Reverberation of cortical spreading depression along closed-loop pathways in rat cerebral cortex.

1972 ◽  
Vol 35 (3) ◽  
pp. 381-388 ◽  
Author(s):  
M Shibata ◽  
J Bures
2005 ◽  
Vol 391 (1-2) ◽  
pp. 51-55 ◽  
Author(s):  
Ranilson de Souza Bezerra ◽  
Ricardo Abadie-Guedes ◽  
Flávio Roberto Mendonça Melo ◽  
Ana Maria de Albuquerque Paiva ◽  
Ângela Amâncio-dos-Santos ◽  
...  

Cephalalgia ◽  
2016 ◽  
Vol 39 (3) ◽  
pp. 333-341 ◽  
Author(s):  
Yan Wang ◽  
Anne E Tye ◽  
Junli Zhao ◽  
Dongqing Ma ◽  
Ann C Raddant ◽  
...  

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.


1993 ◽  
Vol 3 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Jochen Gehrmann ◽  
Guenter Mies ◽  
Petra Bonnekoh ◽  
Richard Banati ◽  
Takehiko Iijima ◽  
...  

2014 ◽  
Vol 39 (12) ◽  
pp. 2431-2439 ◽  
Author(s):  
Emanuela Viggiano ◽  
Davide Viggiano ◽  
Alessandro Viggiano ◽  
Bruno De Luca ◽  
Marcellino Monda

1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.


1993 ◽  
Vol 602 (1) ◽  
pp. 99-103 ◽  
Author(s):  
D.G. Herrera ◽  
D. Maysinger ◽  
R. Gadient ◽  
C. Boeckh ◽  
U. Otten ◽  
...  

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