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

Hippocampus, 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.

The 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.

We 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.

The present findings signify the crucial role of vitamin D on the basic synaptic transmission and synaptic plasticity.