Effects of calcium on drinking fluorosis-induced hippocampal synaptic plasticity impairment in the offspring of rats

Abstract

This study investigated the effects of calcium on fluorosis-induced impairment in learning and memory of offspring rats. Methods Seventy-five newly weaned female Sprague-Dawley (SD) rats were randomly divided into five groups as follows: Control group (Control) drank tap water, and ate the normal diet (calcium content of 0.79%); fluoride group (F) drank 100 mg/L NaF solution, and ate the normal diet; low calcium group (LCa) drank tap water, and ate the low calcium diet (calcium content of 0.063%); low calcium fluoride group (F+LCa) drank 100 mg/L NaF solution, and ate the low calcium diet; high calcium fluoride group (F+HCa) drank 100 mg/L NaF solution, and ate the high calcium diet (calcium content of 7%). After exposing rats to fluoride for three months, male and female rats were mated and 14 and 28 days old offspring were obtained as experimental subjects. Examinations determined the submicroscopic parameters of the synaptic interface and expression levels of specific proteins: doublecortin (DCX) and synaptophysin (p38). (1) High fluorosis significantly reduced synapse density, length of synaptic active zone, thickness of postsynaptic density, and led to abnormal changes in the structural parameter of synaptic gap width, which was significantly reduced or increased. High dietary calcium significantly reversed the abnormal changes in structural parameters, and low calcium aggravated these variations. (2) Dietary calcium resulted in nonsignificant effect on expression levels of DCX and p38. The results suggested that dietary calcium significantly affected hippocampal synaptic plasticity of offspring of mothers exposed to water fluorosis, but its molecular mechanism may not be related to the expression of DCX and p38 in the brain. The findings also demonstrate the important effects of maternal exposure to water fluorosis on offspring brain functions before water improvement.