When good pain turns bad

Classically, pain is viewed as being mediated solely by neurons. However, recent research has shown that activated glial cells (astrocytes and microglia) within the spinal cord amplify pain. These nonneuronal cells play a major role in the creation and maintenance of pathological pain. Glia become activated by immune challenges (viral or bacterial infection) and by substances released by neurons within the pain pathway. Activated glia amplify pain by releasing proinflammatory cytokines. Taken together, research findings suggest a novel approach to human pain control that targets glia. In addition, it is likely that such glial-neuronal interactions are not unique to pain, but rather reflect a general rule of sensory processing.     

小胶质细胞在糖尿病视网膜病变发病机制中的作用

本文阐述近年来通过科学研究,科学工作者坚持科学精神,努力探索小胶质细胞在糖尿病视网膜病变发病机制中所起的作用,提出其可能通过炎症因子的刺激,释放炎症介质,参与免疫炎症反应,从而损伤视网膜血管。了解其作用机制,为糖尿病视网膜病变的防治提供了新的思路。     

Antiaggressive Effects of Zolpidem and Zopiclone in Agonistic Encounters Between Male Mice

The effects of benzodiazepines on various types of aggression have been extensively studied. These substances produce their pharmacological effects by allosterically modulating the action of GABA via specific recognition sites on the GABA_A receptor called omega 1 and omega 2. The antiaggressive profile of non‐benzodiazepine compounds that also act at omega sites, such as zopiclone (a non‐selective omega 1 and 2 ligand) and zolpidem (a selective omega 1 ligand) has been scarcely explored. In this study, we examined the action of zolpidem (0.75‐3 mg/kg, intraperitoneally) and zopiclone (1.5‐6 mg/kg), administered acutely or subchronically for 10 days, on agonistic behavior elicited by isolation in male mice. Individually housed mice were exposed to anosmic “standard opponents” 30 min after drug administration, and the encounters were videotaped and evaluated using an ethologically based analysis. Acute treatment with zopiclone produced a marked antiaggressive effect, reducing offensive behaviors (threat and attack) at all doses used (1.5, 3, and 6 mg/kg) without affecting immobility. Likewise, the intermediate dose of zolpidem (1.5 mg/kg) significantly decreased aggression in a specific manner, without altering immobility, whereas the highest dose (3 mg/kg) provoked a reduction of aggression accompanied by a weak (but significant) increase of immobility. With repeated treatment, no tolerance to the antiaggressive effects of zopiclone and zolpidem was developed. It is concluded that omega sites at the GABA_A receptor could be involved in the control of aggression. Aggr. Behav. 28:416–425, 2002. © 2002 Wiley‐Liss, Inc.