Local opioid inhibition and morphine dependence of supraoptic nucleus oxytocin neurones in the rat <i>in vivo</i>

Ludwig, Mike; Brown, Colin H.; Russell, John A.; Leng, Gareth

doi:10.1111/j.1469-7793.1997.145bc.x

Cited by 38 publications

(30 citation statements)

References 33 publications

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“…Moreover, we have found that -receptor mRNA is expressed in SON VP neurons and non-VP, presumably oxytocin (OT), neurons. A role for -opioid receptors in OT release has been known for some time, although the specific site, either pre-or postsynaptic, has been difficult to delineate (Falke, 1991;Ludwig et al, 1997). Recently, it has also been demonstrated that VP neurons in the rat SON are directly responsive to -opioid agonist and, therefore, are likely to express -opioid receptors (Soldo and Moises, 1998), in agreement with our current findings in the guinea pig.…”

Section: -Opioid Receptor Mrna In Vp Neuronssupporting

confidence: 89%

“…Specifically, endogenous opioid peptides, such as met-enkephalin, which can activate -opioid receptors, are known to have powerful inhibitory effects on hypothalamic neurons involved in regulation of LH and prolactin secretion (Leadem and Yagenova, 1987;Kapoor and Willoughby, 1991;Kehoe et al, 1993;Kalra, 1993;Goodman et al, 1995;Walsh and Clarke, 1996;Herbison, 1998). Opioids have also been found to inhibit activity-dependent release of oxytocin and vasopressin from the supraoptic nucleus (SON), which may be at least in part through a -opioid mechanism because the -opioid agonist DAMGO directly attenuates N-and P-type calcium currents in rat SON neurons (Falke, 1991;Ingram et al, 1996;Ludwig et al, 1997;Soldo and Moises, 1998).…”

mentioning

confidence: 98%

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μ‐opioid receptor mRNA expression in identified hypothalamic neurons

Zheng

Bosch

Rønnekleiv

2005

J of Comparative Neurology

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It has been known for a number of years that mu-opioid receptor agonists (e.g., morphine, beta-endorphin, and enkephalin) inhibit luteinizing hormone (LH), vasopressin (VP), and oxytocin (OT) release and stimulate prolactin secretion in rodents and primates by an action at the level of the brain. Also, electrophysiological studies have established that hypothalamic neurons, including gonadotropin-releasing hormone (GnRH), VP, OT, beta-endorphin, and dopamine neurons, are responsive to mu-receptor activation. Although mu-receptor expression has been demonstrated in the hypothalamus, there have been few studies localizing these receptors in neurosecretory neurons. Therefore, we sought to document mu-opioid receptor mRNA expression in immunocytochemically identified hypothalamic neurons. The brains from both female and male guinea pigs were examined by using in situ hybridization and immunocytochemistry. The studies revealed that mu-receptor mRNA was expressed in different diencephalic regions including the preoptic area, the bed nuclei stria terminalis, the paraventricular nucleus thalamus, and the anterior hypothalamus, as well as the supraoptic (SON), paraventricular (PVH), ventromedial, dorsomedial, and arcuate nuclei of the hypothalamus. Importantly, mu-opioid receptors were expressed in subpopulations of GnRH neurons (33.25 +/- 4.6% and 33.6 +/- 3.7% in females and males, respectively), dopamine neurons (51.7 +/- 5.8% to 75.0 +/- 2.6%, depending on neuronal location), beta-endorphin neurons (68.3.0 +/- 4.4%), and VP neurons (41-70%, depending on neuronal location). Because mu-opioid receptors couple via G-proteins to activate inwardly rectifying potassium channels and to inhibit calcium channels, the presence of these receptors is likely to play a major role in directly controlling the excitability of hypothalamic neurons.

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Section: -Opioid Receptor Mrna In Vp Neuronssupporting

confidence: 89%

mentioning

confidence: 98%

μ‐opioid receptor mRNA expression in identified hypothalamic neurons

Zheng

Bosch

Rønnekleiv

2005

J of Comparative Neurology

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“…Our finding provides an underlying cellular mechanism for an inhibitory action of AVP on AVP neurons that would effectively limit the excitation of these neurons (Ludwig and Leng, 1997). …”

Section: Physiological Implicationsmentioning

confidence: 80%

“…Our result supports such a possibility: AVP released within the nucleus would favor an excitation of OXT neurons while causing inhibition of AVP neurons. The activity of AVP neurons is tuned by AVP, so that the neurons would be quieted during high level of activity (Ludwig et al, 1997). In contrast, OXT that may also be released during high activity of the nucleus will further increase the activity of OXT neurons (Yamashita et al, 1987;Moos and Richard, 1989).…”

