Abstract
Stress-induced renin and prolactin secretion was investigated using a conditioned emotional response paradigm. Three minutes after placement in a chamber the rats received an electric shock to their feet via the grid floor, then were immediately returned to their home cage. This procedure was repeated for 3 consecutive days. On the fourth day, instead of receiving an electric shock, they were removed after 3 min and sacrificed by decapitation. Control rats were treated identically with the exception that shock was not administered at any time. There was a significant increase in plasma renin activity and prolactin level in the stressed rats. The administration of the antianxiety drugs chlordiazepoxide (10 mg/kg i.p.) or midazolam (0.125-2 mg/kg i.p.) blocked the stress-induced increase in prolactin levels but not the stress-induced rise in plasma renin activity. Administration of the β-blocker propranolol (1 mg/kg i.p.) inhibited, but did not completely block, stress-induced rise in plasma renin activity and had no effect on stress-induced prolactin secretion. The opiate antagonist naloxone (0.1-10 mg/kg i.p.) and the acetylcholinesterase inhibitor diisopropyl fluorophosphate (0.5 mg/kg i.p.) did not block stress-induced renin of prolactin secretion. It is concluded that stress-induced prolactin secretion is regulated by a benzodiazepine-mediated mechanism and that stress-induced renin but not prolactin secretion is mediated in part via β-receptors.
Original language | English (US) |
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Pages (from-to) | 257-263 |
Number of pages | 7 |
Journal | Brain research |
Volume | 345 |
Issue number | 2 |
DOIs | |
State | Published - Oct 21 1985 |
Keywords
- benzodiazepine
- diisopropyl fluorophosphate (DFP)
- naloxone
- prolactin
- propranolol
- renin
- stress induction
ASJC Scopus subject areas
- Neuroscience(all)
- Molecular Biology
- Clinical Neurology
- Developmental Biology