Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network
Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2019-08, Vol.116 (32), p.16095-16104 |
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| creator | Cagnan, Hayriye Mallet, Nicolas Moll, Christian K. E. Gulberti, Alessandro Holt, Abbey B. Westphal, Manfred Gerloff, Christian Engel, Andreas K. Hamel, Wolfgang Magill, Peter J. Brown, Peter Sharott, Andrew |
| description | Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/maintenance of excessive beta oscillations in parkinsonism. |
| doi_str_mv | 10.1073/pnas.1819975116 |
| format | Article |
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E. ; Gulberti, Alessandro ; Holt, Abbey B. ; Westphal, Manfred ; Gerloff, Christian ; Engel, Andreas K. ; Hamel, Wolfgang ; Magill, Peter J. ; Brown, Peter ; Sharott, Andrew</creator><creatorcontrib>Cagnan, Hayriye ; Mallet, Nicolas ; Moll, Christian K. E. ; Gulberti, Alessandro ; Holt, Abbey B. ; Westphal, Manfred ; Gerloff, Christian ; Engel, Andreas K. ; Hamel, Wolfgang ; Magill, Peter J. ; Brown, Peter ; Sharott, Andrew</creatorcontrib><description>Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/maintenance of excessive beta oscillations in parkinsonism.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1819975116</identifier><identifier>PMID: 31341079</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Action potential ; Action Potentials ; Aged ; Animals ; Basal ganglia ; Basal Ganglia - physiopathology ; Beta Rhythm - physiology ; Biological Sciences ; Bursts ; Central nervous system diseases ; Cerebral Cortex - physiopathology ; Circuits ; Cortex ; EEG ; Electrical stimuli ; Electroencephalography ; Evolution ; Female ; Firing pattern ; Firing rate ; Frequency dependence ; Ganglia ; Globus pallidus ; Humans ; Life Sciences ; Locking ; Male ; Movement disorders ; Neostriatum ; Neurobiology ; Neurodegenerative diseases ; Neurons ; Neurons - physiology ; Neurons and Cognition ; Oscillations ; Parkinson Disease - physiopathology ; Parkinson's disease ; PNAS Plus ; Rats ; Solitary tract nucleus ; Subthalamic nucleus ; Synchronism ; Synchronization ; Time Factors</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2019-08, Vol.116 (32), p.16095-16104</ispartof><rights>Copyright © 2019 the Author(s). Published by PNAS.</rights><rights>Copyright National Academy of Sciences Aug 6, 2019</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>Copyright © 2019 the Author(s). Published by PNAS. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-2c8cdecb4b0f41867aabfd2248ce3f563330141047dc367f0befcc219a2d1c663</citedby><cites>FETCH-LOGICAL-c477t-2c8cdecb4b0f41867aabfd2248ce3f563330141047dc367f0befcc219a2d1c663</cites><orcidid>0000-0002-6484-8882 ; 0000-0002-1594-3349 ; 0000-0002-1641-115X ; 0000-0002-1152-1114 ; 0000-0003-2904-4384 ; 0000-0003-0557-3935</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/26848469$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/26848469$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27922,27923,53789,53791,58015,58248</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31341079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-02399888$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Cagnan, Hayriye</creatorcontrib><creatorcontrib>Mallet, Nicolas</creatorcontrib><creatorcontrib>Moll, Christian K. E.</creatorcontrib><creatorcontrib>Gulberti, Alessandro</creatorcontrib><creatorcontrib>Holt, Abbey B.</creatorcontrib><creatorcontrib>Westphal, Manfred</creatorcontrib><creatorcontrib>Gerloff, Christian</creatorcontrib><creatorcontrib>Engel, Andreas K.</creatorcontrib><creatorcontrib>Hamel, Wolfgang</creatorcontrib><creatorcontrib>Magill, Peter J.</creatorcontrib><creatorcontrib>Brown, Peter</creatorcontrib><creatorcontrib>Sharott, Andrew</creatorcontrib><title>Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/maintenance of excessive beta oscillations in parkinsonism.</description><subject>Action potential</subject><subject>Action Potentials</subject><subject>Aged</subject><subject>Animals</subject><subject>Basal ganglia</subject><subject>Basal Ganglia - physiopathology</subject><subject>Beta Rhythm - physiology</subject><subject>Biological Sciences</subject><subject>Bursts</subject><subject>Central nervous system diseases</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Circuits</subject><subject>Cortex</subject><subject>EEG</subject><subject>Electrical stimuli</subject><subject>Electroencephalography</subject><subject>Evolution</subject><subject>Female</subject><subject>Firing pattern</subject><subject>Firing rate</subject><subject>Frequency dependence</subject><subject>Ganglia</subject><subject>Globus pallidus</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Locking</subject><subject>Male</subject><subject>Movement