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Jonas Tjaden, Annika Eickhoff, Sarah Stahlke, Julian Gehmeyr, Matthias Vorgerd, Verena Theis, Veronika Matschke, Carsten Theiß

• T-type \(Ca^{2+}\) 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 \(Ca^{2+}\) channel isoforms, Cav3.1 (encoded by \(\it Cacna1g\)), Cav3.2 (encoded by \(\it Cacna1h\)), and Cav3.3 (encoded by \(\it Cacna1i\)), 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 \(Ca^{2+}\) channels with in vivo- and in vitro-grown PCs and showed the distribution of T-type \(Ca^{2+}\) 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.