Section: Avp Differentially Modulates Epscs In Different Populations mentioning

confidence: 99%

Vasopressin Differentially Modulates Non-NMDA Receptors in Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

et al. 2003

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Magnocellular neurons of the supraoptic nucleus release the neuropeptides oxytocin and vasopressin from their dendrites to regulate their synaptic inputs. This study aims to determine the cellular mechanism by which vasopressin modulates excitatory synaptic transmission. Presumably by electroporation through perforated patch, we were able to successfully introduce biocytin into cells in which we performed an electrophysiological study. This method enabled us to determine that roughly half of the recorded neurons were immunoreactive to oxytocin-associated neurophysin and showed two characteristic features: an inward rectification and a sustained outward rectification. The remaining half showed a linear voltage-current relationship and was immunoreactive to vasopressin-associated neurophysin. Using these electrophysiological characteristics and post hoc immunohistochemistry to identify vasopressin or oxytocin neurons, we found that vasopressin decreased evoked EPSCs in vasopressin neurons while increasing EPSCs in oxytocin neurons. In both types of neurons, EPSC decay constants were not affected, indicating that desensitization of non-NMDA receptors did not underlie the EPSC amplitude change. In vasopressin neurons, both vasopressin and a V1a receptor agonist, F-180, decreased AMPA-induced currents, an effect blocked by a V1a receptor antagonist SR49059. In oxytocin neurons, AMPA-induced currents were facilitated by vasopressin, whereas F-180 had no effect. An oxytocin receptor antagonist blocked the facilitatory effect of vasopressin. Thus, we conclude that vasopressin inhibits EPSCs in vasopressin neurons via postsynaptic V1a receptors, whereas it facilitates EPSCs in oxytocin neurons through oxytocin receptors.

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“…In virgin rats, µ- and ĸ-agonists reduce the firing rate of oxytocin cells [8]. Naloxone administration into the SON prevents the decrease of firing rate of oxytocin cells occurred with morphine [9]. During spontaneous parturition, fos (protein product of c-fos) is expressed in SON and brainstem neurons [10].…”

Section: Introductionmentioning

confidence: 99%

Mu Opioid Modulation of Oxytocin Secretion in Late Pregnant and Parturient Rats

et al. 2004

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We have investigated effects of µ- and ĸ-opioid agonists and antagonists on plasma oxytocin levels and noradrenaline content in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of 20-day pregnant rats. β-Endorphin, oxytocin, estrogen and progesterone profiles in late pregnant and parturient rats were also sought. Stage of estrous cycle was monitored by vaginal smear, and pro-estrous animals were left overnight with male. In the first set of experiments, pregnant rats were monitored and decapitated on days 20 and 21 and after the delivery of second pup. In the second set, 20-day pregnant rats were intracerebroventricularly infused with morphine (50 µg/10 µl), U50,488H (ĸ-agonist; 50 µg/10 µl), clocinnamox (µ-antagonist; 50 µg/10 µl) and norbinaltorphimine (ĸ-antagonist; 50 µg/10 µl). Controls received saline alone. Serum estrogen and progesterone levels were measured by enzyme immunoassay, and plasma oxytocin and β-endorphin by radioimmunoassay. Noradrenaline and its metabolite (3,4-dihydroxyphenylglycol) were determined in micropunched hypothalamic nuclei by HPLC-ECD. In parturient rats, oxytocin levels were increased (p < 0.05) and β-endorphin decreased (p < 0.01) compared to 20-day pregnant animals. Serum progesterone concentrations progressively declined towards parturition (p < 0.001). Clocinnamox raised oxytocin levels (p < 0.01) while U50,488H caused decreases (p < 0.05). Noradrenaline content was elevated by clocinnamox in the SON (p < 0.01) and PVN (p < 0.05) compared to control values. Other agonists and antagonists had no significant effect on the noradrenergic neurotransmission or oxytocin secretion. We suggest that noradrenaline may mediate the inhibitory effects of µ-opioids on oxytocin release. Our findings have also shown that ĸ-opioid receptors are not involved in modulation of oxytocin neurons in late pregnant rats.

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Local opioid inhibition and morphine dependence of supraoptic nucleus oxytocin neurones in the rat in vivo

Cited by 38 publications

References 33 publications

μ‐opioid receptor mRNA expression in identified hypothalamic neurons

μ‐opioid receptor mRNA expression in identified hypothalamic neurons

Vasopressin Differentially Modulates Non-NMDA Receptors in Vasopressin and Oxytocin Neurons in the Supraoptic Nucleus

Mu Opioid Modulation of Oxytocin Secretion in Late Pregnant and Parturient Rats

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