OBJECTIVE: We aimed to investigate the expression levels of GABA and GABAA receptor α1 and α2 subunits in patients with major depressive disorder (MDD) during onset and remission. MATERIALS AND METHODS: 48 patients with MDD during onset and 45 patients with MDD during remission who were treated in our university were selected. Moreover, the control group included 46 healthy volunteers recruited in the community. The depression and anxiety symptoms were assessed by Hamilton Depression (HAMD) Scale and Hamilton Anxiety (HAMA) Scale. ELISA was used to determine the serum GABA levels. The mRNA expression of GABAA receptor α1 and α2 subunits in peripheral blood were detected by RT-PCR. RESULTS: The expression levels of serum GABA and of GABAA receptor α1 and α2 subunits in MDD depression attack group were notably decreased in comparison with those in MDD remission group and control group ((4.10 ± 0.73) v.s. (5.91 ± 1.25) and (5.83 ± 1.17) umol/L, F = 5.61, p < 0.001; (0.53 ± 0.32) v.s. (0.91 ± 0.18) and (0.93 ± 0.21), F = 8.37, p < 0.001; (1.45 ± 0.86) v.s. (2.33 ± 1.49) and (2.28 ± 1.50), F = 8.23, p < 0.001). However, there were no marked difference in the levels of these three indices between the MDD remission group and the control group (p > 0.05). Serum GABA levels were negatively correlated with HAMA total score (r = -0.34, p = 0.02), HAMD total score (r = -0.46, p = 0.01) and depression core symptom score (r = -0.32, p = 0.03). CONCLUSIONS: During the onset of MDD, there may be GABA neuronal dysfunction and abnormal expression of GABAA receptor subunits, and those changes showed a state change, which gradually returned to normal during remission.
OBJECTIVE: We aimed to investigate the expression levels of GABA and GABAA receptor α1 and α2 subunits in patients with major depressive disorder (MDD) during onset and remission. MATERIALS AND METHODS: 48 patients with MDD during onset and 45 patients with MDD during remission who were treated in our university were selected. Moreover, the control group included 46 healthy volunteers recruited in the community. The depression and anxiety symptoms were assessed by Hamilton Depression (HAMD) Scale and Hamilton Anxiety (HAMA) Scale. ELISA was used to determine the serum GABA levels. The mRNA expression of GABAA receptor α1 and α2 subunits in peripheral blood were detected by RT-PCR. RESULTS: The expression levels of serum GABA and of GABAA receptor α1 and α2 subunits in MDD depression attack group were notably decreased in comparison with those in MDD remission group and control group ((4.10 ± 0.73) v.s. (5.91 ± 1.25) and (5.83 ± 1.17) umol/L, F = 5.61, p < 0.001; (0.53 ± 0.32) v.s. (0.91 ± 0.18) and (0.93 ± 0.21), F = 8.37, p < 0.001; (1.45 ± 0.86) v.s. (2.33 ± 1.49) and (2.28 ± 1.50), F = 8.23, p < 0.001). However, there were no marked difference in the levels of these three indices between the MDD remission group and the control group (p > 0.05). Serum GABA levels were negatively correlated with HAMA total score (r = -0.34, p = 0.02), HAMD total score (r = -0.46, p = 0.01) and depression core symptom score (r = -0.32, p = 0.03). CONCLUSIONS: During the onset of MDD, there may be GABA neuronal dysfunction and abnormal expression of GABAA receptor subunits, and those changes showed a state change, which gradually returned to normal during remission.
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Keywords:
Gamma-aminobutyric acid; Hamilton anxiety; Hamilton depression; gamma-aminobutyric acid A receptor; major depressive disorder