Evaluation of antidepressant and anxiolytic medications in mice lacking either regulators of G-protein signalling 2 or 4

Advisor(s)

Manoranjan S D'Souza

Confirmation

1

Document Type

Poster

Location

ONU McIntosh Center; McIntosh Activities Room

Start Date

21-4-2023 10:00 AM

End Date

21-4-2023 10:50 AM

Abstract

Regulator of G protein-signaling (RGS) proteins are a family of more than 30 intracellular proteins that negatively modulate signaling pathways of G protein-coupled receptors (GPCRs). GPCRs play an important role in mediating the effects of neurotransmitters like dopamine and serotonin, which in turn play an important role in psychiatric disorders such as anxiety and depression. Importantly, polymorphisms in the RGS2 gene result in increased vulnerability to anxiety and depression in humans. Additionally, mice lacking RGS2 show anxiety- and depression-like behaviors. Similarly, mice lacking RGS4 have shown disruption in dopamine signaling. However, the effects of antidepressants (fluoxetine & desipramine) and anxiolytics (diazepam & buspirone) used in humans have not been systematically evaluated in male and female mice lacking RGS2 and RGS4. This study was designed to address this gap in knowledge. The antidepressant-like and anxiolytic-like effects of these drugs were assessed using the tail suspension and elevated plus maze tests, respectively. Findings from this study will help explain the effects of deletion of either RGS2 or RGS4 on the effects of anxiolytic and antidepressant medications used in humans. The data from the study is currently being analyzed.

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Apr 21st, 10:00 AM Apr 21st, 10:50 AM

Evaluation of antidepressant and anxiolytic medications in mice lacking either regulators of G-protein signalling 2 or 4

ONU McIntosh Center; McIntosh Activities Room

Regulator of G protein-signaling (RGS) proteins are a family of more than 30 intracellular proteins that negatively modulate signaling pathways of G protein-coupled receptors (GPCRs). GPCRs play an important role in mediating the effects of neurotransmitters like dopamine and serotonin, which in turn play an important role in psychiatric disorders such as anxiety and depression. Importantly, polymorphisms in the RGS2 gene result in increased vulnerability to anxiety and depression in humans. Additionally, mice lacking RGS2 show anxiety- and depression-like behaviors. Similarly, mice lacking RGS4 have shown disruption in dopamine signaling. However, the effects of antidepressants (fluoxetine & desipramine) and anxiolytics (diazepam & buspirone) used in humans have not been systematically evaluated in male and female mice lacking RGS2 and RGS4. This study was designed to address this gap in knowledge. The antidepressant-like and anxiolytic-like effects of these drugs were assessed using the tail suspension and elevated plus maze tests, respectively. Findings from this study will help explain the effects of deletion of either RGS2 or RGS4 on the effects of anxiolytic and antidepressant medications used in humans. The data from the study is currently being analyzed.