Postnatal development of multiple opioid receptors in rat brain

Kornblum, Harley I.; Hurlbut, Diana E.; Leslie, Frances M.

doi:10.1016/0165-3806(87)90226-4

Cited by 153 publications

(79 citation statements)

References 51 publications

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“…One can speculate that m-opiate receptors may be involved in the control of pituitary±adrenal function in early postnatal development; however, they showed controversial effects. This hypothesis is consistent with the development of m-receptors in the rat brain during the perinatal period (9) as well as of other opiate receptors including k-receptors, which are detected in the brain of neonatal rats (11), and may be implicated in the control of the pituitary±adrenal axis within the first week of postnatal life (23). In adults, according to experiments performed in vivo and in vitro, the facilitation of ACTH secretion by morphine was correlated with the release of CRF (15,26,27).…”

Section: Discussionsupporting

confidence: 74%

“…The distribution of m-opioid receptor mRNA in the rat brain increases between embryonic days 16 and 22 and continues to increase until postnatal day 7 to a level equivalent to the adult one (9). The coexistence of mand k-but not d-opioid sites has been reported in the human fetal brain (10), and during early neonatal life in the brain of both rat (11) and mouse (12). The development of opiate receptors in the rat brain may be sex hormone dependent, as 6-day-old females display more opiate-binding sites than age-matched males (13).…”

Section: Introductionmentioning

confidence: 99%

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Morphine-induced stimulation of pituitary-adrenocortical activity is mediated by activation of nitric oxide in the early stages of postnatal life in the rat

Lésage

Bernet²,

Montel³

et al. 2001

European Journal of Endocrinology

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Objective: The first aim of the present study was to determine if morphine, a prototypic m-opioid agonist drug, affects pituitary±adrenocortical activity in developing rat pups (first and second weeks of postnatal life). The second aim of this study was to explore, in vivo, if nitric oxide (NO) could be involved in the neurohormonal response to morphine in the early stages of postnatal life. Methods: Plasma ACTH and corticosterone concentrations were determined by RIA in rat pups n 5±14 rats/experimental group) after they had been killed by decapitation. In a first experiment, 1-day and 1-and 2-week-old rats were treated s.c. with morphine (20 mg/kg) or with vehicle (0.9% NaCl) and killed 5±90 min later. In a second experiment, 2-week-old pups were pretreated s.c. with naltrexone (NAL; 0.4 mg/kg or 10 mg/kg), and injected 1 h later with either morphine (20 mg/kg) or vehicle, and killed 30 min later. Some pups injected with only NAL were killed 60 or 90 min later. On the other hand, pups injected with NAL (10 mg/kg) or NAL and morphine were killed 30 min later. In a third experiment, 2-week-old pups were pretreated s.c. with N-v-nitro L arginine methylester (L-NAME; 30 mg/kg or 100 mg/kg), and injected 1 h later with either morphine (20 mg/kg) or vehicle, and killed 30 min later. Moreover, some pups injected with L-NAME (100 mg/kg) or L-NAME with morphine were killed 30 min later. In a final experiment, pups were injected s.c. with either S-nitroso-N-acetylpenicillamine (SNAP; 5 mg/kg) or vehicle, and killed 60 or 90 min later. Results: Morphine administered to rat pups elicited marked rises in both ACTH and corticosterone secretion. Moreover, these responses increased with advancing postnatal age. In 2-week-old rat pups, NAL, a competitive antagonist at m-opioid receptors, administered alone increased both plasma ACTH and corticosterone concentrations 30 min later. L-NAME, a specific NO synthase inhibitor, did not affect plasma ACTH and corticosterone concentrations 30 min later when administered alone. NAL, when concomitantly administered with morphine, was unable to block morphine responses. In contrast, morphine responses were blocked by pretreatment (60 min before) with NAL or with L-NAME. Acute injection of SNAP increased both ACTH and corticosterone release. Conclusion: Our results suggest that opioids have controversial effects on pituitary±adrenocortical activity in the early postnatal period in the rat, and that endogenous NO is one of the major factors in the response of the pituitary±adrenocortical axis to morphine.

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Section: Discussionsupporting

confidence: 74%

Section: Introductionmentioning

confidence: 99%

Morphine-induced stimulation of pituitary-adrenocortical activity is mediated by activation of nitric oxide in the early stages of postnatal life in the rat

Lésage

Bernet²,

Montel³

et al. 2001

European Journal of Endocrinology

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“…The detection of the ␦ receptor mRNA in the DRG at E12.5, the pons at E13.5, and the caudate putamen at E17.5 also significantly extends binding data, which have been unable to detect ␦ binding activity until P1 (Kornblum et al, 1987;Rius et al, 1991). Some anatomical information on the postnatal development of the opioid receptor expression in rodent brain has been provided via ligand autoradiographic analysis (Xia and Haddad, 1991).…”

