| First Author | Bender M | Year | 1997 |
| Journal | Brain Res Mol Brain Res | Volume | 49 |
| Issue | 1-2 | Pages | 271-7 |
| PubMed ID | 9387887 | Mgi Jnum | J:43604 |
| Mgi Id | MGI:1098091 | Doi | 10.1016/s0169-328x(97)00161-7 |
| Citation | Bender M, et al. (1997) D1 receptors mediate dopamine action in the fetal suprachiasmatic nuclei: studies of mice with targeted deletion of the D1 dopamine receptor gene. Brain Res Mol Brain Res 49(1-2):271-7 |
| abstractText | Studies in rodents suggest the presence of a dopaminergic system that influences the function of a biological clock in the hypothalamic suprachiasmatic nuclei (SCN). To provide insights into mechanisms of dopamine action in the SCN, we studied transgenic mice that had either one allele (+-) or both alleles (-/-) of the D1 dopamine receptor gene deleted, along with normal (+/+) littermates. As expected, receptor labelling autoradiography studies using [125I]SCH 23982 showed a complete absence of D1 dopamine receptor binding sites in the SCN of -/- animals. When pregnant mice from +- x +- matings were injected with the D1 receptor agonist SKF 38393, or the dopamine reuptake blocker GBR 12909 at day 19 of gestation, c-fos mRNA expression was observed in the SCN of +/+ fetuses. In contrast, c-fos mRNA induction was not seen in - /- or +- litter mates. Injection of cocaine into pregnant dams also resulted in robust SCN c-fos mRNA expression in +/+ mice. Increases in SCN c-fos mRNA expression were also seen in +- and -/- mice suggesting that cocaine action in the SCN involves both D1 receptor-dependent and - independent mechanisms. Collectively, our studies of transgenic mice deficient in D1 receptors support the presence of a functional dopaminergic system in the fetal SCN. We also identify D1 receptors as the prominent transducer of dopamine action in the fetal SCN. |
