{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T08:02:12Z","timestamp":1790496132223,"version":"4.1.0"},"reference-count":46,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2011,12,1]],"date-time":"2011-12-01T00:00:00Z","timestamp":1322697600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p>Dopamine is related to behaviour (including arousal, motivation and motor control of locomotion), and its turnover in the brain is increased during exercise. We examined the hypothesis that dopamine D<jats:sub>2<\/jats:sub> receptors contribute to exercise hyperpnoea via central neural pathways using the D<jats:sub>2<\/jats:sub>\u2010like receptor antagonist, raclopride. We simultaneously measured ventilation and pulmonary gas exchange for the first time in mice. Mice injected with saline and raclopride (2 mg (kg body weight)<jats:sup>\u22121<\/jats:sup>; <jats:sc>i.p<\/jats:sc>.) were compared for respiratory responses to constant\u2010load exercise at 6 m min<jats:sup>\u22121<\/jats:sup>. Each mouse was set in an airtight treadmill chamber. In the resting state, raclopride\u2010treated mice had reduced respiratory frequency (<jats:italic>f<\/jats:italic><jats:sub>R<\/jats:sub>) and minute ventilation (\n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu1.gif\" xlink:title=\"inline image\"\/>) compared with saline\u2010treated mice, but arterial \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu2.gif\" xlink:title=\"inline image\"\/> and pulmonary gas exchange were not affected, showing that alveolar ventilation was maintained. Inhalation of hyperoxic gas maintained \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu3.gif\" xlink:title=\"inline image\"\/> in saline\u2010treated mice, and hypercapnic ventilatory responses between the two groups were similar. Treadmill exercise produced an abrupt increase in \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu4.gif\" xlink:title=\"inline image\"\/> to a maximal level within 1 min and declined to a steady\u2010state level in both groups. Raclopride\u2010treated mice had reduced <jats:italic>f<\/jats:italic><jats:sub>R<\/jats:sub> and \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu5.gif\" xlink:title=\"inline image\"\/> compared with saline\u2010treated mice during steady states, but showed a similar increase in <jats:italic>f<\/jats:italic><jats:sub>R<\/jats:sub> and \n<jats:inline-graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"graphic\/EPH_1009_mu6.gif\" xlink:title=\"inline image\"\/> at exercise onset. Minute ventilation in the steady state was controlled, along with the increase in pulmonary O<jats:sub>2<\/jats:sub> uptake in both groups, but was lowered in raclopride\u2010treated mice. Thus, D<jats:sub>2<\/jats:sub> receptors participate in resting breathing patterns to raise <jats:italic>f<\/jats:italic><jats:sub>R<\/jats:sub> and exercise hyperpnoea in the steady state, probably through behavioural control and not central motor command, at exercise onset.<\/jats:p>","DOI":"10.1113\/expphysiol.2011.062703","type":"journal-article","created":{"date-parts":[[2011,11,1]],"date-time":"2011-11-01T03:23:40Z","timestamp":1320117820000},"page":"228-238","source":"Crossref","is-referenced-by-count":9,"title":["Dopaminergic modulation of exercise hyperpnoea via D<sub>2<\/sub> receptors in 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