Recent advances into the understanding of molecular mechanism of chronic
pain have been largely developed through the use of genetic manipulations. This is in
part due to the scarcity of selective pharmacological tools, which can be readily solved
by creating knockout or transgenic mice. By identifying new genes that are of import,
our efforts can then be aimed at studying relevant signaling pathways, and combination
of pharmacological manipulations with genetic models can be used to further examine
the specific mechanisms involved in chronic pain. In this review, we will examine the
genetic models that are currently in use to study chronic pain in the anterior cingulate
cortex: knockout mice; transgenic mice; and the strength of combining pharmacology
with these genetic models.
Keywords: Adenylyl cyclase, AMPARs, anterior cingulate cortex, behavior, calcium
calmodulin, chronic pain, electroporation, gene deletion, genetic manipulation, in
vitro, in vivo, inflammatory pain, knockout models, molecular mechanisms, mouse
models, neuropathic pain, NMDARs, regional inhibition, siRNA.
