Adenosine 3',5' -monophosphate in rat cerebral cortex: effect of potassium ions in vivo (cortical spreading depression)

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.

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Microglial Reaction in the Rat Cerebral Cortex Induced by Cortical Spreading Depression

Brain Pathology ◽

10.1111/j.1750-3639.1993.tb00720.x ◽

1993 ◽

Vol 3 (1) ◽

pp. 11-17 ◽

Cited By ~ 114

Author(s):

Jochen Gehrmann ◽

Guenter Mies ◽

Petra Bonnekoh ◽

Richard Banati ◽

Takehiko Iijima ◽

...

Keyword(s):

Cerebral Cortex ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Rat Cerebral Cortex

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

Journal of Neurophysiology ◽

10.1152/jn.1972.35.3.381 ◽

1972 ◽

Vol 35 (3) ◽

pp. 381-388 ◽

Cited By ~ 40

Author(s):

M Shibata ◽

J Bures

Keyword(s):

Cerebral Cortex ◽

Cortical Spreading Depression ◽

Closed Loop ◽

Spreading Depression ◽

Rat Cerebral Cortex

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Increased 20-HETE Synthesis Explains Reduced Cerebral Blood Flow But Not Impaired Neurovascular Coupling after Cortical Spreading Depression in Rat Cerebral Cortex

Journal of Neuroscience ◽

10.1523/jneurosci.2308-12.2013 ◽

2013 ◽

Vol 33 (6) ◽

pp. 2562-2570 ◽

Cited By ~ 43

Author(s):

J. C. Fordsmann ◽

R. W. Y. Ko ◽

H. B. Choi ◽

K. Thomsen ◽

B. M. Witgen ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Cortex ◽

Cerebral Blood Flow ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Neurovascular Coupling ◽

Rat Cerebral Cortex

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Protein kinase C in the rat cerebral cortex during spreading depression

Neuroscience Letters ◽

10.1016/0304-3940(96)12666-5 ◽

1996 ◽

Vol 210 (2) ◽

pp. 79-82 ◽

Cited By ~ 2

Author(s):

Jiri Krivanek ◽

Valeria I. Koroleva

Keyword(s):

Cerebral Cortex ◽

Protein Kinase C ◽

Protein Kinase ◽

Spreading Depression ◽

Rat Cerebral Cortex ◽

Kinase C

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In Vivo Uptake of [3H]Nimodipine into Brain during Cortical Spreading Depression

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/00004647-199705000-00014 ◽

1997 ◽

Vol 17 (5) ◽

pp. 586-590 ◽

Cited By ~ 5

Author(s):

Sachiko Osuga ◽

Antoine M. Hakim ◽

Hitoshi Osuga ◽

Matthew J. Hogan

Keyword(s):

Rat Brain ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Control Group ◽

Similar Measurement ◽

Contralateral Hemisphere ◽

Radiotracer Uptake ◽

Uptake Studies ◽

In Vivo Uptake

We report autoradiographic measurements of the in vivo uptake of [3H]nimodipine during the nonischemic depolarization of cortical spreading depression (CSD) in rat brain. [3H]Nimodipine uptake in brain was determined regionally in rats undergoing CSD (n = 8) and was significantly increased in cortex (14 ± 7%) and hippocampus (10 ± 6%) on the stimulated side relative to the contralateral hemisphere when compared with the same measurements in a control group (n = 8). A similar measurement using the physiologically inert radiotracer [14C]iodoantipyrine to control for potential effects of CSD on radioligand distribution showed a minimal increase (2.4 ± 0.7%) of radiotracer uptake in cortex after CSD. This increase was significantly less than that observed in the [3H]nimodipine uptake studies. We hypothesize that increased in vivo [3H]nimodipine uptake in CSD identifies regions of depolarization and thus infers activation of the L-type voltage sensitive calcium channels.

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