disorders</subject><subject>Neostriatum</subject><subject>Neurobiology</subject><subject>Neurodegenerative diseases</subject><subject>Neurons</subject><subject>Neurons - physiology</subject><subject>Neurons and Cognition</subject><subject>Oscillations</subject><subject>Parkinson Disease - physiopathology</subject><subject>Parkinson's disease</subject><subject>PNAS Plus</subject><subject>Rats</subject><subject>Solitary tract nucleus</subject><subject>Subthalamic nucleus</subject><subject>Synchronism</subject><subject>Synchronization</subject><subject>Time Factors</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1vEzEQxS0EoqFw5gSyxAUO244_4rUvlaoKKFIkLkXiZnm93sTpxl5sbxD_PY5SAvRky_N7b2b8EHpN4IJAyy6nYPIFkUSpdkmIeIIWBBRpBFfwFC0AaNtITvkZepHzFgDUUsJzdMYI41WvFuj7ndtNMZkRu30c5-JjwHHAnSsGd3PKJWMfcNk4PJl070OOwZuAbUzF26oyocedyfW2NmE9eoODKz9jun-Jng1mzO7Vw3mOvn36eHdz26y-fv5yc71qLG_b0lArbe9sxzsYOJGiNaYbekq5tI4NS8EYA1Jn5W1vmWgH6NxgLSXK0J5YIdg5ujr6TnO3c711odRt9JT8zqRfOhqv_68Ev9HruNdCKAAG1eDD0WDzSHZ7vdKHN6BMKSnlnlT2_UOzFH_MLhe989m6cTTBxTlrSgWvs5PlwfbdI3Qb5xTqV1SqpZRQyVWlLo-UTTHn5IbTBAT0IWF9SFj_Tbgq3v6774n_E2kF3hyBbS4xnepUSC65UOw3pDasbQ</recordid><startdate>20190806</startdate><enddate>20190806</enddate><creator>Cagnan, Hayriye</creator><creator>Mallet, Nicolas</creator><creator>Moll, Christian K. 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E.</au><au>Gulberti, Alessandro</au><au>Holt, Abbey B.</au><au>Westphal, Manfred</au><au>Gerloff, Christian</au><au>Engel, Andreas K.</au><au>Hamel, Wolfgang</au><au>Magill, Peter J.</au><au>Brown, Peter</au><au>Sharott, Andrew</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2019-08-06</date><risdate>2019</risdate><volume>116</volume><issue>32</issue><spage>16095</spage><epage>16104</epage><pages>16095-16104</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>Beta frequency oscillations (15 to 35 Hz) in cortical and basal ganglia circuits become abnormally synchronized in Parkinson’s disease (PD). How excessive beta oscillations emerge in these circuits is unclear. We addressed this issue by defining the firing properties of basal ganglia neurons around the emergence of cortical beta bursts (β bursts), transient (50 to 350 ms) increases in the beta amplitude of cortical signals. In PD patients, the phase locking of background spiking activity in the subthalamic nucleus (STN) to frontal electroencephalograms preceded the onset and followed the temporal profile of cortical β bursts, with conditions of synchronization consistent within and across bursts. Neuronal ensemble recordings in multiple basal ganglia structures of parkinsonian rats revealed that these dynamics were recapitulated in STN, but also in external globus pallidus and striatum. The onset of consistent phase-locking conditions was preceded by abrupt phase slips between cortical and basal ganglia ensemble signals. Single-unit recordings demonstrated that ensemble-level properties of synchronization were not underlain by changes in firing rate but, rather, by the timing of action potentials in relation to cortical oscillation phase. Notably, the preferred angle of phase-locked action potential firing in each basal ganglia structure was shifted during burst initiation, then maintained stable phase relations during the burst. Subthalamic, pallidal, and striatal neurons engaged and disengaged with cortical β bursts to different extents and timings. The temporal evolution of cortical and basal ganglia synchronization is cell type-selective, which could be key for the generation/maintenance of excessive beta oscillations in parkinsonism.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>31341079</pmid><doi>10.1073/pnas.1819975116</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-6484-8882</orcidid><orcidid>https://orcid.org/0000-0002-1594-3349</orcidid><orcidid>https://orcid.org/0000-0002-1641-115X</orcidid><orcidid>https://orcid.org/0000-0002-1152-1114</orcidid><orcidid>https://orcid.org/0000-0003-2904-4384</orcidid><orcidid>https://orcid.org/0000-0003-0557-3935</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Action potential Action Potentials Aged Animals Basal ganglia Basal Ganglia - physiopathology Beta Rhythm - physiology Biological Sciences Bursts Central nervous system diseases Cerebral Cortex - physiopathology Circuits Cortex EEG Electrical stimuli Electroencephalography Evolution Female Firing pattern Firing rate Frequency dependence Ganglia Globus pallidus Humans Life Sciences Locking Male Movement disorders Neostriatum Neurobiology Neurodegenerative diseases Neurons Neurons - physiology Neurons and Cognition Oscillations Parkinson Disease - physiopathology Parkinson's disease PNAS Plus Rats Solitary tract nucleus Subthalamic nucleus Synchronism Synchronization Time Factors |
| title | Temporal evolution of beta bursts in the parkinsonian cortical and basal ganglia network |
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