Vitamin D supplementation restores suppressed synaptic plasticity in Alzheimer's disease

Abstract

ObjectivesHippocampus, an appropriate area of brain for assessment of long-term potentiation (LTP), has been found to be susceptible to neural damages caused by Alzheimer's disease. Evidence indicates that vitamin D supports nerve transmission and synaptic plasticity. Vitamin D receptors are expressed in the hippocampus.MethodsThe present study evaluates occurrence of LTP in the control (CON) group fed with normal regimen and, three groups of Aβ-treated rats taking normal (ALZ), vitamin D-free (ALZ − D), or 1,25(OH)2D3 supplemented (ALZ + D) food regimens. In in vivo experiments pre- and post-tetanus field extracellular postsynaptic potentials (fEPSPs) were recorded in the CA3–CA1 pathway.ResultsWe found that the amplitude of baseline fEPSPs was significantly lower in the ALZ group compared with the CON one; lack of vitamin D further declined the amplitude of responses in the ALZ − D animals. While the tetanic stimulation elicited a considerable LTP in the CON rats it was failed to induce LTP in the ALZ animals. Furthermore, the tetanus considerably depressed the amplitude of recordings in the ALZ − D group. 1,25(OH)2D3 supplementation restored post-tetanus potentiation of fEPSPs amplitude in the ALZ + D groups.DiscussionThe present findings signify the crucial role of vitamin D on the basic synaptic transmission and synaptic plasticity.