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Published on: May 26, 2023
The elevated open platform stress suppresses excitatory synaptic transmission in the layer V anterior cingulate
Ryo Kawabata1, Ayumi Fujita2, Yoshihiko Oke3
1Biomedical Chemistry Major, Graduate School of Science and Technology, Kwansei Gakuin University, Sanda, Hyogo, Japan; Department of Neurophysiology, Faculty of Medicine, Hyogo Medical University, Nishinomiya, Hyogo, Japan.
Acute physical stress from the elevated open platform (EOP) in mice causes lasting hypersensitivity by altering synaptic transmission in anterior cingulate cortex (ACC) layer V neurons, impacting stress responses.
Area of Science:
- Neuroscience
- Stress Research
- Synaptic Plasticity
Background:
- Physical stress can induce hyperalgesia, anxiety, and depression.
- Acute physical stress via the elevated open platform (EOP) in mice causes long-lasting mechanical hypersensitivity.
- EOP exposure induces synaptic plasticity in anterior cingulate cortex (ACC) layer II/III pyramidal neurons.
Purpose of the Study:
- To investigate if EOP exposure alters intrinsic properties and synaptic transmission in ACC layer V pyramidal neurons.
- To understand the role of ACC layer V neurons in the behavioral stress response.
Main Methods:
- Whole-cell patch-clamp recordings in brain slice preparations.
- Assessment of intrinsic membrane properties and excitatory/inhibitory synaptic transmission.
- Investigation of thalamo-ACC projections.
Main Results:
- EOP exposure did not alter intrinsic properties of ACC layer V neurons.
- EOP exposure suppressed excitatory synaptic transmission frequency and altered AMPA/GluK receptor kinetics.
- EOP exposure induced short-term depression in thalamo-ACC excitatory synaptic transmission.
Conclusions:
- EOP stress leads to abnormal excitatory synaptic transmission in ACC layer V pyramidal neurons.
- These synaptic changes in ACC layer V neurons may contribute to stress-induced hypersensitivity and behavioral responses.
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