Publications (2)5.78 Total impact
Article: Stress-induced hyperalgesia is associated with a reduced and delayed GABA inhibitory control that enhances post-synaptic NMDA receptor activation in the spinal cord.[show abstract] [hide abstract]
ABSTRACT: GABA and glutamate are both affected by stress and are involved in nociception. Thus, we determined whether stress-induced enhancement of inflammatory hyperalgesia is mediated by an imbalance between glutamate and GABA neurotransmission. Male rats were subjected daily to 10 to 20 minutes per day of either forced swimming (FS) or sham swimming for 3 consecutive days; nonconditioned rats served as controls. Some rats were treated i.p. with ketamine (5 mg/kg), diazepam (2 mg/kg), flumazenil (0.1 mg/kg), or vehicle (0.9% NaCl), 30 to 60 minutes before each conditioning session or nociception assessment. Pain behavior, spinal nociceptive neuronal activation and GABA and glutamate release were respectively evaluated by the formalin test, the expression of c-Fos and in vivo microdialysis of superficial laminae of the lumbar spinal cord, 48 hours after the last conditioning session. Nitric oxide metabolites (NO(x)) were determined as markers of post-synaptic NMDA receptor activation. FS stress enhanced formalin-induced hyperalgesia, increased pain-elicited c-Fos expression, decreased basal and delayed pain-induced GABA release, and increased basal and induced glutamate release. Hyperalgesia and c-Fos overexpression were blocked only by prestress treatment with diazepam and post-stress treatment with ketamine, whereas changes in GABA and glutamate release were reversed by prestress treatment with diazepam. Diazepam effects were blocked by flumazenil. NO(x) increased in lumbar spinal cord of FS rats by a mechanism antagonized by ketamine. Thus, stress-induced hyperalgesia is initiated by a decreased and delayed GABA release and GABA-A receptor activation, whereas it is maintained by increased glutamate release and NMDA glutamate receptor activation at the spinal level.Pain 05/2011; 152(8):1909-22. · 5.78 Impact Factor
Article: [Association between HSV-2 infection and serum anti-rat brain antibodies in patients with autism].[show abstract] [hide abstract]
ABSTRACT: Some cases of autism could be linked to viral infections able to induce autoimmune mechanisms directed against the encephalon. Neurothophic virus infections in animals are associated with clinical signs that are similar to those observed in neurodevelopment disorders. Thus, in this study, we determined the co-existence of antibodies against nerve tissue and viruses with neurothophic competence (HSV-1/2, Epstein-Barr-EBV, cytomegalovirus, measles and rubella) in serum of forty autistic children and forty healthy children. The presence of antibodies against nerve tissue was detected in slices of rat encephalic tissue by indirect immunofluorescence. The levels of anti-viral IgG and IgM antibodies were measured by indirect ELISA. The proportion of autistics with anti-encephalon IgG antibodies (77% anti-amygdala, 70% anti-caudate nucleus, 47.5% anti-cerebellum y anti-brain stem, 45% anti-hippocampus, 40% anti-corpus callosum and 17,5% anti-cortex) was significantly greater than that of controls (10% anti- amygdala y 5% anti- cerebellum) and was directly related to the severity of the autism. The proportion of children with positive levels (greater than 1.1.mg/dL) for anti-HSV IgM antibodies (indicative of acute infection) was significantly greater in autistics (65%) than in healthy children (17.5%). Ninety six percent of the autistics with anti-HSV antibodies also had anti-encephalon antibodies, percentage that was significantly greater than that of autistics negative to the anti-HSV-antibody (43%). In contrast, there were no significant differences for IgG and IgM antibodies for EBV, cytomegalovirus, measles and rubella. This suggests that autoimmunity against encephalic structures elicited by HSV infections could be involved in autism.Investigación clínica 09/2009; 50(3):315-26.