Abstract

Stathmin (STMN), a microtubule-destabilizing factor, can regulate fear, anxiety, and learning. Social defeat stress (SDS) has detrimental effects on mental health and increases the risk of various psychiatric diseases. This study investigated the effects of STMN1 gene knockout (KO) on behavioral parameters and dopaminergic markers using an SDS mouse model. The STMN1 KO mice showed anxious hyperactivity, impaired object recognition, and decreased levels of neutral and social investigating behaviors at baseline compared to wild-type (WT) mice. The impact of SDS on neutral, social investigating and dominant behaviors differed markedly between the STMN1 WT and KO mice. In addition, different levels of total DARPP-32 and pDARPP-32 Thr75 expression were observed among the control, unsusceptible, and susceptible groups of STMN1 KO mice. Our results show that STMN1 has specific roles in locomotion, object recognition, and social interactions. Moreover, SDS had differential impacts on social interactions and dopaminergic markers between STMN1 WT and KO mice.

Highlights

  • The stathmin (STMN) tubulin-binding proteins, including stathmin 1 (STMN1), SCG10 (STMN2), SCLIP (STMN3), and RB3 (STMN4), are highly expressed during early postnatal brain development [1,2].In particular, STMN1 is involved in the formation and disassembly of microtubules (MTs) [1,3]and plays an important role in neurite outgrowth and synaptic plasticity [4]

  • Different levels of total DARPP-32 and pDARPP-32 Thr75 expression were observed among the control, unsusceptible, and susceptible groups of STMN1 KO mice

  • Our results show that STMN1 has specific roles in locomotion, object recognition, and social interactions

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Summary

Introduction

The stathmin (STMN) tubulin-binding proteins, including STMN1, SCG10 (STMN2), SCLIP (STMN3), and RB3 (STMN4), are highly expressed during early postnatal brain development [1,2]. −/− mice are a good animal model for studying the role of the fear in the AMY. Mice are athat good animalon model the role of the AMY in behaviors that depend on Social defeat stress (SDS). The SDS paradigm has been used widely as an animal model for depression, pivotal role in regulating threat-related emotional memory and modulates cognitive functions, anxiety disorders [19], and possibly schizophrenia [20,21]. Considered the SDS model ideal for studying regulating threat-related emotional alsoWe modulates cognitive functions, including reward, the effects of knocking out the fear gene. This study investigated the effects of knocking out the STMN1 gene on behavioral parameters and dopaminergic markers using the SDS model in mice

Experiments were conducted male
Design
Behavioral Measures
Social Avoidance Test
Social Interaction Test
Preparation of Brain Tissue for Western Blot
Statistical Analysis
Results
Western
Discussion
Effects of Stathmin 1 Gene Knockout on Behaviors
Effects of Social Defeat Stress on Stathmin Expression
Effects of Stathmin 1 Gene Knockout on Dopaminergic Markers
Limitations
Conclusions
Full Text
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