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Abnormal motor function and the expression of striatal dopamine D2 receptors in manganese-treated mice
1Department of Public Health, Keimyung University, Taegu 704-701, Korea.
Abstract:
Manganese (Mn) plays an important role in the etiology of several neurobehavioral disorders, but there is a lack of data regarding its specific effects on neurotransduction, especially dopaminergic neurotransduction. We investigated the relationship between motor deficits and alterations in the expression of tyrosine hydroxylase (TH) and dopamine D2-like receptors (DR), including the three dopaminergic subtypes, D2, D3, and D4, in low- and high-dose Mn-treated mice. After administration of Mn (intraperitoneal injections of 20 or 40 mg/kg MnCl(2).4H(2)O once per day for 5 d), motor activity and expression of TH and DR were examined in the striatum of the mouse brain. Mn treatment resulted in significant decrease in coordination and/or impaired motor learning after 5 d of treatment and this effect remained until 10 d after the end of Mn treatment. The expression of dopamine D2-like receptor D2 (DRD2), but not TH, DRD3, or DRD4, in the striatum was dose-dependent, and statistically significant increases were seen at the mRNA and protein levels. These findings indicate that Mn-induced motor deficits may be modulated in part by the expression of DRD2 in the striatum. In addition, our results suggest that the disturbance of dopaminergic neurotransmission mediated by DRD2 may be involved in the pathogenesis of Mn neurotoxicity.
Insights
Manganese (Mn) exposure impairs motor function in mice by altering dopamine D2-like receptor (DRD2) expression in the brain. This suggests a link between Mn neurotoxicity and dopaminergic system disturbances.
Area of Science:
- Neuroscience
- Toxicology
- Neurochemistry
Background:
- Manganese (Mn) is implicated in neurobehavioral disorders.
- Specific effects of Mn on dopaminergic neurotransmission are not well understood.
Purpose of the Study:
- To investigate the relationship between motor deficits and changes in tyrosine hydroxylase (TH) and dopamine D2-like receptors (DRD2, DRD3, DRD4) expression after Mn exposure.
- To explore the role of dopaminergic neurotransmission in Mn neurotoxicity.
Main Methods:
- Mice were administered low or high doses of MnCl2 via intraperitoneal injection for 5 days.
- Motor activity, coordination, and motor learning were assessed.
- Expression levels of TH and DRD2, DRD3, DRD4 were measured in the striatum at mRNA and protein levels.
Main Results:
- Mn treatment caused significant motor deficits, including decreased coordination and impaired motor learning, persisting for up to 10 days post-treatment.
- A dose-dependent and statistically significant increase in dopamine D2-like receptor D2 (DRD2) expression was observed at both mRNA and protein levels in the striatum.
- Expression of tyrosine hydroxylase (TH), DRD3, and DRD4 remained unchanged.
Conclusions:
- Mn-induced motor deficits are partially modulated by alterations in striatal DRD2 expression.
- Disturbances in DRD2-mediated dopaminergic neurotransmission may contribute to the neurotoxic effects of manganese.
