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In Parkinson's disease and its models, abnormal rates and patterns of GPe\u2010STN network activity are linked to motor dysfunction. Following the loss of dopamine, the activities of GPe and STN neurons become more temporally offset and strongly correlated with cortical oscillations below 40\u00a0Hz. Previous studies utilized cortical slow\u2010wave activity and\/or cortical activation (ACT) under anaesthesia to probe the mechanisms underlying the normal and pathological patterning of basal ganglia activity. Here, we combined this approach with <jats:italic>in vivo<\/jats:italic> optogenetic inhibition to identify and interrupt the activity of D2 dopamine receptor\u2010expressing striatal projection neurons (D2\u2010SPNs), parvalbumin\u2010expressing prototypic GPe (PV GPe) neurons, and STN neurons. We found that, in dopamine\u2010depleted mice, (1) the firing rate of D2\u2010SPNs was elevated, especially during cortical ACT, (2) abnormal phasic suppression of PV GPe neuron activity was ameliorated by optogenetic inhibition of coincident D2\u2010SPN activity, (3) autonomous PV GPe neuron firing <jats:italic>ex vivo<\/jats:italic> was upregulated, presumably through homeostatic mechanisms, (4) STN neurons were not hyperactive, despite being disinhibited, (5) optogenetic inhibition of the STN exacerbated abnormal GPe activity, and (6) exaggerated beta band activity was not present in the cortex or GPe\u2010STN network. Together with recent studies, these data suggest that in dopamine\u2010depleted mice abnormally correlated and temporally offset PV GPe and STN neuron activity is generated in part by elevated striatopallidal transmission, while compensatory plasticity prevents STN hyperactivity and limits cortical entrainment.<\/jats:p><\/jats:sec>","DOI":"10.1113\/jp279232","type":"journal-article","created":{"date-parts":[[2020,2,29]],"date-time":"2020-02-29T09:23:51Z","timestamp":1582968231000},"page":"1897-1927","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Dysregulation of external globus pallidus\u2010subthalamic nucleus network dynamics in parkinsonian mice during cortical slow\u2010wave activity and activation"],"prefix":"10.1113","volume":"598","author":[{"given":"Ryan F.","family":"Kovaleski","sequence":"first","affiliation":[{"name":"Department of Physiology, Feinberg School of Medicine Northwestern University  Chicago IL 60611 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua W.","family":"Callahan","sequence":"additional","affiliation":[{"name":"Department of Physiology, Feinberg School of Medicine Northwestern University  Chicago IL 60611 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marine","family":"Chazalon","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux &amp; CNRS UMR 5293 Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives  Bordeaux F\u201033000 France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L.","family":"Wokosin","sequence":"additional","affiliation":[{"name":"Department of Physiology, Feinberg School of Medicine Northwestern University  Chicago IL 60611 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2623-6375","authenticated-orcid":false,"given":"J\u00e9r\u00f4me","family":"Baufreton","sequence":"additional","affiliation":[{"name":"Universit\u00e9 de Bordeaux &amp; CNRS UMR 5293 Institut des Maladies Neurod\u00e9g\u00e9n\u00e9ratives  Bordeaux F\u201033000 France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9759-0163","authenticated-orcid":false,"given":"Mark D.","family":"Bevan","sequence":"additional","affiliation":[{"name":"Department of Physiology, Feinberg School of Medicine Northwestern University  Chicago IL 60611 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