J Korean Neuropsychiatr Assoc.
1999 May;38(3):638-646.
The Effects of Repeated Stress on the Opioidergic Neurotransmission in Rats
- Affiliations
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- 1Department of Psychiatry, Pohang Hospital, College of Medicine, Dongguk University, Pohang, Korea.
- 2Department of Psychiatry, Kyongju Hospital, College of Medicine, Dongguk University, Kyongju, Korea.
- 3Department of Neuropsychiatry, College of Medicine, Yeungnam University, Taegu, Korea.
- 4Department of Pharmacology, College of Medicine, Yeungnam University, Taegu, Korea.
Abstract
- OBJECTIVES: Research into emotional or behavioral stress typically focuses upon the hypothalamic-pituitary-adrenal axis. It is well established that the hypothalamic-pituitary-adrenocortical axis is subject to inhibitory control by opioids in a variety of animal species including pigs. Exposure to acute stress induces the upregulation of opioid receptors and the release of endogenous peptides which mediate the stress-induced analgesia. There is some literature substantiating that repeated stress can lead to changes in opioidergic neurotransmission. However, the changes are highly variable. This study was designed to observe the modulatory effect of repeated immobilization stress on opioidergic neurotransmission.
METHODS
Male Sprague-Dawley rats weighing 150-200g were forced to suffer immobilization stress for 2 hours on each of 14 successive days. Then we examined the maximum binding capacity and affinity of each opioid subtypes(mu, delta, kappa).
RESULTS
Repeated immobilization stress increased the binding of [3H]DPDPE on the delta-subtype opioid receptor in the striatum and hypothalamus. Saturation experiments followed by scatchard analyses of the results showed an increase in the density of delta-subtype opioid receptors, but the affinity of the delta-subtype opioid receptor remained unchanged. Repeated immobilization stress reduced enkephalin activity of striatum and hypothalamus.
CONCLUSIONS
From these results, it could be concluded that repeated immobilization stress up-regulated the delta-subtype opioid receptors and reduced the activity of enkephalin, an endogenous ligand for the delta-subtype opioid receptor.
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