# Neurotransmitter alterations in seasonal affective disorder

## TL;DR

This study finds that people with seasonal affective disorder have lower GABA levels in the hippocampus, suggesting a link to depression and environmental influences.

## Contribution

The study provides new evidence of GABA alterations in SAD, specifically in the hippocampus, using MRSI.

## Key findings

- SAD patients showed significantly reduced GABA+/tCr ratios in the hippocampus compared to healthy controls.
- No significant changes in glutamate or other brain regions were observed in SAD patients.
- The findings suggest common neurobiological mechanisms across depression subtypes.

## Abstract

Seasonal affective disorder (SAD) is a type of unipolar depression characterized by depressive symptoms mainly during the cold season, which were often linked to alterations in the serotonergic system. It is assumed that other neurotransmitter systems, such as glutamate and GABA, are similarly affected. Hence, we investigated differences in glutamate and GABA between SAD patients and healthy control subjects using magnetic resonance spectroscopy imaging (MRSI). Fourteen SAD patients (11 female, 36 ± 11 years) and 14 sex- and age-matched healthy controls, were scanned once between October and February using multi-voxel 3D-GABA-edited MEGA-LASER MRSI at 3 T. Mean GABA+ and Glx (glutamate + glutamine) to total creatine (tCr) ratios were calculated in five brain regions. Mann–Whitney-U-Tests were performed for each region and neurotransmitter ratio independently as well as correlation analyses between neurotransmitter ratios and clinical scores, respectively. A significant reduction in GABA+/tCr ratios in the hippocampus (pcorr = 0.049) between SAD patients and healthy individuals was revealed. No significant changes in other brain regions or correlations with the investigated clinical scores were shown. Our findings of altered GABA concentrations in the hippocampus are in line with neurotransmitter alterations across other subtypes of depression, hinting towards common neurobiological mechanisms and highlights the interplay between environmental factors and neurotransmitter systems.

The online version contains supplementary material available at 10.1038/s41598-026-37634-4.