Published online Feb 19, 2025. doi: 10.5498/wjp.v15.i2.101807
Revised: November 25, 2024
Accepted: December 18, 2024
Published online: February 19, 2025
Processing time: 109 Days and 4.7 Hours
Depression is a prevalent affective disorder, but its pathophysiology remains unclear. Dysfunction in the gamma-aminobutyric acid (GABA)-ergic system may contribute to its onset. Recently, antidepressants (e.g., brexanolone, zuranolone) targeting the GABA-A receptor were introduced. The zona incerta (ZI), an inhi
To explore the relationship between GABAergic neurons in the ZI and depre
A chronic restraint stress (CRS) model was utilized to induce depression in mice. Whole-cell patch-clamp recordings assessed the excitability changes of GABAergic neurons in the ZI. Additionally, chemogenetic techniques were employed to modulate ZI GABAergic neurons. The performance of the mice in behavioral tests for depression and anxiety was observed.
The findings indicated that GABAergic neurons in the ZI were closely associated with depression-like behaviors in mice. Twenty-eight days after the CRS model was established, depression-like and anxiety-like behaviors were observed in the mice. The excitability of GABAergic neurons in the ZI was reduced. Chemogenetic activation of these neurons alleviated CRS-induced depression-like and anxiety-like behaviors. Conversely, inhibition of GABAergic neurons in the ZI led to changes in emotion-related behavioral outcomes in mice.
Activity of GABAergic neurons in the ZI was closely associated with depression-like phenotypes in mice, suggesting that these neurons could be a potential therapeutic target for treating depression.
Core Tip: Gamma-aminobutyric acid (GABA)-ergic dysfunction may play a role in the onset of depression. Case reports have indicated that deep brain stimulation of the zona incerta (ZI), which is abundant in GABAergic neurons, can modify depressive and anxiety symptoms. However, direct evidence linking ZI GABAergic neurons to depression-related behaviors in rodents is limited. This study demonstrated chronic resistant stress induced depression-like and anxiety-like behaviors in mice and reduced neuronal excitability. Chemogenetic activation alleviated these symptoms, whereas inhibition altered the behavior of normal mice. These findings suggested that ZI GABAergic neurons may serve as potential therapeutic targets for depression.