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Chronic ceftriaxone treatment rescues hippocampal memory deficit in AQP4 knockout mice via activation of GLT-1

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N -methyl-D-aspartate receptors (NMDARs) activation leading to intracellular calcium (Ca 2+ ) influx and rapid activation of various protein kinases [e.g., calcium/calmodulin dependent kinases (CaMKs), protein kinases A (PKA), and C (PKC), extracellular signal-regulated protein kinase (ERK)] and phosphatases [e.g., protein phosphatase 1 (PP1), calcineurin] (Ho et al., 2011)

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