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Elucidating The Cellular Markers In The Extended Amygdala Associated With Acute Morphine‐Induced Withdrawal
Author(s) -
Brown Michael Kameron,
Radke Anna K,
Meisel Robert L.,
Gewirtz Jonathan C.
Publication year - 2010
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.24.1_supplement.lb612
Subject(s) - amygdala , stria terminalis , creb , extended amygdala , morphine , immediate early gene , anxiety , c fos , nucleus , central nucleus of the amygdala , neuroscience , psychology , endocrinology , medicine , chemistry , gene expression , gene , psychiatry , transcription factor , biochemistry
Anxiety is a classic symptom of withdrawal that often occurs in humans and animals. Preliminary studies show that anxiety in animals occurs four hours after acute morphine exposure. However, the question of the neurological structures associated with this phenomenon remains unanswered. Structures such as the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST) have been shown to have crucial overlapping roles in mediating anxiety. Therefore through the use of the immediate early genes (IEGs) c‐Fos and p‐CREB, which serve as molecular markers, we investigated whether structures in the extended amygdala are involved in acute morphine‐induced anxiety in spontaneous and precipitated withdrawal. Cellular activation was observed through c‐Fos staining of the CeA, two hours after withdrawal from morphine. Definitive conclusions could not be drawn from the c‐Fos staining in the BNST. The p‐CREB staining in the CeA suggests that this region was activated by spontaneous withdrawal from morphine. The p‐CREB staining in the BNST suggests that this region of the brain may be activated by both precipitated and spontaneous withdrawal. Together the data from this experiment supports the hypothesis that extended amygdala structures are involved in acute‐morphine induced withdrawal. Supported by NIH T34GM008411