# The mechanism of parvalbumin interneurons regulating glutamatergic neurons involvement in stress induced anxiety in the basolateral amygdala of male mice

## TL;DR

This study explores how stress affects brain cells in mice, leading to anxiety and how restoring these cells can reduce anxiety.

## Contribution

The study identifies how parvalbumin interneurons regulate glutamatergic neurons in stress-induced anxiety in mice.

## Key findings

- Stress reduces parvalbumin interneurons in the basolateral amygdala of mice.
- Reduced parvalbumin interneurons lead to increased glutamatergic neuron excitability and anxiety.
- Activating parvalbumin interneurons can alleviate stress-induced anxiety in mice.

## Abstract

Modern life’s fast-paced and the unexpected conditions contribute to escalating stress levels, often leading to anxiety disorders and posing significant challenges to physical and mental health. In judicial practice, the parties often suffer from anxiety disorder under the great stress. However, the precise mechanisms underlying stress-induced anxiety disorders remain incompletely understood. This study aims to explore the neural mechanisms by which stress-induced imbalances in the basolateral amygdala (BLA) parvalbumin interneurons (PV-INs) and glutamatergic neurons lead to anxiety. This study used behavioral analysis, morphology, patch clamp electrophysiology, and viral interference techniques to detect the number of BLA PV-INs and glutamatergic neurons, as well as the excitability of glutamatergic neurons. Results demonstrated that acute and chronic stress adversely affect PV-INs in the BLA, diminishing their numbers and resulting in glutamatergic neurons disinhibition, thereby enhancing glutamatergic neurons excitability and precipitating anxiety behaviour. The anxiety disorder can be effectively improved by activating PV-INs. This study reveals the mechanism of internal amygdala PV-INs regulation leading to anxiety disorders under acute and chronic stress.