Opposite effects of morphine on feeding and drinking in rats relative to administration time.

Kunihara, Mineo; Kanbayashi, Miyuki; Ohshima, Takao

doi:10.1254/jjp.33.829

Cited by 21 publications

(10 citation statements)

References 19 publications

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“…Such an effect has been previously reported for morphine (Leshem 1981 a;Kunihara et al 1983), where a triphasic effect on feeding resulted in an overall reduction of intake during 24 h.…”

supporting

confidence: 80%

“…A large body of evidence attesting to the opiates' hyperphagic influence (Grandison and Guidotti 1977;Cooper and Sanger 1984;Gold and Sternbach 1984;Morley et al 1984) has served to draw attention away from the earlier reports of morphine-induced anorexia (Frenk and Rogers 1979;Marks-Kaufman and Kanarek 1980;Sanger and McCarthy 1980;Cooper 1981;Leshem 1981a;Kunihara et al 1983). There are good reasons for this bias in favour of opiate-induced hyperphagia.…”

mentioning

confidence: 99%

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Morphine induces delayed anorexia in rats

Leshem

1988

Psychopharmacology

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The delayed suppression of feeding caused by morphine was investigated in the rat. A single injection of morphine evoked a triphasic influence on feeding: a brief (1 h) severe anorexia was followed by hyperphagia (3 h) and a mild (20%) yet persistent (4-24 h) anorexia. This latter anorexic effect was at least partially naltrexone reversible, and the duration of this antagonism (8 h) was longer than that of naltrexone's anorexic effect (4 h). Delayed morphine anorexia cannot be ascribed to morphine's initial stuporific influence, and it was not dependent upon previous feeding or deprivation. It was not due to gastric distension. The specificity and significance of this anorexia is discussed.

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“…Such an effect has been previously reported for morphine (Leshem 1981 a;Kunihara et al 1983), where a triphasic effect on feeding resulted in an overall reduction of intake during 24 h.…”

supporting

confidence: 80%

mentioning

confidence: 99%

Morphine induces delayed anorexia in rats

Leshem

1988

Psychopharmacology

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“…That is, body weight loss due to cessation of morphine administration was not induced in the schedule of morphine administra tion employed in the present study, and it is unlikely that the increase in body weight in morphine-treated rats is the result of recovery from morphine withdrawal-induced body weight loss after injection of morphine at 6:00. Recently it was reported that a single dose of morphine evoked a dose-dependent change in feeding (21,22): a brief (1 hr) anorexia was followed by hyperphagia (3 hr). Therefore, the body weight increases after saline in the rats treated with morphine for 1 6 days might be the result of the hyperphagic effect of morphine.…”

Section: Discussionmentioning

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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“…However, it has been rarely studied that opioids such as morphine have different effects on food intake which are related to feeding con ditions or administration time (5, 6). We previously reported that in non-fasted rats, morphine increased food intake for 2 hr following the injection during the light period, but decreased it during the dark period; and in fasted rats, morphine decreased food intake regardless of adminis tration time (7). This report suggests that the two differnt effects of morphine disturb the baseline levels of feeding in naive rats; morphine could stimulate feeding when rats were in a satiated state (in non-fasted rats during the light period), whereas morphine could suppress feeding when rats were in a hungry state (in non-fasted rats during the light period and in fasted rats).…”

mentioning

confidence: 93%

Adrenal Function Affects Morphine-Induced Feeding during Dark Per ad, but not during Light Period in Rats

Kunihara

Kanbayashi

Ohshima

1984

Japanese Journal of Pharmacology

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Abstract-The present study was undertaken to investigate the relationships between morphine-induced feeding and the adrenal functions. Morphine (5 mg/kg) was intraperitoneally administered at 10:45 (light period) or 18:45 (dark period). The orectic effects of morphine during the light period in normal rats were not influenced by adrenalectomy; however, the anorectic effects during the dark period in normal rats were attenuated by both adrenalectomy and adrenodemedullation. Corticos terone (10 mg/kg) itself had no effects on feeding during the light and dark period. Morphine did not alter blood insulin levels during the light period, but markedly decreased it during the dark period independently of feeding. These results show that morphine has two different effects on feeding by administration time, and they suggest that the adrenal affects morphine-induced feeding only during the dark period (hungry state), presumably through insulin release, but not during the light period (satiated state).

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Opposite effects of morphine on feeding and drinking in rats relative to administration time.

Cited by 21 publications

References 19 publications

Morphine induces delayed anorexia in rats

Morphine induces delayed anorexia in rats

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

Adrenal Function Affects Morphine-Induced Feeding during Dark Per ad, but not during Light Period in Rats

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