Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity.
- Publisher:
- AMER ASSOC ADVANCEMENT SCIENCE
- Publication Type:
- Journal Article
- Citation:
- Sci Adv, 2023, 9, (25), pp. eade8247
- Issue Date:
- 2023-06-23
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Becchi, S | |
dc.contributor.author | Chieng, B | |
dc.contributor.author | Bradfield, LA | |
dc.contributor.author | Capellán, R | |
dc.contributor.author | Leung, BK | |
dc.contributor.author | Balleine, BW | |
dc.date.accessioned | 2024-01-15T04:48:35Z | |
dc.date.available | 2024-01-15T04:48:35Z | |
dc.date.issued | 2023-06-23 | |
dc.identifier.citation | Sci Adv, 2023, 9, (25), pp. eade8247 | |
dc.identifier.issn | 2375-2548 | |
dc.identifier.issn | 2375-2548 | |
dc.identifier.uri | http://hdl.handle.net/10453/174450 | |
dc.description.abstract | The loss of neurons in parafascicular thalamus (Pf) and their inputs to dorsomedial striatum (DMS) in Lewy body disease (LBD) and Parkinson's disease dementia (PDD) have been linked to the effects of neuroinflammation. We found that, in rats, these inputs were necessary for both the function of striatal cholinergic interneurons (CINs) and the flexible encoding of the action-outcome (AO) associations necessary for goal-directed action, producing a burst-pause pattern of CIN firing but only during the remapping elicited by a shift in AO contingency. Neuroinflammation in the Pf abolished these changes in CIN activity and goal-directed control after the shift in contingency. However, both effects were rescued by either the peripheral or the intra-DMS administration of selegiline, a monoamine oxidase B inhibitor that we found also enhances adenosine triphosphatase activity in CINs. These findings suggest a potential treatment for the cognitive deficits associated with neuroinflammation affecting the function of the Pf and related structures. | |
dc.format | Print-Electronic | |
dc.language | eng | |
dc.publisher | AMER ASSOC ADVANCEMENT SCIENCE | |
dc.relation.ispartof | Sci Adv | |
dc.relation.isbasedon | 10.1126/sciadv.ade8247 | |
dc.rights | info:eu-repo/semantics/openAccess | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Dementia | |
dc.subject.mesh | Neuroinflammatory Diseases | |
dc.subject.mesh | Cholinergic Neurons | |
dc.subject.mesh | Parkinson Disease | |
dc.subject.mesh | Corpus Striatum | |
dc.subject.mesh | Cholinergic Agents | |
dc.subject.mesh | Cognition | |
dc.subject.mesh | Corpus Striatum | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Parkinson Disease | |
dc.subject.mesh | Dementia | |
dc.subject.mesh | Cholinergic Agents | |
dc.subject.mesh | Cognition | |
dc.subject.mesh | Cholinergic Neurons | |
dc.subject.mesh | Neuroinflammatory Diseases | |
dc.subject.mesh | Rats | |
dc.subject.mesh | Animals | |
dc.subject.mesh | Dementia | |
dc.subject.mesh | Neuroinflammatory Diseases | |
dc.subject.mesh | Cholinergic Neurons | |
dc.subject.mesh | Parkinson Disease | |
dc.subject.mesh | Corpus Striatum | |
dc.subject.mesh | Cholinergic Agents | |
dc.subject.mesh | Cognition | |
dc.title | Cognitive effects of thalamostriatal degeneration are ameliorated by normalizing striatal cholinergic activity. | |
dc.type | Journal Article | |
utslib.citation.volume | 9 | |
utslib.location.activity | United States | |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
utslib.copyright.status | open_access | * |
dc.date.updated | 2024-01-15T04:48:27Z | |
pubs.issue | 25 | |
pubs.publication-status | Published | |
pubs.volume | 9 | |
utslib.citation.issue | 25 |
Abstract:
The loss of neurons in parafascicular thalamus (Pf) and their inputs to dorsomedial striatum (DMS) in Lewy body disease (LBD) and Parkinson's disease dementia (PDD) have been linked to the effects of neuroinflammation. We found that, in rats, these inputs were necessary for both the function of striatal cholinergic interneurons (CINs) and the flexible encoding of the action-outcome (AO) associations necessary for goal-directed action, producing a burst-pause pattern of CIN firing but only during the remapping elicited by a shift in AO contingency. Neuroinflammation in the Pf abolished these changes in CIN activity and goal-directed control after the shift in contingency. However, both effects were rescued by either the peripheral or the intra-DMS administration of selegiline, a monoamine oxidase B inhibitor that we found also enhances adenosine triphosphatase activity in CINs. These findings suggest a potential treatment for the cognitive deficits associated with neuroinflammation affecting the function of the Pf and related structures.
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