Modification of dopamine release by nociceptin in conscious rat striatum

Konya, Hiroyuki; Masuda, Hiroshi; Itoh, Kiyofumi; Nagai, Kazuo; Kakishita, Eizo; Matsuoka, Akira

doi:10.1016/s0006-8993(98)00075-4

Cited by 37 publications

(24 citation statements)

References 23 publications

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“…Furthermore, dopamine release in the nucleus accumbens of anaesthetized rats was reduced by nociceptin administered intracerebroventricularly or into the ventral tegmental area (Murphy et al 1996(Murphy et al , 1997; administration of nociceptin into the ventral tegmental area, in addition, increased the levels of GABA, glutamate and aspartate in this brain region (Murphy et al 1997). In conscious rats, nociceptin, administered via the dialysis probe, increased striatal dopamine release (Konya et al 1998) It was the aim of the present study to examine whether nociceptin inhibits the release of noradrenaline in superfused mouse brain cortex slices and, if so, whether this effect (1) extends to other species, (2) is mediated via ORL 1 receptors and (3) is a direct presynaptic action on the noradrenergic axons.…”

Section: Introductionmentioning

confidence: 94%

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Schlicker

Werthwein

Kathmann

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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A fourth type of opioid receptor, termed ORL1, has been cloned and nociceptin (also known as orphanin FQ) has been identified as an endogenous ligand at this receptor. We examined whether nociceptin affects the release of noradrenaline in the brain. For this purpose, cerebral cortex slices from the mouse, rat or guinea-pig were preincubated with [3H]noradrenaline and then superfused with medium containing desipramine and rauwolscine. Tritium overflow was evoked electrically (0.3 Hz) or by introduction of Ca2+ 1.3 mM into Ca2+-free K+-rich (15 mM) medium. Nociceptin 1 microM reduced the electrically evoked tritium overflow from mouse, rat and guinea-pig brain cortex slices by 80, 71 and 36%, respectively. Naloxone 10 microM did not change the effect of nociceptin. All subsequent experiments were performed on mouse brain cortex slices and in the presence of naloxone 10 microM. The concentration-response curve of nociceptin (maximum inhibition by 80%, pEC50 7.5) was shifted to the right by the non-selective ORL1 receptor antagonist naloxone benzoylhydrazone and the selective ORL1 receptor antagonist [Phe1psi(CH2-NH)Gly2]-nociceptin(1-13)NH2 (pA2 6.6 and 7.2, respectively). Naloxone benzoylhydrazone did not affect the evoked overflow by itself whereas [Phe1psi(CH2-NH)Gly2]nociceptin(1-13)NH2 caused an inhibition by maximally 35% (pEC50 7.0; intrinsic activity alpha 0.45). The inhibitory effect of [Phe1psi(CH2-NH)Gly2]-nociceptin(1-13)NH2 was counteracted by naloxone benzoylhydrazone. Nociceptin also reduced the Ca2+-evoked tritium overflow in mouse brain cortex slices superfused in the presence of tetrodotoxin. This effect was also antagonized by naloxone benzoylhydrazone, which, by itself, did not affect the evoked tritium overflow. In conclusion, nociceptin inhibits noradrenaline release more markedly in the mouse than in the rat or guinea-pig brain cortex. The effect of nociceptin in the mouse brain cortex involves ORL1 receptors, which are located presynaptically on noradrenergic neurones.

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Section: Introductionmentioning

confidence: 94%

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Schlicker

Werthwein

Kathmann

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Furthermore, an injection of N/OFQ (1 mM) directly into the VTA, is sufficient to attenuate cocaine-induced increases in NAc dopamine and locomotor activity (Murphy and Maidment, 1999). However, it should be noted that striatal administration of high concentrations of N/OFQ can have opioid-like activity, inducing a naloxone reversible increase in dopamine levels in the nucleus accumbens (NAc) (Konya et al, 1998). …”

Section: Introductionmentioning

confidence: 99%

Retrodialysis of N/OFQ into the nucleus accumbens shell blocks cocaine-induced increases in extracellular dopamine and locomotor activity

Vazquez-DeRose

Stauber

Khroyan

et al. 2013

European Journal of Pharmacology

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Nociceptin (N/OFQ) has been implicated in a variety of neurological disorders, most notably in reward processes and drug abuse. N/OFQ suppresses extracellular dopamine in the nucleus accumbens (NAc) after intracerebroventricular injection. This study sought to examine the effects of retrodialyzed N/OFQ on the cocaine-induced increase in extracellular dopamine levels in the NAc, as well as locomotor activity, in freely moving rats. 1.0µM, 10µM, and 1mM N/OFQ, in the NAc shell, significantly suppressed the cocaine-induced dopamine increase in the NAc, while N/OFQ alone had no significant effect on dopamine levels. Co-delivery of the selective NOP receptor antagonist SB612111 ([(−)-cis-1-Methyl-7-[[4-(2,6-dichlorophenyl)piperidin-1-yl]methyl]-6,7,8,9-tetrahydro-5H-benzocyclohepten-5-ol] reversed the N/OFQ suppression of cocaine-induced dopamine in the NAc, suggesting that this is an NOP receptor-mediated effect. Using a novel system to assess locomotion, we measured various motor activities of the animals with simultaneous microdialysis from the home cage. Cocaine produced an expected increase in total activity, including horizontal movement and rearing behavior. Retrodialysis of N/OFQ with cocaine administration affected all motor activities, initially showing no effect on behavior, but over time inhibiting cocaine-induced motor behaviors. These results suggest that N/OFQ can act directly in the NAc shell to block cocaine-induced increases in extracellular dopamine levels. Extracellular dopamine and locomotor activity can be dissociated within the NAc and may reflect motor output differences in shell versus core regions of the NAc. These studies confirm the widespread involvement of NOP receptors in drug addiction and further validate the utility of an NOP receptor agonist as a medication for treatment of drug addiction.

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“…Furthermore, administration of nociceptin into the ventricle or the ventral tegmental area inhibited dopamine release in the nucleus accumbens of the anaesthetized rat (Murphy et al, 1996;1997). By contrast, nociceptin, administered intrastriatally to conscious rats, increased dopamine release in the striatum (Konya et al, 1998) and, when administered to the ventral tegmental area of the anaesthetized rat, facilitated GABA and glutamate release in this brain region (Murphy et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

Werthwein

Bauer

Nakazi

et al. 1999

British J Pharmacology

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In conclusion, nociceptin inhibits noradrenaline release in the mouse cortex via ORL 1 receptors, which interact with presynaptic a 2 -autoreceptors on noradrenergic neurones. The e ect of nociceptin does not desensitize nor does it involve NO, prostanoids or adenosine. Nociceptin also attenuates noradrenaline release from several subcortical regions and serotonin release from cortical slices by a naloxone benzoylhydrazone-sensitive mechanism.

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Modification of dopamine release by nociceptin in conscious rat striatum

Cited by 37 publications

References 23 publications

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Retrodialysis of N/OFQ into the nucleus accumbens shell blocks cocaine-induced increases in extracellular dopamine and locomotor activity

Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

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Modification of dopamine release by nociceptin in conscious rat striatum

Cited by 37 publications

References 23 publications

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Nociceptin inhibits noradrenaline release in the mouse brain cortex via presynaptic ORL1 receptors

Retrodialysis of N/OFQ into the nucleus accumbens shell blocks cocaine-induced increases in extracellular dopamine and locomotor activity

Further characterization of the ORL1 receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro

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Further characterization of the ORL₁ receptor‐mediated inhibition of noradrenaline release in the mouse brain in vitro