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May 31, 2019

RPG Seminar Series (Speaker: Mr. WONG Cheuk Ning / Miss SAW Ying Ling)

Date: Friday, 31 May 2019

Venue: Seminar Room 4, G/F
Laboratory Block, Faculty of Medicine Building
21 Sassoon Road, Hong Kong

Time: 5:00 p.m.

Title: The role of heparanase in hippocampal’s synaptic homeostasis
Speaker: Mr. WONG Cheuk Ning (MPhil candidate)

When NMDA was added exogenously into both rat hippocampal neuronal culture and astrocytes culture, both hippocampal neurons and astrocytes response to the addition of NMDA by increasing the exosome release. However, the level of exosome release from astrocytes is higher than in hippocampal neurons. Since both heparanase 1 and heparanase 2 could affect neuronal surface AMPA receptor density thereby lowering the synaptic plasticity. Therefore, there is a possibility that the release of the heparanase 1 and heparanase 2 contained exosome from the astrocytes and hippocampal neurons is a protective mechanism to protect the neurons itself from over-excitable state by stimulating the internalization of the neuronal surface AMPA receptor. The action lowering the neuronal surface AMPA receptor density may suggest that the heparanase expressed in the hippocampus act as a regulator in synaptic homeostasis.

Title: Prelimbic cortical stimulation ameliorates the neuroinflammatory-¬induced depressive--like and social behavioral deficits in rat models
Speaker: Miss SAW Ying Ling (MPhil candidate)

Deep brain stimulation (DBS) is a promising neuromodulation therapy for treatment-resistant depression. Although previous research have reported the comorbidity of neuroinflammation and depression, the underlying mechanisms of stimulation¬induced antidepressive effects on neuroinflammatory elements remain largely unknown. In this study, we aimed to investigate the anti¬neuroinflammatory role of DBS of the prelimbic cortex in rat models of depression. Animals went under a chronic unpredictable stress (CUS) protocol or CUS in combination with lipopolysaccharide (LPS) induction and subsequently received either DBS or sham stimulation in the prelimbic cortex (PrL). Our findings demonstrate PrL¬DBS enhances social interaction and antidepressant¬like behavior in CUS and CUS+LPS groups. Additionally, gene expression studies show significant decreases in markers for microglial activation and neuroinflammation in the prefrontal cortex when compared to non¬treated animals. In conclusion, DBS¬induced changes in the neuroinflammatory environment were mediated by both the neuroinflammatory¬dependent and ¬independent mechanisms in these animal models of depression.