Corticotropin-Releasing Factor Stimulation of Adrenocorticotropin and<i>β</i>-Endorphin Release: Effects of Acute and Chronic Stress*

Young, Elizabeth A.; Akil, Huda

doi:10.1210/endo-117-1-23

Cited by 135 publications

(64 citation statements)

References 14 publications

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“…Since the response of fi-EP and PRL to morphine and U-50,488H was not reduced in arthritic rats, the data complement those of previous studies (Kawakami et al, 1979;Young and Akil, 1985) in indicating that the response of &EP and PRL to releasing factors is not modified by chronic stress.…”

Section: Endogenous and Exogenous Opioid Control Of Nociception In Arsupporting

confidence: 88%

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

Millan¹,

Członkowski²,

Pilcher³

et al. 1987

J. Neurosci.

111

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Intradermal inoculation of rats at the tail base with Mycobacterium butyricum led to the gradual development of an arthritic swelling of the limbs which peaked at 3 weeks and subsided thereafter. Arthritic rats displayed a loss of body weight, hypophagia, and hypodipsia in addition to a disruption of the diurnal rhythms of ingestive behavior and of core temperature. The activity of adenohypophyseal beta- endorphin-(beta-EP) secreting corticotrophs, in contrast to prolactin- (PRL) secreting lactotrophs, was increased in arthritic rats. Indeed, hypertrophy of the adrenal glands was seen. Arthritic rats also showed an elevation in spinal cord levels of immunoreactive dynorphin (DYN), an endogenous ligand of the kappa-opioid receptor. The paws and tail of arthritic rats showed lower thresholds in response to noxious pressure (hyperalgesia), higher thresholds in response to noxious heat (hypoalgesia), and no change in their response to noxious electrical stimulation. Neither naloxone nor ICI-154, 129 (a preferential delta- receptor antagonist) modified the responses of the paw or tail to pressure. However, MR 2266 (an antagonist with higher activity at kappa- receptors) decreased thresholds to pressure in arthritic, but not control, rats; that is, it potentiated the hyperalgesia. This action was stereospecific. None of the antagonists modified the response to heat. MR 2266 did not affect the response to pressure in rats with acute inflammation produced by yeast. Thus, the potentiation of pressure hyperalgesia by MR 2266 in chronic arthritic rats is highly selective. Arthritic rats showed a reduced response to the analgesic effect of a kappa-agonist (U-50,488H), whereas the response to a mu- agonist (morphine) was enhanced. These effects were specific to nociception in that their influence upon endocrine secretion (PRL and beta-EP) was otherwise changed. The secretion of beta-EP and PRL was stimulated by both morphine and U-50,488H, and the influence of U- 50,488H upon the release of beta-EP (from the adenohypophysis) was enhanced in arthritic rats. It is suggested that polyarthritis is a complex condition entailing many changes, both behavioral and endocrinological. Further, arthritic rats cannot simply be described as “hyperalgesic”: of critical importance is the nature of the nociceptive stimulus applied. The parallel alterations in spinal cord pools of DYN and kappa-receptors (see also Millan et al., 1986) and the changes in the influence on nociception of kappa-agonists and kappa-antagonists suggest an increased activity of spinal DYN. Thus, spinal kappa- receptors may play a role in the modulation of nociception under chronic pain.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Endogenous and Exogenous Opioid Control Of Nociception In Arsupporting

confidence: 88%

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

Millan¹,

Członkowski²,

Pilcher³

et al. 1987

J. Neurosci.

111

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“…Various other treatments that can alter both the pituitary content and the plasma levels of ACTH and iJ-EP/iJ-LPH in the rat have not shown ACTH to be increased at the expense of iJ-EP/iJ-LPH (Lim et af. 1982;Young and Akil 1985). One major difference, however, between cited research on chronic stress/acute stress (Young and Akil, 1985;Shimoi et af.…”

Section: Discussionmentioning

confidence: 99%

“…1982;Young and Akil 1985). One major difference, however, between cited research on chronic stress/acute stress (Young and Akil, 1985;Shimoi et af. 1986) and the present investigation is that the regulation of ACTH and iJ-EP/iJ-LPH in the above groups was studied in rats, in response to a standard footshock applied for about 30 min daily.…”

Section: Discussionmentioning

confidence: 99%

Effect of Myiasis and Acute Restraint Stress on Plasma Levels of Immunoreactive , ß-Endorphin, Adrenocorticotrophin (ACTH) and Cortisol in the Sheep

Shutt¹,

Smith²,

Wallace³

et al. 1988

Aust. Jnl. Of Bio. Sci.

