Doxapram increases corticotropin-releasing factor immunoreactivity and mRNA expression in the rat central nucleus of the amygdala
Autor: | Boe Gwun Chun, Song Hyen Choi, Min Soo Lee, Sang Ha Park, Eunju Do, Sung Jin Kim, Kyung Ho Shin, Bo-Hyun Moon |
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Rok vydání: | 2005 |
Předmět: |
Male
endocrine system medicine.medical_specialty Corticotropin-Releasing Hormone Physiology Central nervous system Biology Biochemistry Amygdala Rats Sprague-Dawley Cellular and Molecular Neuroscience Endocrinology Internal medicine Basal ganglia medicine Animals RNA Messenger In Situ Hybridization Central nucleus of the amygdala Doxapram Immunohistochemistry Rats Stria terminalis medicine.anatomical_structure Gene Expression Regulation Paraventricular nucleus of hypothalamus Panic Disorder Central Nervous System Stimulants Septal Nuclei Nucleus hormones hormone substitutes and hormone antagonists Paraventricular Hypothalamic Nucleus medicine.drug |
Zdroj: | Peptides. 26:2246-2251 |
ISSN: | 0196-9781 |
DOI: | 10.1016/j.peptides.2005.03.036 |
Popis: | Doxapram causes panic anxiety in humans. To determine whether doxapram alters corticotropin-releasing factor (CRF) expression in the central nucleus of the amygdala (CeA), paraventricular nucleus of hypothalamus (PVN), or bed nucleus of the stria terminalis (BNST), we used immunohistochemistry to measure CRF peptide in these brain areas after doxapram injection. Doxapram injection significantly increased CRF-like immunoreactivity (CRF-IR) within the CeA, but not in the BNST or PVN, and this increase was significant 2 h after injection. In addition, doxapram significantly increased CRF mRNA expression within the CeA, and this was most prominent 30 min after injection. These results suggest that doxapram selectively increases CRF expression within the CeA, and that this is mediated by increased CRF gene transcription. This increase in CRF-IR within the CeA might explain the doxapram-induced anxiety reaction. |
Databáze: | OpenAIRE |
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