File Download

There are no files associated with this item.

Conference Paper: Altered dendritic spine plasticity in a mouse depression model

TitleAltered dendritic spine plasticity in a mouse depression model
Authors
Issue Date2016
PublisherThe University of Hong Kong.
Citation
The 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 48, abstract no. P36 How to Cite?
AbstractDepressive disorder is a most prevalent psychiatric disorder worldwide and is estimated to be affecting 350 millions of the global population. In the prefrontal cortex (PFC) of depression patients, hypofunction is accompanied with structural deficits, including decreased cell number, neuronal atrophy and decreased number of spine synapses. In rodents, chronic stress exposure induces depressive-like behaviour and results in structural impairment of dendrites of layer 2/3 and 5 pyramidal neurons in PFC, including reduced dendritic spine density and atrophy of apical dendrites. However, it is unclear whether dendritic deficits contribute to depression development. Ketamine, a NMDA receptor blocker, is found to exert rapid, lasting antidepressant effect at a single, sub-anaesthetic dose. Ketamine can also rapidly reverse chronic stress-induced synaptic deficit. Yet, data on the effect of ketamine on dendritic spine plasticity in long-term is lacking. In this study, we used in vivo two-photon transcranial imaging of Thy1-YFP H line mice to investigate dendritic spine plasticity in the chronic restraint stress (CRS) depression model. We found that CRS increased dendritic spine elimination and reduced spine formation of layer V pyramidal neurons in the frontal association cortex. In addition, CRS-induced alterations in spine plasticity precede the onset of behavioural symptoms. Importantly, we found that ketamine treatment counteracted the effects of stress on dendritic spine plasticity. REFERENCES: 1. Duman, R. S., & Aghajanian, G. K. (2012). Synaptic dysfunction in depression: potential therapeutic targets. Science, 338(6103), 68-72. 2. Licznerski, P., & Duman, R. S. (2013). Remodeling of axo-spinous synapses in the pathophysiology and treatment of depression. Neuroscience, 251, 33-50.
DescriptionConference Theme: Nature and Nurture in Brain Functions
Persistent Identifierhttp://hdl.handle.net/10722/231517

 

DC FieldValueLanguage
dc.contributor.authorNg, HLL-
dc.contributor.authorHuang, Y-
dc.contributor.authorChang, RCC-
dc.contributor.authorLai, SWC-
dc.date.accessioned2016-09-20T05:23:40Z-
dc.date.available2016-09-20T05:23:40Z-
dc.date.issued2016-
dc.identifier.citationThe 2016 Neuroscience Symposium and Annual Scientific Conference of the Hong Kong Society of Neurosciences, The University of Hong Kong, Hong Kong, 18 May 2016. In Programme Book, 2016, p. 48, abstract no. P36-
dc.identifier.urihttp://hdl.handle.net/10722/231517-
dc.descriptionConference Theme: Nature and Nurture in Brain Functions-
dc.description.abstractDepressive disorder is a most prevalent psychiatric disorder worldwide and is estimated to be affecting 350 millions of the global population. In the prefrontal cortex (PFC) of depression patients, hypofunction is accompanied with structural deficits, including decreased cell number, neuronal atrophy and decreased number of spine synapses. In rodents, chronic stress exposure induces depressive-like behaviour and results in structural impairment of dendrites of layer 2/3 and 5 pyramidal neurons in PFC, including reduced dendritic spine density and atrophy of apical dendrites. However, it is unclear whether dendritic deficits contribute to depression development. Ketamine, a NMDA receptor blocker, is found to exert rapid, lasting antidepressant effect at a single, sub-anaesthetic dose. Ketamine can also rapidly reverse chronic stress-induced synaptic deficit. Yet, data on the effect of ketamine on dendritic spine plasticity in long-term is lacking. In this study, we used in vivo two-photon transcranial imaging of Thy1-YFP H line mice to investigate dendritic spine plasticity in the chronic restraint stress (CRS) depression model. We found that CRS increased dendritic spine elimination and reduced spine formation of layer V pyramidal neurons in the frontal association cortex. In addition, CRS-induced alterations in spine plasticity precede the onset of behavioural symptoms. Importantly, we found that ketamine treatment counteracted the effects of stress on dendritic spine plasticity. REFERENCES: 1. Duman, R. S., & Aghajanian, G. K. (2012). Synaptic dysfunction in depression: potential therapeutic targets. Science, 338(6103), 68-72. 2. Licznerski, P., & Duman, R. S. (2013). Remodeling of axo-spinous synapses in the pathophysiology and treatment of depression. Neuroscience, 251, 33-50.-
dc.languageeng-
dc.publisherThe University of Hong Kong.-
dc.relation.ispartofNeuroscience Symposium 2016 & Annual Scientific Conference of the Hong Kong Society of Neurosciences-
dc.titleAltered dendritic spine plasticity in a mouse depression model-
dc.typeConference_Paper-
dc.identifier.emailChang, RCC: rccchang@hku.hk-
dc.identifier.emailLai, SWC: coraswl@hku.hk-
dc.identifier.authorityChang, RCC=rp00470-
dc.identifier.authorityLai, SWC=rp01895-
dc.identifier.hkuros266373-
dc.identifier.spage48, abstract no. P36-
dc.identifier.epage48, abstract no. P36-
dc.publisher.placeHong Kong-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats