Neuroscience letters
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Neuroscience letters · Dec 2005
Pharmacological interactions between calcium/calmodulin-dependent kinase II alpha and TRPV1 receptors in rat trigeminal sensory neurons.
Multiple lines of evidence suggest that calcium/calmodulin-dependent kinase II alpha (CaMKIIalpha) plays an important role in the spinal dorsal horn in nociceptive models of chemical, inflammatory and nerve injury. Moreover, CaMKIIalpha phosphorylates the vanilloid receptor type 1 (TRPV1), thereby regulating vanilloid agonist binding to the receptor. Herein, we have explored a possible interaction of CaMKIIalpha activity with the TRPV1 receptor in rat trigeminal ganglion (TG) neurons in vitro. ⋯ CAP also stimulated a significant approximately 50% increase in autophosphorylation of CaMKIIalpha at Thr286/287. Immunocytochemistry for phospho-CaMKIIalpha indicated that this effect specifically occurred in TRPV1-positive TG neurons. These findings indicate that phopho-CaMKIIalpha is likely to play a role in presynaptic primary afferents in animal models of nociceptive hypersensitivity and provide support for CaMKIIalpha modulation of TRPV1 activity in sensory neurons.
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Neuroscience letters · Dec 2005
Nicotinic receptor involvement in antinociception induced by exposure to cigarette smoke.
Direct exposure of rats to tobacco smoke induces antinociception. We presently investigated if this antinociception is mediated via nicotinic and/or mu-opioid receptors. Adult male rats were surgically implanted with Alzet osmotic minipumps that delivered either saline (control), the nicotinic antagonist mecamylamine, or the opiate antagonist naltrexone (3 mg/kg/day i.v. for 21 days). ⋯ Controls exposed to filtered smoke (with approximately 50% lower nicotine concentration) also exhibited significant analgesia on the first exposure day with rapid development of tolerance. Exposure to high levels of cigarette smoke, or to filtered smoke with a lower nicotine concentration in the vapor phase, induces antinociception with rapid development of tolerance. The antinociceptive effect appears to be mediated via nicotinic and mu-opioid receptors.