Effects of subchronic aluminum exposure on spatial memory, ultrastructure and L-LTP of hippocampus in rats

Abstract

-Epidemiological investigations have indicated that aluminum (Al), as an important environmental neurotoxicant, could cause damage to the cognitive function which was closely related with neurodegenerative diseases. Long-term potentiation (LTP) is one form of synaptic plasticity in association with cognitive function. Previous studies have demonstrated that Al impaired early phase long-term potentiation (E-LTP) in vivo and in vitro. However, Al-induced damage to late phase long-term potentiation (L-LTP) has poorly been studied. The present study was designed to observe the effects of subchronic Al exposure on the spatial memory, hippocampus ultrastructure and L-LTP in rats. Pregnant Wistar rats were assigned to four groups. Neonatal rats were exposed to Al by parental lactation from parturition to weaning for 3 weeks and then fed with the distilled water containing 0, 0.2%, 0.4% and 0.6% aluminum chloride (AlCl 3 ) respectively from weaning to postnatal 3 months. The levels of Al in blood and hippocampus were quantitated by atomic absorption spectrophotometer. Morris water maze test was performed to study spatial memory. The induction and maintenance of L-LTP in area of Schaffer collateral-CA1 synapse was recorded by extracellular microelectrode recording technology in hippocampus of experimental rats. Hippocampus was collected for transmission electron microscopy observation. The results showed that the Al concentrations in blood and hippocampus of Al-exposed rats were higher than those of the control rats. Al could impair spatial memory ability of rats. Neuronal and synaptic ultrastructure from Al-exposed rats presented pathological changes; the incidence of L-LTP has a decrease trend while population spike (PS) amplitude was much smaller significantly stimulated by high-frequency stimulation (HFS) in Al-exposed rats. Our findings showed that Al exposure caused spatial memory damage, under which the neuronal and synaptic ultrastructure changes maybe were their morphological basis and the impaired L-LTP of hippocampus could be their electrophysiological basis.

A review of the bioactivity of hydraulic calcium silicate cements

“…These results have led to the preparation of experiment bioactive tricalcium silicate 76,77 and dicalcium silicate 78 cements for endodontic applications. The use of these experimental calcium silicate cements should alleviate potential concerns regarding aluminium-induced neurotoxicity 79–81 that may arise with the clinical use of clinker-derived tricalcium aluminate-containing HCSCs.…”

Bioactivity of Mineral Trioxide Aggregate and Mechanism of Action

“…These results have led to the preparation of experiment bioactive tricalcium silicate [30,48] and dicalcium silicate [25] cements for endodontic applications. The use of these experimental calcium silicate cements should alleviate potential concerns regarding aluminium-induced neurotoxicity [69,141,171] that may arise with the clinical use of clinker-derived tricalcium aluminate-containing hydraulic calcium (alumino)silicate cements.…”

Neuroprotective effects of eugenol against aluminiuminduced toxicity in the rat brain

“…As a result of the wide usage of such a well-established neurotoxin (3)(4)(5), Al has become a global public health problem. Reports have also defined it as an important etiological factor in the progression of several neurodegenerative disorders as it influences more than 200 biologically important reactions (6,7). Aluminium-induced brain toxicity was reported in rats by many authors, including administration of aluminium chloride hexahydrate (25 mg kg -1 day -1 ) for one month by oral gavage (8), daily oral treatment with aluminium chloride (100 mg kg ) orally for four consecutive weeks (9,10).…”