Astrogliosis and compensatory neurogenesis after the very first ethanol binge drinking‐like exposures in adolescent rat

Background

Multiple ethanol binge drinking-like exposures during adolescence in rat induce neuroinflammation, neurogenesis loss and cognitive deficits at adulthood. Interestingly, the very first ethanol binge drinking-like exposures during adolescence also induce cognitive and synaptic plasticity impairments in the hippocampus at short term while the cellular mechanisms of these effects remain unclear. Here, we sought to determine which of the cellular effects of ethanol might play a role in cognitive and synaptic plasticity disturbances observed in adolescent male rat after only two binge-like ethanol exposures.

Methods

Using immunochemistry, we determined neurogenesis, neuronal loss, astrogliosis, neuroinflammation and synaptogenesis in the hippocampus of adolescent rat 48h after two binge-like ethanol exposures (3 g/kg, i.p, 9 hours apart). Flow cytometry was used to analyze activated microglia and to identify the TLR4 expressing cell types.

Results

Increased DCX immunoreactivity was detected in the subgranular zone (SGZ) of the dentate gyrus (DG) together with astrogliosis in the SGZ and a lower number of mature neurons in the DG and in CA3, suggesting compensatory neurogenesis. Synaptic density decreased in the stratum oriens of CA1 revealing structural plasticity. There was no change in microglial TLR4 expression nor in the number of activated microglia, suggesting a lack of neuroinflammatory processes although neuronal TLR4 was decreased in CA1 and DG.

Conclusions

Our findings demonstrate that the cognitive deficits associated with hippocampal synaptic plasticity alterations that we previously characterized 48h after the very first binge-like exposures are associated with hippocampal structural plasticity, astrogliosis and decreased neuronal TLR4 expression, but not with microglia reactivity.

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