A Cacna1a knockin migraine mouse model with increased susceptibility to cortical spreading depression.

By A. M. van den Maagdenberg, D. Pietrobon, T. Pizzorusso, S. Kaja, L. Broos, T. Cesetti, Rob C. G. van de Ven, A. Tottene, Jos van der Kaa, J. Plomp and 2 more. Neuron, 2004

672 citations recorded by the source corpus.

Subfields: Pathology and Forensic Medicine, Psychiatry and Mental health, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/f46485a5c61e8f7571f1603407faa62e065b6ce2

How researchers see this paper

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

In Pathology and Forensic Medicine

1. G. Zamponi
2. R. Noseda
3. R. Burstein
4. P. Goadsby

In Psychiatry and Mental health

1. P. Goadsby
2. G. Zamponi
3. R. Noseda
4. R. Burstein

In Sensory Systems

1. P. Goadsby
2. R. Burstein

Citations in the corpus

• The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (2015, background): “It has become clear that expression of such mutants in heterologous systems is not ideal, because these mutations appear to manifest themselves differently when the channels are present in a native neuronal environment [compare Hans et al. (1999) with Van den Maagdenberg et al. (2004)].”
• PATHOPHYSIOLOGY OF MIGRAINE (2006, background): “Linking the channel disturbance for the first time to the aura process has demonstrated that human mutations expressed in a knock-in mouse produce a reduced threshold for cortically spreading depression (van den Maagdenberg et al, 2004).”
• Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain (2013, background): “In agreement with the human data, mice carrying FHM mutations have shown increased susceptibility to CSD and altered synaptic transmission [36,68,125,127].”