α-Neurexins couple Ca2+ channels to synaptic vesicle exocytosis

By M. Missler, Weiqi Zhang, A. Rohlmann, Gunnar Kattenstroth, R. Hammer, K. Gottmann, T. Sūdhof. Nature, 2003

595 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4b93eea1b5bb1fd30d9202758463386e4406706d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. T. Sūdhof
2. Ann Marie Craig
3. H. Zoghbi
4. Mark F. Bear
5. S. Harrison

In Cellular and Molecular Neuroscience

1. T. Sūdhof
2. Mark F. Bear
3. H. Zoghbi
4. Ann Marie Craig
5. Yunhee Kang
6. Weiqi Zhang
7. M. Missler
8. G. Aramuni

In Molecular Biology

1. T. Sūdhof
2. H. Zoghbi
3. Mark F. Bear
4. Ann Marie Craig
5. Weiqi Zhang
6. M. Missler
7. G. Aramuni
8. S. Harrison

Citations in the corpus

• Extracellular Domains of α-Neurexins Participate in Regulating Synaptic Transmission by Selectively Affecting N- and P/Q-Type Ca2+ Channels (2005, methodology): “1A): (1) the original neurexin 1 transgene ( Nrx::HRP) (Missler et al., 2003) and (2) a newly generated neurexin 1 transgene ( Nrx::HRP).”
• Neuroligins determine synapse maturation and function. (2006, unknown): “This ratio is very similar to that observed in respiratory brainstem slices from newborn wild-type mice (Missler et al., 2003).”
• Neuroligins and neurexins link synaptic function to cognitive disease (2008, background): “I suggest that these molecules are required for synapse function but not for synapse formation, that they affect trans-synaptic activation of synaptic transmission but are not essential for synaptic cohesion of the presynaptic and postsynaptic specializations, and that their dysfunction impairs the ”
• Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “Presynaptic Ca 2+ channel function was compromised in the α -NRXN-null mice based on decreased presynaptic Ca 2+ currents, especially N-type Ca 2+ currents (Missler et al. 2003).”
• Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2. (2007, unknown): “Indeed, results from knockout (KO) mice demonstrated that neither NLs nor a-neurexins are required for the initial formation of synapses, but both are essential for synaptic function and mouse survival (Missler et al., 2003; Varoqueaux et al., 2006).”
• Neurexin-neuroligin signaling in synapse development. (2007, background): “The link between a-neurexins and presynaptic Ca channels is essential for function of both glutamatergic and GABAergic synapses in vivo [46].”