NEUROTRANSMITTERS IN THE CNS OF THE VITAMIN-D DEFICIENT, HYPOCALCEMIC RAT

Sprague-Dawley rats were made chronically vitamin D deficient (VDD) and hypocalcemic, or VDD and normocalcemic. Rickets, severely reduced body weight, hair shedding, lethargy, muscular paralysis and a high mortality rate are characteristic features of the male VDD/hypocalcemic animals. An assessment was made of the neurotransmitter status of the VDD-hypocalcemic and VDD/normocalcemic animals. In nine out of eleven regions of the CNS studied, the increase in GABA induced by the GABA-T inhibitor ethanolamine sulphate (EOS) was significantly higher (P < 0.05 or P < 0.01) in the VDD/hypocalcemic group vs the normal controls. However, the EOS-mediated increase in GABA was similar in the VDD/normocalcemic and normal control groups suggesting that hypocalcemia is the likely cause of the increased GABA turnover in the VDD/hypocalcemic rats. Glutamate, dopamine, dihydroxyphenylacetic acid, homovanillic acid and norepinephrine, were also analysed in representative regions of the CNS. Their concentrations were not affected in any consistent way in either the VDD/hypocalcemic group or VDD/normocalcemic groups vs the normal controls. Therefore, despite the chronic, severe pathology induced by vitamin D deficiency and hypocalcemia, the neurotransmitters studied appeared to be normal in the CNS of these animals.