Frontiers in pharmacology
January 1, 2024
Xulin Chen, Xian Wang, Caijuan Li et al.
7 citations
Over the past 20 years, research on NMDA receptors as targets for depression treatment has grown steadily, with 5,092 publications identified. The United States leads in collaborations, publications, and citations. Co-cited reference analysis revealed 15 main clusters. Recent hotspots include ketamine (an NMDA receptor antagonist) for treatment-resistant depression, oxidative stress, synaptic plasticity, and neuroplasticity-related factors such as brain-derived neurotrophic factor. While ketamine's application and mechanisms in major depressive disorder remain a hot topic, its side effects have spurred investigation into new rapid-acting antidepressants.
Neuropharmacology
May 15, 2025
Yazhou Wen, Jin Zhou, Huiling Yu et al.
2 citations
Prenatal chronic restraint stress (CRS) in mice induced postpartum depression-like behaviors in mothers and sex-specific behavioral changes in their adolescent offspring: female offspring showed depression-like behaviors, while male offspring exhibited memory deficits. Esketamine, given to mothers on postpartum days 1-5, improved these maternal depression-like behaviors and also corrected the behavioral abnormalities in adolescent offspring. Additionally, prenatal CRS caused heightened secretion of ACTH and CORT in adolescent offspring during acute restraint stress, indicating hyperresponsiveness of the stress hormone system. Esketamine's effects on these hormone levels were not reported.
Molecular psychiatry
May 13, 2026
Fukang Zhang, Shuyuan Fan, Shiqi Li et al.
Exposure to 60% nitrous oxide (N2O), but not 30%, induced conditioned place preference (CPP) reward behavior in rodents and increased the excitability and glutamatergic transmission of dopamine neurons in the ventral tegmental area (VTA). N2O specifically elevated homocysteine levels in the deep cerebellar nuclei (DCN), but blocking homocysteine production did not reduce the rewarding behavior or glutamatergic transmission. Instead, N2O directly enhanced AMPA receptor-mediated glutamatergic transmission and increased activity in both DCN and VTA dopamine neurons. Inhibiting the DCN-VTA circuit via optogenetic long-term depression or chemogenetic inhibition of VTA dopamine neurons reduced N2O-induced CPP. Attenuating N2O-induced potentiation of the DCN-VTA circuit may offer a therapeutic strategy for N2O-related reward behavior.