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Diazepam binding inhibitor (DBI) increases after acute stress in rat
C Ferrarese1, T Mennini, N Pecora
1Department of Neurology, University of Milan, Ospedale San Gerardo, Monza, Italy.
Neuropharmacology
|December 1, 1991
Summary
Stress increases diazepam binding inhibitor (DBI) in the brain and adrenal gland. This DBI may regulate steroidogenesis via mitochondrial benzodiazepine receptors (MBR) during stress responses.
Area of Science:
- Neuroendocrinology
- Stress Physiology
Background:
- Diazepam binding inhibitor (DBI) interacts with GABAA/benzodiazepine receptors (GBR) and mitochondrial benzodiazepine receptors (MBR).
- DBI acting at MBR influences ACTH-induced steroidogenesis.
- Stress alters GBR and MBR levels, suggesting a role for DBI in stress adaptation.
Purpose of the Study:
- To investigate modifications in DBI, GBR, and MBR levels in response to acute noise stress.
- To examine these changes in various brain regions and the adrenal gland.
Main Methods:
- Utilized an acute noise stress model in rats.
- Analyzed DBI, GBR, and MBR content in brain areas (hippocampus) and adrenal glands.
Main Results:
- Acute stress elevated DBI and ODN-like immunoreactivity in the hippocampus.
- Hippocampal GBR decreased while MBR increased following DBI elevation.
- Adrenal cortex DBI and MBR content increased within the first hour post-stress, correlating with corticosterone levels.
Conclusions:
- DBI levels and MBR content are modulated by acute stress in the brain and adrenal gland.
- DBI, through MBR, may play a regulatory role in stress-induced steroidogenic function.