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Updated: Jun 16, 2026
P50 Sensory Gating in Infants
Published on: December 26, 2013
A follow-up study on features of sensory gating P50 in treatment-resistant depression patients
Yong Wang1, Yi-Ru Fang, Xing-Shi Chen
1Division of Mood Disorder, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, China.
Background:
Depressive disorder is a well-known chronic, recurrent and disabling mental disease with high direct and indirect costs to society in both western and eastern cultures. Approximately 40% of depressed patients show only partial or no response to initial or even multiple antidepressant medications and are usually called treatment-resistant depression (TRD) patients. The present work was to measure the features of sensory gating (SG) P50 in TRD patients with the intent of understanding the characteristics of this disease.
Methods:
In 50 TRD patients, 39 non-treatment-resistant depression (NTRD) patients and 51 healthy controls (HC), auditory evoked potential P50 was measured using the conditioning/testing paradigm presented with auditory double clicks stimuli, and 36 TRD patients had repeated measurements after an 8-week venlafaxine treatment course.
Results:
All the depressive disorder patients, including the TRD and NTRD groups, showed an increased testing stimulus wave (S2-P50) amplitude compared to controls (P < 0.01 and P < 0.05), but there was no significant difference between the TRD and NTRD groups (P > 0.05). There were significant differences in the ratio of testing stimulus (S2) and conditioning stimulus (S1) (S2/S1) and in the value of 100 x (1 - S2/S1) among the three groups. Compared to the baseline, TRD patients had no significant changes of features and different expression of P50 after acute treatment (P > 0.05). Meanwhile, a statistically significant positive correlation of S2/S1 with the scores of the 17-item Hamilton Rating Scale for Depression (HAMD-17) (P < 0.01), and a significantly negative correlation of S1 - S2, 100 x (1 - S2/S1) with the scores of HAMD-17 (P < 0.01) were observed in the TRD patients' baseline measurement, but there was no correlation after venlafaxine treatment (P > 0.05).
Conclusions:
Both the TRD and NTRD patients had obvious SG deficits, with a more severe deficit in TRD patients. Although, with a correlated relationship to the severity of depressive symptoms, SG P50 deficit might be suggested as a trait marker for TRD, and a combination of S2/S1 ratio, S1 - S2 and 100 x (1 - S2/S1), was recommended for electrophysiological measurement in TRD patients.
