In vivo evaluation of the hippocampal glutamate, GABA and the BDNF levels associated with spatial memory performance in a rodent model of neuropathic pain.

BACKGROUND: Patients with chronic pain usually suffer from learning and memory impairment which may significantly decrease their quality of life. Despite laboratory and clinical studies, the mechanism underlying this memory impairment remains elusive. We evaluated the effect of chronic pain on the glutamate and GABA levels and BDNF expression in the CA1 region of hippocampus as a possible explanation for memory impairment related to neuropathic pain. METHODS: In this respect, 30 male rats were randomly allocated to 3 groups as control, sham and neuropathic. Neuropathic pain was induced by a chronic constriction injury of the sciatic nerve (CCI) and mechanical allodynia and the spatial memory was assessed using the Von Frey filaments and Morris water maze respectively. To determine the potential mechanisms, the in vivo extracellular levels of glutamate and γ-aminobutyric acid (GABA) were measured by microdialysis and the brain-derived neurotrophic factor (BDNF) expression was determined by using western blots technique in the hippocampus on days 14 and 21 post-CCI. RESULTS: We showed that CCI impaired spatial learning and memory in Morris water maze (MWM) task. BDNF expression level and glutamate concentration significantly decreased in rats with chronic constriction injury of the sciatic nerve (P<0.001, F=7.3, F=23.23). In addition, GABA increased in hippocampal CA1 region (P<0.001, F=39.2) when the pain threshold was minimum. Nevertheless, these changes reversed while pain was relieved spontaneously. CONCLUSION: Chronic pain induced by constriction of the sciatic nerve impairs the spatial learning and memory function in rats. This effect exerts through the increase in GABA concentration and decrease in the glutamate and BDNF levels in the CA1 region of the hippocampus.

Association of serum alpha-tocopherol, retinol and ascorbic acid with the risk of cataract development.

OBJECTIVE: Several studies on cataract have suggested that antioxidant micronutrients such as alpha-tocopherol, retinol and ascorbic acid may help to protect against cataractogenesis. Our objective was to determine the serum concentration of these antioxidant vitamins in subjects with cataract to see if there is any correlation between the levels of essential vitamins and the development of cataract. METHODS: The study was performed on a total of 88 patients and healthy controls who were given physical examinations that included a complete eye examination. Ascorbic acid was measured in serum with UV/Vis spectrophotometry, and fat-soluble vitamins were measured in serum by high-performance liquid chromatography according to previously published methods. RESULTS: The mean serum concentration of alpha-tocopherol in patients (9.16 +/- 2.53 microg/ml) with cataract was lower than in the control group (p < 0.001). Patients had a moderately lower ascorbic acid concentration than the control group, which was not statistically significant. The subjects' serum retinol levels were similar to control group levels and not statistically significant. CONCLUSION: While this is a small-scale case study it can nonetheless be viewed as presenting support to help narrow the possibility that antioxidative agents may play a role in delaying cataract formation.