PMID- 22890077 OWN - NLM STAT- MEDLINE DCOM- 20130501 LR - 20220408 IS - 1873-7544 (Electronic) IS - 0306-4522 (Linking) VI - 223 DP - 2012 Oct 25 TI - Chronic restraint stress decreases glial fibrillary acidic protein and glutamate transporter in the periaqueductal gray matter. PG - 209-18 LID - S0306-4522(12)00827-5 [pii] LID - 10.1016/j.neuroscience.2012.08.007 [doi] AB - Stress affects brain activity and promotes long-term changes in multiple neural systems. Exposure to stressors causes substantial effects on the perception and response to pain. In several animal models, chronic stress produces lasting hyperalgesia. Postmortem studies of stress-related psychiatric disorders have demonstrated a decrease in the number of astrocytes and the level of glial fibrillary acidic protein (GFAP), a marker for astrocyte, in the cerebral cortex. Since astrocytes play vital roles in maintaining neuroplasticity via synapse maintenance and secretion of neurotrophins, impairment of astrocytes is thought to be involved in the neuropathology. In the present study we examined GFAP and excitatory amino acid transporter 2 (EAAT2) protein levels in the periaqueductal gray matter (PAG) after subacute and chronic restraint stresses to clarify changes in descending pain modulatory system in the rat with stress-induced hyperalgesia. Chronic restraint stress (6h/day for 3 weeks), but not subacute restraint stress (6h/day for 3 days), caused a marked mechanical hypersensitivity and aggressive behavior. The chronic restraint stress induced a significant decrease of GFAP protein level in the PAG (32.0 +/- 8.9% vs. control group, p<0.05). In immunohistochemical analysis the remarkable decrease of GFAP was observed in the ventrolateral PAG. The EAAT2 protein level in the 3 weeks stress group (79.6 +/- 6.8%) was significantly lower compared to that in the control group (100.0 +/- 6.1%, p<0.05). In contrast there was no significant difference in the GFAP and EAAT2 protein levels between the control and 3 days stress groups These findings suggest a dysfunction of the PAG that plays pivotal roles in the organization of strategies for coping with stressors and in pain modulation after chronic restraint stress. CI - Copyright (c) 2012 IBRO. Published by Elsevier Ltd. All rights reserved. FAU - Imbe, H AU - Imbe H AD - Department of Physiology, Wakayama Medical University, Kimiidera 811-1, Wakayama City 641-8509, Japan. imbe@wakayama-med.ac.jp FAU - Kimura, A AU - Kimura A FAU - Donishi, T AU - Donishi T FAU - Kaneoke, Y AU - Kaneoke Y LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20120810 PL - United States TA - Neuroscience JT - Neuroscience JID - 7605074 RN - 0 (Amino Acid Transport System X-AG) RN - 0 (Glial Fibrillary Acidic Protein) SB - IM MH - Aggression/psychology MH - Amino Acid Transport System X-AG/*metabolism MH - Animals MH - Gene Expression Regulation/*physiology MH - Glial Fibrillary Acidic Protein/*metabolism MH - Hyperalgesia/physiopathology MH - Male MH - Pain Threshold/physiology MH - Periaqueductal Gray/*metabolism MH - Rats MH - Rats, Sprague-Dawley MH - *Restraint, Physical MH - Synaptosomes/metabolism MH - Time Factors EDAT- 2012/08/15 06:00 MHDA- 2013/05/02 06:00 CRDT- 2012/08/15 06:00 PHST- 2012/03/30 00:00 [received] PHST- 2012/08/01 00:00 [revised] PHST- 2012/08/02 00:00 [accepted] PHST- 2012/08/15 06:00 [entrez] PHST- 2012/08/15 06:00 [pubmed] PHST- 2013/05/02 06:00 [medline] AID - S0306-4522(12)00827-5 [pii] AID - 10.1016/j.neuroscience.2012.08.007 [doi] PST - ppublish SO - Neuroscience. 2012 Oct 25;223:209-18. doi: 10.1016/j.neuroscience.2012.08.007. Epub 2012 Aug 10.