Abstract
Previous studies suggest that in people with major depressive disorder (MDD), there exists a perturbation of the normal balance between the excitatory and inhibitory neurotransmitter systems in the visual cortex, indicating the possibility of altered visual cortical excitability. However, investigations into the neural activities of the visual cortex in MDD patients yielded inconsistent findings. The present study aimed to evaluate the visual cortical excitability utilizing a paired-pulse stimulation paradigm in patients with MDD and to access the paired-pulse behavior of recording visual evoked potentials (VEPs) as a marker of MDD. We analyzed the amplitudes of VEPs and paired-pulse suppression (PPS) at four different stimulus onset asynchronies (SOAs) spanning 93 ms to 133 ms. Further, the relationship between PPS and the symptom severity of depression was investigated using Spearman's correlation. We found that, whereas the first VEP amplitude remained unchanged, the second VEP amplitude was significantly higher in the MDD group compared to the healthy controls. As a result, the amplitude ratio (second VEP amplitude/first VEP amplitude) increased, indicating reduced PPS and thus increased excitability in the visual cortex. Moreover, we found the amplitude ratios had a significantly positive correlation with the symptom severity of depression in MDD, indicating a clinically useful biomarker for MDD. Our findings provide new insights into the changes in the excitation-inhibition balance of visual cortex in MDD, which could pave the way for specific clinical interventions.
Highlights
Major depressive disorder (MDD) is a common mental disease that is characterized by affective disturbances and neurocognitive impairment, for which the development of clinically useful biomarkers remains a challenge [1].Though the underlying mechanism of MDD has not been fully understood, wide-spread connectivity alterations in the structure and function of cortical regions, including occipital cortical abnormalities linked with impaired visual perception, have been reported in MDD patients [2]
Post-hoc t-tests with Bonferroni correction showed the amplitude ratios (A2s/A1) were significantly higher at stimulus onset asynchronies (SOAs) of 93 ms (F = 66.481, p < 0.001), 107 ms (F = 84.846, p < 0.001), 120 ms (F = 30.536, p < 0.001) and 133 ms (F = 9.469, p = 0.003) in the MDD group compared to the healthy controls (Table 4)
Because the amplitude ratio was calculated by dividing A2s by A1, the two components were analyzed separately to identify which component was responsible for the increased amplitude ratio in the MDD group (Figure 2B)
Summary
Though the underlying mechanism of MDD has not been fully understood, wide-spread connectivity alterations in the structure and function of cortical regions, including occipital cortical abnormalities linked with impaired visual perception, have been reported in MDD patients [2]. MDD patients, such as visual motion, visual contrast and visual integration, using psychophysical measures. The results revealed higher motion suppression [3], decreased contrast suppression [4] and deficits in integration of visual inputs in MDD [5]. The psychophysical deficits in visual perception in MDD are closely related to the abnormality of biochemical changes in the occipital cortex. In MDD, there was a reduction in glutamate levels in the occipital cortex, and, more importantly, the balance between GABA and glutamate levels was disrupted [8]
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