| Autor: |
Murcia V; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. murciava17@mail.vmi.edu., Johnson L; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. johnsonlk17@mail.vmi.edu., Baldasare M; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. baldasaremp16@mail.vmi.edu., Pouliot B; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. pouliotba16@mail.vmi.edu., McKelvey J; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. mckelveyjm16@mail.vmi.edu., Barbery B; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. barberyb18@mail.vmi.edu., Lozier J; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. lozierja@vmi.edu., Bell WE; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. bellwe@vmi.edu., Turner JE; Department of Biology, Center for Molecular, Cellular, and Biological Chemistry, Virginia Military Institute, Lexington, VA 24450, USA. turnerje@vmi.edu. |
| Abstrakt: |
Nitric oxide (NO) has been shown to affect motor function. Specifically, NO has been shown to act through regulation of dopamine (DA) release, transporter function, and the elicitation of neuroprotection/neurodegeneration of neurons. Recently, zebrafish have been proposed to be a new model for the study of various types of motor dysfunctions, since neurotoxin damage to their nigrostriatal-like neurons exhibit motor anomalies similar to those of mammalian models and human patients. Results from this study demonstrate that when NO synthesis is inhibited in zebrafish, using a neuronal NO synthase inhibitor (nNOSI), a condition called 'listless' occurs, where the fish lack swimming abilities, are rigid, and have difficulty maintaining balance. Additionally, co-treatment with either NO or estrogen (E2), an upstream regulator of NO synthase, can rescue fish from the 'listless' phenotype caused by exposure to the neurotoxin 6-hydroxydopamine (6 OHDA). In turn, NO deprived zebrafish were rescued from the 'listless' phenotype when co-treated with L-DOPA, a precursor to DA. Interestingly, the longer fish are exposed to a 6 OHDA + nNOSI co-treatment, the slower the recovery after washout, compared to a single treatment of each. Most significantly, NO involvement in the motor homeostasis of the embryonic zebrafish was shown to be expressed through the NO-cGMP-dependent pathway, and response to nNOSI treatments is developmentally regulated. In conclusion, these results indicate that there is a link between E2, NO, and DA systems that regulate motor functions in the embryonic zebrafish. |
