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GLIA Porto 2019: Abstracts Oral Presentations, Posters, Indexes

A traumatic childhood is among the most important risk factors for developing stress-related psychopathologies such as posttraumatic stress disorder or depression later in life. In rodents, it can be modeled by juvenile stress, resulting in increased anxiety and impaired coping with stressful challenges in adulthood. In the current study, we found that juvenile stress led to a reduced synaptic efficacy, as indicated by decreased ratios of field excitatory postsynaptic potential slope to fiber volley amplitude at Schaffer collaterals in the ventral CA1. However, this was associated with increased long-term potentiation (LTP) of synaptic transmission after high-frequency stimulation. Recent studies suggest that the active neurotransmission at excitatory terminals is maintained by the glutamateglutamine cycle in astrocytes. We therefore tested whether these processes also guide the lasting changes on plasticity observed after juvenile stress by blocking a key enzyme, the astrocytic glutamate degrading enzyme glutamine synthetase (GS). Indeed, the pharmacological inhibition of GS by methionine sulfoximine in slices from naïve rats mimicked the effect of juvenile stress on vCA1-LTP. Supplying glutamine to overcome the GS deficiency normalized vCA1-LTP in slices from juvenile stressed rats to control levels. This functional GS deficiency was further paralleled by an allostatic reduction of GS mRNA expression levels in the ventral CA1 Stratum radiatum in rats with a history of juvenile stress. Together, our results suggest a critical role for the astrocytic glutamine/glutamate cycle in mediating long-term effects of juvenile stress on plasticity in the ventral CA1, a region associated with anxiety and emotional memory processing.