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Altered c ‐ fos expression in the parabrachial nucleus in a rodent model of CFA‐induced peripheral inflammation
Author(s) -
Bellavance Lisa L.,
Beitz Alvin J.
Publication year - 1996
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19960311)366:3<431::aid-cne5>3.0.co;2-5
Subject(s) - parabrachial nucleus , nociception , lateral parabrachial nucleus , spinal cord , neuroscience , hyperalgesia , biology , noxious stimulus , nucleus , medicine , receptor
Increases in the expression of immediate early genes have been shown to occur in the lumbar spinal cord dorsal horn after peripheral inflammation. Given that the pontine parabrachial nucleus has been implicated in nociceptive as well as antinociceptive processes and is reciprocally connected with the spinal cord dorsal horn, it seems likely that peripheral inflammation will cause alterations in immediate early gene expression in this nucleus. To test this hypothesis we examined cFos‐like immunoreactivity in a rodent complete Freund's adjuvant‐induced peripheral inflammatory model of persistent nociception. Unilateral hind paw injections of complete Freund's adjuvant produced inflammation, hyperalgesia of the affected limb, and alterations in open field behaviors. Immunocytochemical analysis demonstrated a bilateral increase in cFos‐like immunoreactivity in the lateral and Kolliker‐Fuse subdivisions of the parabrachial nucleus at 6 and 24 hours postinjection and an ipsilateral decrease below basal levels in the Kolliker‐Fuse subdivision at 96 hours postinjection when compared to saline controls. Taken together, these results suggest that select parabrachial neurons are activated by noxious somatic inflammation. These active parabrachial neurons are likely to participate in ascending nociceptive and/or descending antinociceptive pathways. © 1996 Wiley‐Liss, Inc.