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Activity in neurons from the nodose ganglia after treatment with CP 55,940 and cholecystokinin
Author(s) -
Rose Juliane M,
Freeman Kimberly G,
Edwards Gaylen L
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb614
Subject(s) - cholecystokinin , nodose ganglion , neuron , agonist , medicine , cannabinoid receptor , endocannabinoid system , endocrinology , cannabinoid , receptor , chemistry , neuropeptide , biology , neuroscience , vagus nerve , stimulation
Previous work has shown that endocannabinoids increase feeding, while cholecystokinin (CCK) has an anorexigenic effect on food intake. Receptors for these hormones are located on cell bodies of vagal afferent nerves in the nodose ganglia. An interaction of CCK with endocannabinoid receptors has been suggested (J. Neurosci. 24:2708, 2004). The purpose of these studies is to explore the effect of pretreatment with a cannabinoid agonist, CP 55,940 (CP), on nodose neuron activation by CCK. To determine the effect of CP and CCK on neuron activation, rats were anesthetized and nodose ganglia were extirpated. The neurons were dissociated and plated. The cells were treated with media, CP, CCK, or CP followed by CCK. Immunohistochemistry was performed to stain the cells for cFos as a measure of cell activation. Neurons were identified using neurofilament immunoreactivity. The neurons on each slip were counted using fluorescence imaging, and the number of neurons that were c‐Fos and neurofilament positive were counted. Pretreatment with CP 55,940 decreased the percentage of neurons expressing cFos‐immunreactivity in response to CCK. This observation suggests that endocannabinoids inhibit CCK activation of nodose ganglion neurons. (Supported by Univ of Georgia Research Foundation and College of Veterinary Medicine)