Glutamate neurotransmission is affected in prenatally stressed offspring

Ezequiela Adrover, Maria Eugenia Pallarés, Carlos Javier Baier, Melisa C Monteleone, Fernando A Giuliani, Helle S Waagepetersen, Marcela A Brocco, Ricardo Cabrera, Ursula Sonnewald, Arne Schousboe, Marta C Antonelli

    16 Citations (Scopus)

    Abstract

    Previous studies from our laboratory have shown that male adult offspring of stressed mothers exhibited higher levels of ionotropic and metabotropic glutamate receptors than control rats. These offspring also showed long-lasting astroglial hypertrophy and a reduced dendritic arborization with synaptic loss. Since metabolism of glutamate is dependent on interactions between neurons and surrounding astroglia, our results suggest that glutamate neurotransmitter pathways might be impaired in the brain of prenatally stressed rats. To study the effect of prenatal stress on the metabolism and neurotransmitter function of glutamate, pregnant rats were subjected to restrain stress during the last week of gestation. Brains of the adult offspring were used to assess glutamate metabolism, uptake and release as well as expression of glutamate receptors and transporters. While glutamate metabolism was not affected it was found that prenatal stress (PS) changed the expression of the transporters, thus, producing a higher level of vesicular vGluT-1 in the frontal cortex (FCx) and elevated levels of GLT1 protein and messenger RNA in the hippocampus (HPC) of adult male PS offspring. We also observed increased uptake capacity for glutamate in the FCx of PS male offspring while no such changes were observed in the HPC. The results show that changes mediated by PS on the adult glutamatergic system are brain region specific. Overall, PS produces long-term changes in the glutamatergic system modulating the expression of glutamate transporters and altering synaptic transmission of the adult brain.

    Original languageEnglish
    JournalNeurochemistry International
    Volume88
    Pages (from-to)73-87
    Number of pages15
    ISSN0197-0186
    DOIs
    Publication statusPublished - 1 Sept 2015

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