Version 1
: Received: 7 May 2024 / Approved: 7 May 2024 / Online: 7 May 2024 (23:49:57 CEST)
How to cite:
Brockhaus, J.; Kahl, I.; Ahmad, M.; Repetto, D.; Reissner, C.; Missler, M. Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+-Influx. Preprints2024, 2024050405. https://doi.org/10.20944/preprints202405.0405.v1
Brockhaus, J.; Kahl, I.; Ahmad, M.; Repetto, D.; Reissner, C.; Missler, M. Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+-Influx. Preprints 2024, 2024050405. https://doi.org/10.20944/preprints202405.0405.v1
Brockhaus, J.; Kahl, I.; Ahmad, M.; Repetto, D.; Reissner, C.; Missler, M. Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+-Influx. Preprints2024, 2024050405. https://doi.org/10.20944/preprints202405.0405.v1
APA Style
Brockhaus, J., Kahl, I., Ahmad, M., Repetto, D., Reissner, C., & Missler, M. (2024). Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+-Influx. Preprints. https://doi.org/10.20944/preprints202405.0405.v1
Chicago/Turabian Style
Brockhaus, J., Carsten Reissner and Markus Missler. 2024 "Conditional Knockout of Neurexins Alters the Contribution of Calcium Channel Subtypes to Presynaptic Ca2+-Influx" Preprints. https://doi.org/10.20944/preprints202405.0405.v1
Abstract
Presynaptic Ca2+-influx through voltage-gated Ca2+-channels (VGCC) is a key signal for synaptic vesicle release. Synaptic neurexins can partially determine the strength of transmission by regulating VGCCs. However, it is unknown whether neurexins modulate Ca2+-influx via all VGCC subtypes similarly. Here, we performed live cell imaging of synaptic boutons from primary hippocampal neurons with a Ca2+-indicator. We used the expression of inactive and active Cre recombinase to compare control to conditional knockout neurons lacking either all or selected neurexin variants. We found that reduced total presynaptic Ca2+-transients caused by the deletion of all neurexins were primarily due to the reduced contribution of P/Q-type VGCCs. The deletion of neurexin1α alone also reduced the total presynaptic Ca2+-influx but increased Ca2+-influx via N-type VGCCs. Moreover, we tested whether the decrease of Ca2+-influx induced by activation of cannabinoid receptor 1 (CB1-receptor) is modulated by neurexins. Unlike earlier observations emphasizing a role for β-neurexins, we found that the decrease of presynaptic Ca2+-transients induced by CB1-receptor activation depended more strongly on the presence of α-neurexins in hippocampal neurons. Together, our results suggest that neurexins have unique roles in the modulation of presynaptic Ca2+-influx through VGCC subtypes and that different neurexin variants may affect specific VGCCs.
Biology and Life Sciences, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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