The significance of increase in striatal D(2) receptors in epileptic EL mice.
The present study systematically and quantitatively analyzed the immunohistochemical distribution of various substances involved in synthesis, binding, and transport of dopamine in the forebrain of epileptic mice (EL mouse strain) using a brain mapping analyzer. A reduction in serum calcium levels decreases calcium/calmodulin-dependent-dopamine synthesis in the brain and subsequently increases susceptibility to epileptic convulsions and induces abnormal behavior in EL mice. The immunohistochemical levels of D(2) receptors in the medial area of the neostriatum were significantly higher in EL mice than in ddY mice (mother strain of EL mice), while there were no differences in the levels of tyrosine hydroxylase, calcium/calmodulin-dependent protein kinase II, calmodulin, D(1) receptors, and dopamine transporters. Together with our previous findings, the results suggest that the decrease in serum calcium levels and subsequent decrease in brain dopamine synthesis comprise the primary physiologic disorder in EL mice, and convulsions or increased D(2) receptors are secondarily-induced phenomena to improve or compensate for the principal disorder.[1]References
- The significance of increase in striatal D(2) receptors in epileptic EL mice. Sutoo, D., Akiyama, K. Brain Res. (2003) [Pubmed]
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