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Cutaneous myiasis in sheep arising from the activity of Lucilia cuprina larvae can result in significant physiological changes in susceptible animals. The stress imposed on the pituitary-adrenal axis of the sheep in response to myiasis and acute restraint is the subject of this investigation. Merino wethers were exposed to handling restraint, and blood sampling, during examination for blowfly strike; where necessary, they were treated for cutaneous myiasis. Significant changes in the plasma concentrations of immunoreactive J3-endorphin (J3-EP), ACTH and cortisol were found in sheep with extensive myiasis, as compared with unstruck sheep or those with only localized myiasis. In five susceptible sheep with extensive cutaneous myiasis, mean plasma levels of J3-EP, ACTH and cortisol were 307 ± 71 pg ml-1, 953 ± 58 pg ml-1 and 232 ± 46 nmoll-1 respectively, compared with 818 ± 89 pg ml-1, 641 ± 41 pg ml-1 and 107 ± 17 nmol I-I in six unstruck sheep handled similarly. Whereas significant increases in plasma ACTH and cortisol can result from pituitary-adrenal responses to acute emotional or surgical stress, and are usually accompanied by a concomitant release of J3-EP from the pituitary, the present findings indicate a marked reduction in J3-EP levels and a significant increase in ACTH and cortisol in sheep following blowfly strike and acute handling restraint. This result suggests that cutaneous myiasis in susceptible sheep can alter the pituitaryadrenal response to acute restraint stress, and this could occur either by an alteration of precursor processing in the pituitary or by the selective release of ACTH.

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“…Secondly, cortisol levels rise during acute stress but are low after chronic stress due to feedback inhibition of its synthesis (Dallman & Jones, 1973;Young & Akil, 1985). Since cortisol enhances the affinity of the GABA receptor (Majewska et al, 1985), the stimulation of GABAergic function would also act as a compensatory and adaptive mechanism to overcome the lack of positive hormonal influence upon this neuronal system (which is found in the early phases of stress), thus contributing to prevent the behavioural disturbances otherwise produced chronically by stressors.…”

Section: Discussionmentioning

confidence: 99%

Changes in central GABAergic function following acute and repeated stress

Losada

1988

British J Pharmacology

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The function of γ‐aminobutyric acid (GABA)ergic systems in response to acute and repeated stressful manipulations was evaluated in both the corpus striatum and frontal cerebral cortex of the rat. In the corpus striatum the activity of the synthetic enzyme for GABA (glutamic acid decarboxylase, GAD) and the levels of GABA were reduced by acute immobilization stress (1 h). GABA turnover was reduced only by acute cold stress (3 h, 4°C). In the frontal cerebral cortex no changes were observed after acute stressful manipulations, but repeated stress (0.5 h immobilization per day for 14 days) enhanced both GAD activity and GABA turnover, and reduced GABA levels. In conclusion, it would appear that the GABAergic system in the corpus striatum of the rat is most sensitive to acute stress and that the system in the frontal cerebral cortex area is preferentially responsive to chronic stress. It is speculated that the cortical GABAergic system is responsible for adaptive responses to the adverse conditions prevailing during chronic stress.

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Corticotropin-Releasing Factor Stimulation of Adrenocorticotropin andβ-Endorphin Release: Effects of Acute and Chronic Stress*

Cited by 135 publications

References 14 publications

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

A model of chronic pain in the rat: functional correlates of alterations in the activity of opioid systems

Effect of Myiasis and Acute Restraint Stress on Plasma Levels of Immunoreactive , ß-Endorphin, Adrenocorticotrophin (ACTH) and Cortisol in the Sheep

Changes in central GABAergic function following acute and repeated stress

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