Induction of calcitonin gene-related peptide expression in rats by cortical spreading depression

Author:

Wang Yan1,Tye Anne E2,Zhao Junli1,Ma Dongqing13,Raddant Ann C4,Bu Fan13,Spector Benjamin L4,Winslow Nolan K4,Wang Minyan13,Russo Andrew F2456

Affiliation:

1. Centre for Neuroscience and

2. Department of Biological Sciences, Xi’an Jiaotong-Liverpool University (XJTLU), SIP, Suzhou 215123, China

3. Neuroscience Program, Departments of

4. Molecular Physiology and Biophysics, and

5. Neurology, University of Iowa, Iowa City, IA 52242, USA;

6. Veterans Affairs Medical Center, Iowa City, IA 52246, USA

Abstract

Objective The neuropeptide calcitonin gene-related peptide (CGRP) has now been established as a key player in migraine. However, the mechanisms underlying the reported elevation of CGRP in the serum and cerebrospinal fluid of some migraineurs are not known. A candidate mechanism is cortical spreading depression (CSD), which is associated with migraine with aura and traumatic brain injury. The aim of this study was to investigate whether CGRP gene expression may be induced by experimental CSD in the rat cerebral cortex. Methods CSD was induced by topical application of KCl and monitored using electrophysiological methods. Quantitative PCR and ELISA were used to measure CGRP mRNA and peptide levels in discrete ipsilateral and contralateral cortical regions of the rat brain 24 hours following CSD events and compared with sham treatments. Results The data show that multiple, but not single, CSD events significantly increase CGRP mRNA levels at 24 hours post-CSD in the ipsilateral rat cerebral cortex. Increased CGRP was observed in the ipsilateral frontal, motor, somatosensory, and visual cortices, but not the cingulate cortex, or contralateral cortices. CSD also induced CGRP peptide expression in the ipsilateral, but not contralateral, cortex. Conclusions Repeated CSD provides a mechanism for prolonged elevation of CGRP in the cerebral cortex, which may contribute to migraine and post-traumatic headache.

Publisher

SAGE Publications

Subject

Neurology (clinical),General Medicine

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