| Abstract | In the current study, using a hippocampus-dependent paradigm to assess whether NE could restore cognitive deficits initiated by systemic bacterial endotoxin post-training administration to elucidate if there is a connection between AMPAR GluR1-related mechanisms and cognitive recovery after innate immune initiation. To uncover the hippocampus basis of the interaction, we used the trace-cued aversion-conditioning model, which is well documented as hippocampus-dependent in function, to assess if NE can restore the function of the hippocampus. To the best of the authors' knowledge, the peripheral administration of norepinephrine to assess the restorative qualities to the hippocampus after bacterial endotoxin exposure has disrupted cognition has not been previously studied. |
