level in the cerebrospinal fluid (CSF) was elevated in the SO-O group (P < 0.001) but not in the OVX-W or OVX-O groups. CONCLUSIONS: These results bring novel data when related to the glutamatergic system in the SO-O group. This has suggested that the action mechanism of omega-3 was not dependent on glutamate levels in the CSF of the OVX group, but it played a regulatory role in the sham-operated animals. To confirm this, more studies are needed to explore this field when relating to the estrogen and glutamate receptor changes in specific brain regions.

The genetic influence of the brain-derived neurotrophic factor Val66Met polymorphism in chronic low back pain

Abstract Background: The Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene is a potential biomarker of vulnerability to pain. Thus, the present study aimed to investigate the association of this polymorphism with clinical and biopsychosocial factors in patients with chronic low back pain (CLBP). Methods: A total of 107 individuals with CLBP answered questionnaires that were validated and adapted for the Brazilian population, including the Brief Inventory of Pain, the Central Sensitization Inventory, the Roland Morris Disability Questionnaire, the Tampa Scale for Kinesiophobia, the Pain Catastrophizing Scale, the Survey of Pain Attitude-Brief, and the Hospital Anxiety and Depression Scale. All of the subjects were genotyped for the BDNF Val66Met polymorphism. Results: The sample showed moderate scores of disability, central sensitization, and kinesiophobia, in addition to mild anxiety, hopelessness, and ruminant thoughts. No significant association was observed between the Val66Met polymorphism and the variables analyzed. Besides, there was no relationship between the BDNF Val66Met polymorphism with CSI, catastrophization, or disabilities that were generated by CLBP. Conclusions: The results showed that the Val66Met polymorphism of the BDNF gene was not associated with clinical and biopsychosocial characteristics of CLBP in the sample studied.

Analgesic effects of the CTK 01512-2 toxin in different models of orofacial pain in rats.

BACKGROUND: Orofacial pain is clinically challenging, having therapeutic failures and side effects. This study evaluated the antinociceptive activities of the CTK 01512-2 toxin, the TRPA1 channel antagonist, and the selective inhibitor of the N-type voltage-gated calcium channels (N-type VGCC), in different pain models. MATERIALS AND METHODS: The trigeminal ganglia were stimulated in vitro with capsaicin. The in vivo models received subcutaneous (sc) injections of formalin into the upper lip of the rats, Freund's Complete Adjuvant (FCA) into the temporomandibular joint (TMJ), and infraorbital nerve constrictions (IONC). CTK 01512-2 at concentrations of 30, 100, and 300 pmol/site, intrathecally (ith), and MVIIA at 10, 30, and 100 pmol/site in the formalin test, guided the doses for the models. The glutamate levels in the CSF of the rats that were submitted to IONC were analyzed. RESULTS: CTK 01512-2 decreased the nociceptive behavior in the inflammatory phase of the formalin test (65.94 ± 7.35%) and MVIIA in the neurogenic phase (81.23 ± 3.36%). CTK 01512-2 reduced facial grooming with FCA in the TMJ (96.7 ± 1.6%), and in the IONC neuropathy model, it decreased heat hyperalgesia (100%) and cold hyperalgesia (81.61 ± 9.02%). The levels of glutamate in the trigeminal ganglia in vitro (81.40 ± 8.59%) and in the CSF in vivo (70.0 ± 9.2%) were reduced. CONCLUSIONS: The roles of TRPA1 in pain transduction and the performance of CTK 01512-2 in the inhibition of the N-type VGCCs were reinforced. This dual activity may represent an advantage in clinical treatments.