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Conference Paper: Investigating inflammatory responses in a corticosterone-induced model of depression

TitleInvestigating inflammatory responses in a corticosterone-induced model of depression
Authors
Issue Date2021
Citation
The 15th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders (AD/PD™ 2021), Virtual Conference, 9-14 March 2021, Poster 662 How to Cite?
AbstractAims: In this project, we aim to use a corticosterone-induced model to investigate the inflammatory responses that occur in depression, which may further increase the risk of developing neurodegenerative diseases in the future. Methods: Corticosterone was administered daily to Sprague-Dawley (SD) rats for 14, 21 or 28 days. Afterwards, a series of behavioral tests were performed to assess their anxiety, memory and depressive behaviors. Different brain regions and tissues were collected to conduct immunohistochemical analysis and qPCR. Results: Following 21 days of corticosterone administration, subjects displayed decreased adrenal and bodyweight, indicating successful absorption of corticosterone into the system. From the Open Field test, we observed the development of anxiety-like behaviors. Additionally, in the 21-day time point, we observed the development of systemic inflammation from qPCR analysis, but no significant neuroinflammation. Conclusions: In these experiments, we utilized a corticosterone-induced model of depression to investigate the possible inflammatory links between depression and neurodegenerative diseases. 21 days of corticosterone treatment was sufficient to lead to the development of anxiety-like symptoms, as well as leading to the development of systemic inflammation, yet no neuroinflammation. This is the first time we have observed this phenomenon, which deserves further investigation. Future work will be conducted to see how the inflammatory response changes over different durations of corticosterone treatment, and the impact this has on the brain. Acknowledgement: SLD is awarded by Hong Kong PhD Fellowship.
DescriptionTopic: Theme K: Psychiatric Symptoms in Neurodegenerative Diseases / K1. Disease Mechanisms, Pathophysiology - no. P662 / #1258
Persistent Identifierhttp://hdl.handle.net/10722/306102

 

DC FieldValueLanguage
dc.contributor.authorDUNNETT, SL-
dc.contributor.authorWANG, PH-
dc.contributor.authorChang, RCC-
dc.date.accessioned2021-10-20T10:18:49Z-
dc.date.available2021-10-20T10:18:49Z-
dc.date.issued2021-
dc.identifier.citationThe 15th International Conference on Alzheimer’s and Parkinson’s Diseases and related neurological disorders (AD/PD™ 2021), Virtual Conference, 9-14 March 2021, Poster 662-
dc.identifier.urihttp://hdl.handle.net/10722/306102-
dc.descriptionTopic: Theme K: Psychiatric Symptoms in Neurodegenerative Diseases / K1. Disease Mechanisms, Pathophysiology - no. P662 / #1258-
dc.description.abstractAims: In this project, we aim to use a corticosterone-induced model to investigate the inflammatory responses that occur in depression, which may further increase the risk of developing neurodegenerative diseases in the future. Methods: Corticosterone was administered daily to Sprague-Dawley (SD) rats for 14, 21 or 28 days. Afterwards, a series of behavioral tests were performed to assess their anxiety, memory and depressive behaviors. Different brain regions and tissues were collected to conduct immunohistochemical analysis and qPCR. Results: Following 21 days of corticosterone administration, subjects displayed decreased adrenal and bodyweight, indicating successful absorption of corticosterone into the system. From the Open Field test, we observed the development of anxiety-like behaviors. Additionally, in the 21-day time point, we observed the development of systemic inflammation from qPCR analysis, but no significant neuroinflammation. Conclusions: In these experiments, we utilized a corticosterone-induced model of depression to investigate the possible inflammatory links between depression and neurodegenerative diseases. 21 days of corticosterone treatment was sufficient to lead to the development of anxiety-like symptoms, as well as leading to the development of systemic inflammation, yet no neuroinflammation. This is the first time we have observed this phenomenon, which deserves further investigation. Future work will be conducted to see how the inflammatory response changes over different durations of corticosterone treatment, and the impact this has on the brain. Acknowledgement: SLD is awarded by Hong Kong PhD Fellowship.-
dc.languageeng-
dc.relation.ispartofThe 15th International Conference on Alzheimer’s Disease & Parkinson’s Disease 2021-
dc.titleInvestigating inflammatory responses in a corticosterone-induced model of depression-
dc.typeConference_Paper-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.hkuros326688-
dc.identifier.spagePoster 662-
dc.identifier.epagePoster 662-

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