Section: Discussionmentioning

confidence: 99%

“…In the mouse, receptor binding activity can be detected in homogenates as early as embryonic day 12.5 (E12.5) (Rius et al, 1991), whereas receptor binding is first detected at E14.5. In contrast, CNS ␦ receptor binding sites cannot be detected at all prenatally (Kornblum et al, 1987;Rius et al, 1991). In the rat spinal cord, and binding sites first appear at E15, whereas ␦ sites are not detected until postnatal day 1 (P1) (Attali et al, 1990).…”

mentioning

confidence: 99%

Developmental Expression of the μ, κ, and δ Opioid Receptor mRNAs in Mouse

Zhu¹,

Hsu²,

Pintar³

1998

J. Neurosci.

153

109

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To characterize further the establishment of the opioid system during prenatal mouse development, we have examined the spatial and temporal expression patterns of , , and ␦ opioid receptor mRNAs and find that the expression patterns of these mRNAs are distinct at all ages. Within the embryo, is the first opioid receptor expressed, with transcripts detected in the gut epithelium as early as embryonic day 9.5 (E9.5). By E10.5, receptor expression is first detected in the facial-vestibulocochlear preganglion complex, whereas ␦ receptor mRNA is first detected at E12.5 in several peripheral tissues, including the olfactory epithelium, heart, limb bud, and tooth. In the brain, both and mRNAs are first detected at E11.5 in the basal ganglia and midbrain, respectively. During mid-gestation and late gestation, the expression of both and receptors extends to other brain regions that exhibit high expression in the adult, including the medial habenula, hypothalamus, pons, and medulla for and the basal ganglia, thalamus, hypothalamus, raphe, and ventral tegmental area for . Thus by E17.5, many aspects of the adult expression patterns of and receptors already have been established. Compared with and , ␦ receptor mRNA expression in the brain begins relatively late, and the expression levels remain very low even at E19.5. In contrast to its late appearance in the brain, however, ␦ is the first opioid receptor expressed in the dorsal root ganglion, at E12.5, before its expression in the spinal cord begins at E15.5. receptor is the first opioid receptor expressed in the spinal cord, at E11.5. These results extend previous ligand-binding data to significantly earlier ages and suggest that early developmental events in both neural and non-neural tissues may be modulated by opioid receptors. Several examples of possible autocrine and paracrine loops of opioid peptide and receptor expression have been identified, suggesting a role for these local circuits in developmental processes.

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“…In particular, µ and δ opioid receptors sometimes display allosteric interactions which may relate to these receptors' ability to associate and form a single functionally unique receptor complex 6 . Yet, there are several problems with these interpretations for astrocyte growth: (i) Even at dilute (10 −10 M) concentrations there may be sufficient cross-reactivity between ligands and opioid receptors so that [Met 5 ]enkephalin might act on µ opioid receptors 19 or that morphine might bind to δ opioid sites 9 . (ii) Most importantly, the present studies were performed on 1-day-old mouse pups (maintained for as long as 8 days in vitro).…”

Section: Discussionmentioning

confidence: 99%

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

Stiene‐Martin

Gurwell

Hauser

1991

Developmental Brain Research

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SUMMARYTo determine whether exogenous opiate drugs with abuse liability directly modify neural growth, the present study investigated the effects of morphine on astrocyte proliferation and differentiation in primary cultures of murine glial cells. The results indicate that morphine decreases glial cell production in a dose-dependent, naloxone reversible manner. Most notably, gliogenesis virtually ceased in the presence of 10 −6 M morphine during the first week in culture, whereas 10 −8 M or 10 −10 M morphine caused an intermediate suppression of growth compared to control or 10 −6 M morphine treated cultures. Moreover, morphine-treatment inhibited [ 3 H]thymidine incorporation by glial fibrillary acidic protein (GFAP) immunoreactive, flat (type 1) astrocytes, suggesting that the decrease in glial cell production was due in part to an inhibition of astrocyte proliferation. Morphine also caused significant increases in both cytoplasmic area and process elaboration in flat (type 1) astrocytes indicating greater morphologic differentiation. In the above experiments, morphine-dependent alterations in astrocyte growth were antagonized by naloxone, indicating that morphine action was mediated by specific opioid receptors. These observations suggest that opiate drugs can directly modify neural growth by influencing two critical developmental events in astrocytes, i.e., inhibiting proliferation and inducing morphologic differentiation.

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Postnatal development of multiple opioid receptors in rat brain

Cited by 153 publications

References 51 publications

Morphine-induced stimulation of pituitary-adrenocortical activity is mediated by activation of nitric oxide in the early stages of postnatal life in the rat

Morphine-induced stimulation of pituitary-adrenocortical activity is mediated by activation of nitric oxide in the early stages of postnatal life in the rat

Developmental Expression of the μ, κ, and δ Opioid Receptor mRNAs in Mouse

Morphine alters astrocyte growth in primary cultures of mouse glial cells: evidence for a direct effect of opiates on neural maturation

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