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10.1523/JNEUROSCI.4036-14.2015 http://scihub22266oqcxt.onion/10.1523/JNEUROSCI.4036-14.2015 C4452552!4452552!26041913     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26041913&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 500 Internal Server Error in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Neurosci 2015 ; 35 (22): 8442-50 Nephropedia Template TP {{tp|p=26041913|t=2015. Microglia Disrupt Mesolimbic Reward Circuitry in Chronic Pain |pdf=|usr=}}{{26041913}} gab.com Text Microglia Disrupt Mesolimbic Reward Circuitry in Chronic Pain JO: J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26041913 #FOAvip Chronic pain attenuates midbrain dopamine (DA) transmission, as evidenced by a decrease in opioid-evoked DA release in the ventral striatum, suggesting that the occurrence of chronic pain impairs reward-related behaviors. However, mechanisms by which pain modifies DA transmission remain elusive. Using in vivo microdialysis and microinjection of drugs into the mesolimbic DA system, we demonstrate in mice and rats that microglial activation in the VTA compromises not only opioid-evoked release of DA, but also other DA-stimulating drugs, such as cocaine. Our data show that loss of stimulated extracellular DA is due to impaired chloride homeostasis in midbrain GABAergic interneurons. Treatment with minocycline or interfering with BDNF signaling restored chloride transport within these neurons and recovered DA-dependent reward behavior. Our findings demonstrate that a peripheral nerve injury causes activated microglia within reward circuitry that result in disruption of dopaminergic signaling and reward behavior. These results have broad implications that are not restricted to the problem of pain, but are also relevant to affective disorders associated with disruption of reward circuitry. Because chronic pain causes glial activation in areas of the CNS important for mood and affect, our findings may translate to other disorders, including anxiety and depression, that demonstrate high comorbidity with chronic pain. Twit Text FOAVip Microglia Disrupt Mesolimbic Reward Circuitry in Chronic Pain ????J Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=26041913 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26041913 #FOAvip English Wikipedia <ref>{{Cite pmid|26041913}}</ref> Microglia Disrupt Mesolimbic Reward Circuitry in Chronic Pain #MMPMID26041913 Taylor AMW; Castonguay A; Taylor AJ; Murphy NP; Ghogha A; Cook C; Xue L; Olmstead MC; De Koninck Y; Evans CJ; Cahill CM J Neurosci 2015[Jun]; 35 (22): 8442-50 PMID26041913show ga Chronic pain attenuates midbrain dopamine (DA) transmission, as evidenced by a decrease in opioid-evoked DA release in the ventral striatum, suggesting that the occurrence of chronic pain impairs reward-related behaviors. However, mechanisms by which pain modifies DA transmission remain elusive. Using in vivo microdialysis and microinjection of drugs into the mesolimbic DA system, we demonstrate in mice and rats that microglial activation in the VTA compromises not only opioid-evoked release of DA, but also other DA-stimulating drugs, such as cocaine. Our data show that loss of stimulated extracellular DA is due to impaired chloride homeostasis in midbrain GABAergic interneurons. Treatment with minocycline or interfering with BDNF signaling restored chloride transport within these neurons and recovered DA-dependent reward behavior. Our findings demonstrate that a peripheral nerve injury causes activated microglia within reward circuitry that result in disruption of dopaminergic signaling and reward behavior. These results have broad implications that are not restricted to the problem of pain, but are also relevant to affective disorders associated with disruption of reward circuitry. Because chronic pain causes glial activation in areas of the CNS important for mood and affect, our findings may translate to other disorders, including anxiety and depression, that demonstrate high comorbidity with chronic pain. äMicroglia Disrupt Mesolimbic Reward Circuitry in Chronic Pain (epmc).pdf DeepDyve Pubget Overpricing