Stimulation-Produced Analgesia From the Occipital or Retrosplenial Cortex of Rats Involves Serotonergic and Opioid Mechanisms in the Anterior Pretectal Nucleus

The electrical stimulation of the occipital (OC) or retrosplenial (RSC) cortex produces antinociception in the rat tail-flick test. These cortices send inputs to the anterior pretectal nucleus (APtN) which is implicated in antinociception and nociception. At least muscarinic cholinergic, opioid, and serotonergic mechanisms in the APtN are involved in stimulation-produced antinociception (SPA) from the nucleus. In this study, the injection of 2% lidocaine (.25 mu L) or methysergide (40 and 80 ng/.25 mu L) into the APtN reduced the duration but did not change the intensity of SPA from the OC, whereas both duration and intensity of SPA from the RSC were significantly reduced in rats treated with lidocaine or naloxone (10 and 50 ng/.25 mu L), injected into the ANN. Naloxone or methysegide injected into the APtN was ineffective against SPA from the OC or RSC, respectively. Atropine (100 ng/.25 mu L) injected into the ANN was ineffective against SPA from either the OC or RSC. We conclude that the APtN acts as an intermediary for separate descending pain inhibitory pathways activated from the OC and RSC, utilizing at least serotonin and endogenous opioid as mediators in the nucleus. Perspective: Stimulation-induced antinociception from the retrosplenial or occipital cortex in the rat tail-flick test depends on the activation of separate descending pain inhibitory pathways that utilize the APtN as a relay station. (C) 2011 by the American Pain SocietyFAPESPCAPE

Depressed female smokers have higher levels of soluble tumor necrosis factor receptor 1

Aim: To examine clinical and biomarkers in depressed female smokers, in order to better clarify the process that link mood disorders, childhood trauma and smoking in women. Methods: The clinical sample comprised women with unipolar or bipolar depression, divided into subgroups of smokers and never-smoker. The control groups comprised two subgroups non-depressed women, separated into smokers and never-smokers. A structured questionnaire was used to assess socio-demographic and clinical data. The following scales were used: 17-item version Hamilton Depression Rating Scale, Hamilton Anxiety Rating scale (HAM-A), Sheehan disability scale, the Child Trauma Questionnaire. The following biomarkers were investigated: lipid profile, including total cholesterol, high-density lipoprotein cholesterol (HDLc), low-density lipoprotein cholesterol, triglycerides the Castelli's Risk indexes I and II; and cytokines, including interleukins (IL)-1β, IL-6, IL-10, IL-12, soluble tumor necrosis factor receptor 1 (sTNF-R1). Results: Depressed female smokers showed a number of significant positive correlations: emotional neglect and sTNF-R1 (p = 0.02); waist circumference and sTNF-R1 (p = 0.001); body mass index and sTNF-R1 (p < 0.01); HAM-A and sTNF-R1 (p = 0.03); IL-1β and sTNF-R1 (p < 0.01); IL-10 and sTNF-R1 (p = 0.001); IL-12 and sTNF-R1 (p < 0.01);Castelli index I and sTNF-R1 (p < 0.01); Castelli index II and sTNF-R1 (p < 0.01); and a significantly negative correlation between HDLc and sTNF-R1(p = 0.014). Conclusion: This study suggests that depressed female smokers who experienced more childhood trauma and had more anxiety symptoms are associated with the activation of inflammatory processes and alterations in components of lipid profile. Keywords: Tobacco use disorder, Depression, Inflammation, Metabolism, Child abus