EA1-linked Kv1.1 dysfunction enhances susceptibility to cerebellar spreading depression and a transient cerebellar refractory state

Ilenio Servettini; Alfredo Megaro; Martino Caramia; Luigi Sforna; Antonio Michelucci; Luigi Catacuzzeno

doi:10.1016/j.bbadis.2026.168302

May 1, 2026Biochimica et Biophysica Acta (BBA) - Molecular Basis of DiseaseOpen Access

EA1-linked Kv1.1 dysfunction enhances susceptibility to cerebellar spreading depression and a transient cerebellar refractory state

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Key Points

The research aims to understand how the EA1-linked Kv1.1 mutation influences cerebellar spreading depression in mice.
Investigated the pharmacological differences between cerebellar and cortical spreading depression
Analyzed synaptic suppression duration during EA1 attacks
Assessed the effects of the Kv1.1 V408A mutation in mice.
CeSD showed distinct pharmacological characteristics compared to cortical SD.
Ea1 attacks correlated with transient synaptic suppression duration.
Mice with the Kv1.1 V408A mutation demonstrated increased susceptibility to CeSD.

Implication

Examines how Kv1.1 mutation affects cerebellar spreading depression, implying increased susceptibility in affected individuals.

Abstract

• Mice cerebellar spreading depression (CeSD) differs pharmacologically from cortical SD. • CeSD induces a transient synaptic suppression that mirrors the duration of EA1 attacks. • The EA1-associated Kv1.1 V408A mutation increases susceptibility to the CeSD in mice.

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Cite This Study

Servettini et al. (2026) studied this question.

synapsesocial.com/papers/6a168a340c924ddd1bd58dd5 https://doi.org/10.1016/j.bbadis.2026.168302

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EA1-linked Kv1.1 dysfunction enhances susceptibility to cerebellar spreading depression and a transient cerebellar refractory state

Key Points

Implication

Abstract

Discussion

Cite This Study

EA1-linked Kv1.1 dysfunction enhances susceptibility to cerebellar spreading depression and a transient cerebellar refractory state

Key Points

Implication

Abstract

Discussion

Cite This Study

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