| dc.contributor.advisor | Nitsche, Michael Prof. Dr. | |
| dc.contributor.author | Mueller, Lynn Elena | |
| dc.date.accessioned | 2018-11-05T10:30:30Z | |
| dc.date.available | 2018-11-20T23:50:06Z | |
| dc.date.issued | 2018-11-05 | |
| dc.identifier.uri | http://hdl.handle.net/11858/00-1735-0000-002E-E4EF-D | |
| dc.identifier.uri | http://dx.doi.org/10.53846/goediss-7120 | |
| dc.identifier.uri | http://dx.doi.org/10.53846/goediss-7120 | |
| dc.language.iso | eng | de |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | |
| dc.subject.ddc | 610 | de |
| dc.title | The effect of apomorphine on anodal tDCS-induced cortical plasticity in the human motor cortex | de |
| dc.type | doctoralThesis | de |
| dc.contributor.referee | Nitsche, Michael Prof. Dr. | |
| dc.date.examination | 2018-11-13 | |
| dc.description.abstracteng | The aim of this thesis was to study the effect of apomorphine on non-focal anodal tDCS-induced plasticity and thus further examine the influence of the dopaminergic system on motor cortex plasticity in humans. In a randomized double blind study design, 12 healthy subjects received in four different sessions intracutaneous injections of placebo or 0.1, 0.2, 0.3 mg of apomorphine, a global dopamine agonist, while the effect of anodal tDCS-induced motor cortical plasticity was examined. In accordance with previous research, in the placebo medication condition cortical excitability was significantly enhanced by anodal tDCS. For all dosages of apomorphine explored in the present experiment, anodal tDCS-induced plasticity effects were abolished. 0.1, 0.2, and 0.3 mg apomorphine are comparable to low doses of other dopamine agents, such as L-dopa. Hence, those findings are in line with previous research showing that low doses of dopamine lead to an abolishment of plasticity induction. Low doses of apomorphine (i.e. ~0.004 mg/kg) are assumed to mainly stimulate presynaptic dopamine receptors, whose activation leads to a decrease in dopamine neurotransmission through negative feedback mechanisms and thus to a reduction in dopaminergic firing rate. As the activation of presynaptic dopamine receptors reduce excitatory glutamatergic transmission, this can explain why apomorphine abolished the anodal tDCS effect.
However, some questions remain to be explored, for instance the influence of higher doses of apomorphine on tDCS-induced plasticity and consequently more research is needed to fully understand the role of dopamine in neuroplasticity. | de |
| dc.contributor.coReferee | Hülsmann, Swen Prof. Dr. | |
| dc.contributor.thirdReferee | Wedekind, Dirk Prof. Dr. | |
| dc.subject.eng | apomorphine | de |
| dc.subject.eng | neuroplasticity | de |
| dc.identifier.urn | urn:nbn:de:gbv:7-11858/00-1735-0000-002E-E4EF-D-4 | |
| dc.affiliation.institute | Medizinische Fakultät | de |
| dc.subject.gokfull | Medizin (PPN619874732) | de |
| dc.description.embargoed | 2018-11-20 | |
| dc.identifier.ppn | 1039858562 | |