Abstract
Recent studies showed that cyanobacteria-derived microcystin-leucine-arginine (MCLR) can cause hippocampal pathological damage and trigger cognitive impairment; but the underlying mechanisms have not been well understood. The objective of the present study was to investigate the mechanism of MCLR-induced cognitive deficit; with a focus on endoplasmic reticulum (ER) stress. The Morris water maze test and electrophysiological study demonstrated that MCLR caused spatial memory injury in male Wistar rats; which could be inhibited by ER stress blocker; tauroursodeoxycholic acid (TUDCA). Meanwhile; real-time polymerase chain reaction (real-time PCR) and immunohistochemistry demonstrated that the expression level of the 78-kDa glucose-regulated protein (GRP78); C/EBP homologous protein (CHOP) and caspase 12 were significantly up-regulated. These effects were rescued by co-administration of TUDCA. In agreement with this; we also observed that treatment of rats with TUDCA blocked the alterations in ER ultrastructure and apoptotic cell death in CA1 neurons from rats exposed to MCLR. Taken together; the present results suggested that ER stress plays an important role in potential memory impairments in rats treated with MCLR; and amelioration of ER stress may serve as a novel strategy to alleviate damaged cognitive function triggered by MCLR.
Highlights
There has been increasing attention on toxic blooms of cyanobacteria over the past few decades
Dysfunction of cognition and synaptic plasticity could be prevented by tauroursodeoxycholic acid (TUDCA), suggesting that endoplasmic reticulum (ER) stress plays a critical role in underlying memory deficits in rats treated with MCLR
We tested the effects of MCLR on spatial learning and memory function using a Morris water maze
Summary
There has been increasing attention on toxic blooms of cyanobacteria over the past few decades. Abundant proof from aquatic and terrestrial animals confirmed that MCs can cross the blood-brain-barrier to induce neurotoxicity [7,8,9,10] Neurological symptoms, such as dizziness, tinnitus, vertigo visual disturbance, have been reported in patients intravenously exposed to MCLR [11,12]. MCLR was found to induce spatial memory deficit, histological and ultrastructural injuries, serious oxidative damage, as well as neuronal apoptosis in hippocampus of rats [14]. We studied for evidence about MCLR-induced ER stress in the hippocampus and its role in underlying synaptic plasticity and cognitive impairment. Dysfunction of cognition and synaptic plasticity could be prevented by TUDCA, suggesting that ER stress plays a critical role in underlying memory deficits in rats treated with MCLR
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