Jonas Tjaden
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jonas Tjaden has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Annika Eickhoff
Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, Universitätsstr. 150, 44801 Bochum, Germany
1 shared publication - Carsten Theiss
Institute of Anatomy, Department of Cytology, Ruhr-University Bochum, 44801 Bochum, Germany
1 shared publication - Julian Gehmeyr
Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, Universitätsstr. 150, 44801 Bochum, Germany
1 shared publication - Matthias Vorgerd
Department of Neurology with Heimer Institute for Muscle Research, Faculty of Medicine, University Hospital Bergmannsheil, Ruhr University Bochum, 44789 Bochum, NRW, Germany
1 shared publication - Sarah Stahlke
Institute of Anatomy, Department of Cytology, Ruhr-University Bochum, 44801 Bochum, Germany
1 shared publication - Verena Theis
Department of Cytology, Institute of Anatomy, Ruhr-University Bochum, Universitaetsstr. 150, Building MA, Level 5, 44780 Bochum, Germany
1 shared publication
Latest Publications
- Open Access
Expression Pattern of T-Type Ca2+ Channels in Cerebellar Purkinje Cells after VEGF Treatment
T-type Ca2+ channels, generating low threshold calcium influx in neurons, play a crucial role in the function of neuronal networks and their plasticity. To further investigate their role in the complex field of research in plasticity of neurons on a molecular level, this study aimed to analyse the impact of the vascular endothelial growth factor (VEGF) on these channels. VEGF, known as a player in vasculogenesis, also shows potent influence in the central nervous system, where it elicits neuronal growth. To investigate the influence of VEGF on the three T-type Ca2+ channel isoforms, Cav3.1 (encoded by Cacna1g), Cav3.2 (encoded by Cacna1h), and Cav3.3 (encoded by Cacna1i), lasermicrodissection of in vivo-grown Purkinje cells (PCs) was performed, gene expression was analysed via qPCR and compared to in vitro-grown PCs. We investigated the VEGF receptor composition of in vivo- and in vitro-grown PCs and underlined the importance of VEGF receptor 2 for PCs. Furthermore, we performed immunostaining of T-type Ca2+ channels with in vivo- and in vitro-grown PCs and showed the distribution of T-type Ca2+ channel expression during PC development. Overall, our findings provide the first evidence that the mRNA expression of Cav3.1, Cav3.2, and Cav3.3 increases due to VEGF stimulation, which indicates an impact of VEGF on neuronal plasticity.
Open AccessExpression Pattern of T-Type Ca2+ Channels in Cerebellar Purkinje Cells after VEGF Treatment
T-type Ca2+ channels, generating low threshold calcium influx in neurons, play a crucial role in the function of neuronal networks and their plasticity. To further investigate their role in the complex field of research in plasticity of neurons on a molecular level, this study aimed to analyse the impact of the vascular endothelial growth factor (VEGF) on these channels. VEGF, known as a player in vasculogenesis, also shows potent influence in the central nervous system, where it elicits neuronal growth. To investigate the influence of VEGF on the three T-type Ca2+ channel isoforms, Cav3.1 (encoded by Cacna1g), Cav3.2 (encoded by Cacna1h), and Cav3.3 (encoded by Cacna1i), lasermicrodissection of in vivo-grown Purkinje cells (PCs) was performed, gene expression was analysed via qPCR and compared to in vitro-grown PCs. We investigated the VEGF receptor composition of in vivo- and in vitro-grown PCs and underlined the importance of VEGF receptor 2 for PCs. Furthermore, we performed immunostaining of T-type Ca2+ channels with in vivo- and in vitro-grown PCs and showed the distribution of T-type Ca2+ channel expression during PC development. Overall, our findings provide the first evidence that the mRNA expression of Cav3.1, Cav3.2, and Cav3.3 increases due to VEGF stimulation, which indicates an impact of VEGF on neuronal plasticity.