Pituitary-Adrenal Activation Following Intrahypothalamic Microinjection of Morphine

Lotti, Victor J.; Kokka, Norio; George, Rani Mary

doi:10.1159/000121765

Cited by 75 publications

(25 citation statements)

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“…This response has been presumed to be mediated solely by the hypothalamic-pituitary axis or by a direct action at the pituitary (Kokka and George, 1974;Lotti et al, 1969;Zimmerman and Critchlow, 1973). The present results indicate that h .0' morphine can also influence the steroidogenic response to ACTH by a direct action on the adrenal cortex.…”

Section: Discussionsupporting

confidence: 46%

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Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Heybach

Vernikos

1981

European Journal of Pharmacology

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Section: Discussionsupporting

confidence: 46%

“…Intrahvpothalamic (Lotti et al, 1969) and peripheral (Kokka and George, 1974) morphine injections stimulate the secretion of adrenocorticotrophic hormone (ACTH) from the pituitary, as reflected by increased plasma levels of adrenal corticosterone in the rat. This stimulation is also abolished by naloxone pretreatment (Kokka and George, 1974).…”

mentioning

confidence: 99%

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Heybach

Vernikos

1981

European Journal of Pharmacology

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“…However, as several lines of evidence (George and Way, 1959;Lotti et al, 1969;Gibson et al, 1979;Buckingham and Cooper, 1984) show, it is assumed that the opiate has no direct action on the pituitary gland. Recently, we also have found that (D-ala2, met5)-enkephalinamide, a potent methionineenkephalin analog, has no direct effect on the anterior pituitary corticotrophs in pituitary cell cultures (in submission).…”

Section: Resultsmentioning

confidence: 99%

Effect of morphine on hypothalamic corticotropin-releasing factor(CRF) and pituitary-adrenocortical activity.

1986

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The effects of intraperitoneal and intra-third ventricular administration of morphine on the hypothalamic corticotropin-releasing factor (CRF) and the pituitary-adrenocortical activity were examined in unanesthetized, freely moving rats.Hypothalamic CRF was measured by rat CRF radioimmunoassay. Intraperitoneal or intra-third ventricular administration of morphine increased blood concentrations of ACTH and corticosterone while intraperitoneal administration tended to increase CRF concentration in the whole hypothalamus including the median eminence and intra-third ventricular administration increased CRF concentration in the hypothalamus excluding the median eminence.However, morphine seemed to inhibit the increase in CRF concentration in the hypothalamus induced by the ether-laparotomy stress. The main site of morphine action on the hypothalamo-pituitary-adrenocortical system seemed to be in the hypothalamic area.

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“…Intrahypothalamic and intraventricular morphine injec tions elevate PCS (9,10), and the increase in PCS induced by acute morphine administered systemically is blocked by hypophysectomy or lesions of the median eminence (11,12). Responses of PCS to exogenous corticotropin releasing factor (CRF) and adrenocorticotropic hormone (ACTH) are not attenuated in morphine-tolerant rats, showing that an attenuated PCS response to morphine, i.e., tolerance to the PCS effect, does not occur at the pituitary and adrenal levels (8).…”

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confidence: 99%

Quantitative Properties of Plasma Corticosterone Elevation Induced by Naloxone-Precipitated Withdrawal in Morphine-Dependent Rats

Kishioka¹,

Nishida²,

Fukunaga³

et al. 1994

Japanese Journal of Pharmacology

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ABSTRACT-Elevation of plasma corticosterone (PCS) has been used as an indicator of morphine withdrawal, but it is not clear whether the magnitude of elevation is related to the intensity of the dependence. The dose-dependent effects of naloxone on PCS and body weight were studied in male Sprague-Dawley rats rendered physically dependent on morphine by injecting increasing doses of 40-120 mg/kg/day, s.c. twice daily for 1-6 days. Naloxone (0.01-2.0 mg/kg, s.c.) was administered 3 hr after the last morphine administration. Naloxone elevated PCS levels in a dose-dependent manner in all groups treated with morphine, and the elevation was correlated with the number of days of morphine treatment. Naloxone also reduced dose-dependently the body weight in all groups treated with morphine; in this case, a reverse correlation was obtained between the body weight changes and the PCS levels. It was confirmed that PCS elevation is a quantitative sign of naloxone-precipitated morphine withdrawal and that the elevation is indicative of the degree of morphine physical dependence.Keywords: Morphine dependence, Plasma corticosterone, Body weight loss, Naloxone withdrawal Plasma corticosterone (PCS) has been shown to be elevated during both spontaneous and naloxone-precipi tated withdrawal from acute and chronic morphine ex posure, and the elevation of PCS has been used as a meas ure of morphine dependence (1 -4). Interestingly, the ele vation of PCS is also induced by acute morphine adminis tration (1, 5) and the development of tolerance to this hor mone effect follows chronic exposure to morphine (6 8).Intrahypothalamic and intraventricular morphine injec tions elevate PCS (9, 10), and the increase in PCS induced by acute morphine administered systemically is blocked by hypophysectomy or lesions of the median eminence (11,12). Responses of PCS to exogenous corticotropin releasing factor (CRF) and adrenocorticotropic hormone (ACTH) are not attenuated in morphine-tolerant rats, showing that an attenuated PCS response to morphine, i.e., tolerance to the PCS effect, does not occur at the pituitary and adrenal levels (8). Secretion of CRF is stimu lated during the periods of both acute morphine adminis tration (13) and morphine withdrawal (14). These results suggest that the stimulation of PCS secretion and the de velopment of tolerance to the PCS effect of morphine both occurred in the region of the central nervous system involved in the neural control of the hypothalamo-pitui tary-adrenal (HPA) axis. Additionally, the effect of mor phine on PCS is mediated selectively through mu opioid receptor, which in turn is involved in the development of tolerance to the PCS effect of morphine and morphine withdrawal (8,15). Accordingly, if the increase in PCS is a quantitative sign of morphine withdrawal, the understanding of the neural mechanism of PCS elevation during morphine withdrawal would contribute to the elucidation of the un derlying neural mechanism of morphine tolerance and/or dependence. However, little is known about whether the...

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Pituitary-Adrenal Activation Following Intrahypothalamic Microinjection of Morphine

Cited by 75 publications

References 0 publications

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Effect of morphine on hypothalamic corticotropin-releasing factor(CRF) and pituitary-adrenocortical activity.

Quantitative Properties of Plasma Corticosterone Elevation Induced by Naloxone-Precipitated Withdrawal in Morphine-Dependent Rats

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