N-Cadherin Regulates GluA1-Mediated Depressive-Like Behavior in Adolescent Female Rat Offspring following Prenatal Stress.

BACKGROUND: The incidence of depression is twice higher in women than in men, and gender differences in the prevalence rates first emerge around puberty. Prenatal stress (PS) induces gender-dependent depressive-like behavior in adolescent offspring, but the neuro-physiological mechanisms remain unclear. Our study aimed to investigate the possible neuro-physiological mechanisms of gender-dependent depressive-like behavior in PS adolescent offspring and further explored the possibility of treating depression in adolescent female rats. METHODS: The pregnant rats were exposed to restraint stress in the third trimester for 7 days. The depressive-like behavior and the expression of N-cadherin and AMPARs in the hippocampus of adolescent offspring rats were assessed. 10 mg/kg AMPAR antagonist CNQX and 10 mg/kg N-cadherin antagonist ADH-1 were intraperitoneally injected into female adolescent offspring, respectively; 0.2 µg AMPAR agonist CX546 was administered to the dentate gyrus of male adolescent offspring to determine the role of N-cadherin-AMPARs in depressive-like behavior of the offspring following PS. RESULTS: We found that PS increased N-cadherin expression, which upregulated GluA1 expression in the dentate gyrus, mediating depressive-like behavior in adolescent female rat offspring by reducing PSD-95. In addition, ADH-1 and CNQX improved depressive-like behavior in adolescent female offspring following PS. Furthermore, injection of the CX546 into the dentate gyrus induced depressive-like behavior in PS male offspring. CONCLUSION: The gender-dependent expression of N-cadherin-GluA1 pathway in adolescent offspring in the dentate gyrus was the key factor in gender differences of depressive-like behavior following PS.

Homocysteine-mediated gender-dependent effects of prenatal maternal depression on motor development in newborn infants.

BACKGROUND: The present study aimed to determine whether there were gender differences in the effects of prenatal maternal depression on motor development in newborn infants, and further to explore the role of plasma homocysteine in the delayed motor development in male newborn infants following prenatal maternal depression. METHODS: The term pregnant women within 37-42 weeks of gestation were assessed depressive symptoms by Hamilton Rating Scale for Depression. According to the gender of the newborn infants, all the subjects were divided into four groups: female control group (n = 45), male control group (n = 47), female depression group (n = 50), male depression group (n = 60). Motor development in newborn infants were assessed by Neonatal Behavioral Assessment Scale. Plasma homocysteine concentrations both in mothers and newborn infants were measured by enzymatic cycling assay. RESULTS: There were the worse scores of the items of motor development and significantly higher plasma homocysteine concentrations  in the male newborn infants of depression group than those of the female depression group and female control group, male control group, respectively. Plasma homocysteine concentrations significantly correlated with the items of motor development in all newborn infants, including the depression group and control group. LIMITATIONS: We should further explore homocysteine-mediated gender-dependent effects of prenatal maternal depression on motor development in newborn infants in the long-term follow-up. CONCLUSIONS: Prenatal maternal depression could result in delayed motor development in male newborn infants, but not female newborn infants. Plasma homocysteine may mediate gender-dependent effects of prenatal maternal depression on motor development in newborn infants.