[Effect of GABA(B) Receptor Signal to Corticosterone-induced Neuron Apoptosis]

To investigate whether corticosterone results in neuron apoptosis through regulating γ-aminobutyric acid (GABA) receptor.

In vivo: the hyperglycemic rat model with applying chronic restraint stress to healthy male SD rats (3 months) was established, after paraffin embedding the brain was sliced, and the level of neuron apoptosis was tested by detecting active Caspase-3 with immune-histochemical staining and TUNEL. The level of corticosterone in serum was detected by using ELISA. In vitro: the level of active Caspase-3 in NG108-15 cells (neuroblastoma and glioma cell line) after treated with corticosterone (10(-7) mol/L) was detected with Western blot. In NG108-15 cells recombinanted with GABA(B2) receptor, after administrating separately with the GABA(B) agonist baclofen (100 µmol/L) and antagonist CGP35348 (100 µmol/L), the level of active Caspase-3 under the effect of corticosterone (10(-7) mol/L) was detected.

Active Caspase-3 positive apoptotic cells and TUNEL-positive cells were detected in solitary nucleus of hyperglycemia rat induced by chronic restraint stress, and the level of serum corticosterone had recovered after an initial ascent. NG108-15 cells could express GABA(B1) receptor endogenously, and the expression of active Caspase-3 increased after corticosterone treatment (P < 0.05). In NG108-15 cells transfected with GABA(B2) receptor subunits, baclofen could reduce the effect of corticosterone- induced active Caspase-3 upexpression, while CGP35348 enhanced this effect (P < 0.05).

Corticosterone may lead to abnormal neuron excitability and neuron apoptosis by means of inhibiting GABA receptor B.