title: Early-life-stress affects the homeostasis of glutamatergic synapses.
abstract: Early-life stress induces several neuropsychological disorders in adulthood, including depression. Such disorders may be induced by functional alteration of the glutamatergic system. However, their underlying mechanisms have not yet been fully clarified. Furthermore, the involvement of glucocorticoids, which are representative stress hormones, has not yet been fully clarified. In this study, we used maternal deprivation (MD) mice as an early-life-stress model, and studied the changes in the glutamatergic system in adulthood. The glutamate concentration and neuronal activity in the somatosensory cortex (SSC) increased under basal conditions in MD mice. Stressful physical stimulation (SPS) increased the concentration of corticosterone, but not of glutamate, in the control mouse SSC. On the other hand, in the MD mice, although the basal concentration of corticosterone in the SSC increased, no SPS-induced increase was observed. In contrast, the concentration of glutamate increased greatly during SPS. It was significantly high for 30 min after stimulation. The expression level of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/N-methyl-d-aspartate receptors in the MD mice was also changed compared with that in the control mice after stimulation. These findings indicate that early-life stress disrupts the homeostasis of glutamatergic synapses.
authors.affiliation: Department of Integrative Physiology, Gunma University Graduate School of Medicine, Maebashi, Gunma, 371-8511, Japan.
authors.forename: Syutaro
authors.initials: S
authors.lastname: Toya
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Takatsuru
authors.forename: Michifumi
authors.initials: M
authors.lastname: Kokubo
authors.forename: Izuki
authors.initials: I
authors.lastname: Amano
authors.forename: Noriaki
authors.initials: N
authors.lastname: Shimokawa
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Koibuchi
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D003345:Corticosterone / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D018698:Glutamic Acid / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology; D008297:Male; D008426:Maternal Deprivation; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000502:physiology*; D010812:Physical Stimulation; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D013003:Somatosensory Cortex / Q000254:growth & development / Q000503:physiopathology*; D013315:Stress, Psychological / Q000503:physiopathology*; D013569:Synapses / Q000502:physiology*; D055698:Touch Perception / Q000502:physiology
chemical_list: D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D003345:Corticosterone
keywords: AMPA receptor; NMDA receptor; early-life stress; in vivo microdialysis