Abstract
a-Calcitonin gene-related peptide (aCGRP) is a pleiotropic peptide neuromodulator that is widely expressed throughout the central and peripheral nervous systems. Although CGRP has been implicated in numerous physiological processes (including peripheral vasodilatation, acetylcholine receptor biosynthesis, nociception, and neurogenic inflammation), the precise physiological roles of CGRP remain to be elucidated. To provide a better understanding of the physiological role(s) mediated by this peptide neurotransmitter, we have generated aCGRP-null mice by targeted modification in embryonic stem cells.
Highlights
ALTERATIONS IN NEUROGENIC INFLAMMATORY RESPONSES IN MICE LACKING α-Calcitonin gene-related peptide (αCGRP)
Numerous studies have indicated that the release of CGRP and tachykinins from the peripheral endings of sensory nerves leads to a neurogenic inflammatory response characterized by an edematous reaction resulting from local vasodilatation and plasma extravasation
Direct assessment of plasma extravasation in capsaicin-treated animals, using intravenous administration of Evans Blue, paralleled the results observed with changes in ear thickness (∆T) as plasma extravasation was reduced in α-Calcitonin gene-related peptide (αCGRP)-null mice by 56% when compared to control animals
Summary
ALTERATIONS IN NEUROGENIC INFLAMMATORY RESPONSES IN MICE LACKING αCGRP Numerous studies have indicated that the release of CGRP and tachykinins from the peripheral endings of sensory nerves leads to a neurogenic inflammatory response characterized by an edematous reaction resulting from local vasodilatation and plasma extravasation.
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