{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T18:41:38Z","timestamp":1789497698763,"version":"build-2803163510"},"reference-count":56,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2019,12,12]],"date-time":"2019-12-12T00:00:00Z","timestamp":1576108800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2020,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background and Purpose<\/jats:title>\n                    <jats:p>Chronic inflammation may play a role in the pathogenesis of Parkinson's disease (PD). Noradrenaline is an endogenous neurotransmitter with anti\u2010inflammatory properties. In the present investigation, we assessed the immunomodulatory and neuroprotective efficacy of pharmacologically targeting the CNS noradrenergic system in a rat model of PD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Experimental Approach<\/jats:title>\n                    <jats:p>\n                      The impact of treatment with the \u03b2\n                      <jats:sub>2<\/jats:sub>\n                      \u2010adrenoceptor agonists clenbuterol and formoterol was assessed in the intranigral LPS rat model of PD. The immunomodulatory potential of formoterol to influence the CNS response to systemic inflammation was also assessed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key Results<\/jats:title>\n                    <jats:p>\n                      LPS\u2010induced deficits in motor function (akinesia and forelimb\u2010use asymmetry) and nigrostriatal dopamine loss were rescued by both agents. Treatment with the noradrenaline reuptake inhibitor atomoxetine reduced striatal dopamine loss and motor deficits following intranigral LPS injection. Co\u2010treatment with the \u03b2\n                      <jats:sub>2<\/jats:sub>\n                      \u2010adrenoceptor antagonist ICI 118,551 attenuated the protective effects of atomoxetine. Systemic LPS challenge exacerbated reactive microgliosis, IL\u20101\u03b2 production, dopamine cell loss in the substantia nigra, nerve terminal degeneration in the striatum, and associated motor impairments in animals that previously received intranigral LPS. This exacerbation was attenuated by formoterol treatment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion and Implications<\/jats:title>\n                    <jats:p>\n                      The results indicate that pharmacologically targeting \u03b2\n                      <jats:sub>2<\/jats:sub>\n                      \u2010adrenoceptors has the propensity to regulate the neuroinflammatory phenotype\n                      <jats:italic>in vivo<\/jats:italic>\n                      and may be a potential neuroprotective strategy where inflammation contributes to the progression of dopaminergic neurodegeneration. In accordance with this, clinical agents such as \u03b2\n                      <jats:sub>2<\/jats:sub>\n                      \u2010adrenoceptor agonists may prove useful as immunomodulatory agents in the treatment of neurodegenerative conditions associated with brain inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.14862","type":"journal-article","created":{"date-parts":[[2019,9,11]],"date-time":"2019-09-11T03:14:10Z","timestamp":1568171650000},"page":"282-297","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Pharmacological targeting of \u03b2\n                    <sub>2<\/sub>\n                    \u2010adrenoceptors is neuroprotective in the LPS inflammatory rat model of Parkinson's disease"],"prefix":"10.1111","volume":"177","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2472-7795","authenticated-orcid":false,"given":"Eoin","family":"O'Neill","sequence":"first","affiliation":[{"name":"Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience Trinity College Dublin  Dublin 2 Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin D.","family":"Yssel","sequence":"additional","affiliation":[{"name":"Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience Trinity College Dublin  Dublin 2 Ireland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caoimhe","family":"McNamara","sequence":"additional","affiliation":[{"name":"Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences and Trinity College Institute of Neuroscience Trinity College Dublin  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