Abstract
A role for the occipital or retrosplenial cortex in nociceptive processing has not
been demonstrated yet, but connections from these cortices to brain structures involved
in descending pain-inhibitory mechanisms were already demonstrated. This study demonstrated
that the electrical stimulation of the occipital or retrosplenial cortex produces
antinociception in the rat tail-flick and formalin tests. Bilateral lesions of the
dorsolateral funiculus abolished the effect of cortical stimulation in the tail-flick
test. Injection of glutamate into the same targets was also antinociceptive in the
tail-flick test. No rats stimulated in the occipital or retrosplenial cortex showed
any change in motor performance on the Rota-rod test, or had epileptiform changes
in the EEG recording during or up to 3 hours after stimulation. The antinociception
induced by occipital cortex stimulation persisted after neural block of the retrosplenial
cortex. The effect of retrosplenial cortex stimulation also persisted after neural
block of the occipital cortex. We conclude that stimulation of the occipital or retrosplenial
cortex in rats leads to antinociception activating distinct descending pain-inhibitory
mechanisms, and this is unlikely to result from a reduced motor performance or a postictal
phenomenon.
Perspective
This study presents evidence that stimulation of the retrosplenial or occipital cortex
produces antinociception in rat models of acute pain. These findings enhance our understanding
of the role of the cerebral cortex in control of pain.
Key words
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Article info
Publication history
Published online: April 26, 2010
Accepted:
January 25,
2010
Received in revised form:
January 14,
2010
Received:
October 20,
2009
Footnotes
Supported by FAPESP and FAPESP-Cinapse. G.M.R. was the recipient of a CAPES fellowship. N.G.C holds a CNPq-Brazil Research fellowship.
Identification
Copyright
© 2010 American Pain Society. Published by Elsevier Inc. All rights reserved.
