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Papers of the Week


Papers: 13 Jun 2020 - 19 Jun 2020


Animal Studies

PAIN TYPE:
Migraine/Headache


2020 Jun


Sci Adv


6


23

Editor's Pick

Astrocyte dysfunction increases cortical dendritic excitability and promotes cranial pain in familial migraine.

Authors

Romanos J, Benke D, Pietrobon D, Zeilhofer H U, Santello M
Sci Adv. 2020 Jun; 6(23):eaaz1584.
PMID: 32548257.

Abstract

Astrocytes are essential contributors to neuronal function. As a consequence, disturbed astrocyte-neuron interactions are involved in the pathophysiology of several neurological disorders, with a strong impact on brain circuits and behavior. Here, we describe altered cortical physiology in a genetic mouse model of familial hemiplegic migraine type 2 (FHM2), with reduced expression of astrocytic Na,K-ATPases. We used whole-cell electrophysiology, two-photon microscopy, and astrocyte gene rescue to demonstrate that an impairment in astrocytic glutamate uptake promotes NMDA spike generation in dendrites of cingulate cortex pyramidal neurons and enhances output firing of these neurons. Astrocyte compensation of the defective ATPase in the cingulate cortex rescued glutamate uptake, prevented abnormal NMDA spikes, and reduced sensitivity to cranial pain triggers. Together, our results demonstrate that impaired astrocyte function alters neuronal activity in the cingulate cortex and facilitates migraine-like cranial pain states in a mouse model of migraine.