Inhibition by sigma receptor ligand, MS-377, of N -methyl- D -aspartate-induced currents in dopamine neurons of the rat ventral tegmental area

Yamazaki, Yu; Ishioka, Miwa; Matsubayashi, Hiroaki; Amano, Taku; Sasa, Masashi

doi:10.1007/s00213-002-1023-4

Cited by 11 publications

(6 citation statements)

References 27 publications

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“…This contrasts to a previous locomotor activity study where the antagonists prevented methamphetamine’s stimulatory effect (Nguyen et al, 2005). Additionally, previous research found that both antagonists produced inhibitory effects on dopamine systems in ventral tegmental area and hippocampus (Meurs et al, 2007; Yamazaki et al, 2002). However, dopamine neuron inhibition has not previously been reported in striatum.…”

Section: Discussionmentioning

confidence: 91%

“…Interestingly, pentazocine inhibited NMDA-stimulated [ 3 H]dopamine release from rat striatal slices (Gonzalez-Alvear and Werling, 1994). BD-1063 inhibited NMDA-induced current in rat ventral tegmental area dopamine neurons (Yamazaki et al, 2002). Additionally, BD-1047 attenuated neuropeptide Y-induced increases in hippocampus extracellular dopamine levels (Meurs et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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The sigma receptor agonist SA4503 both attenuates and enhances the effects of methamphetamine

Rodvelt

Oelrichs

Blount

et al. 2011

Drug and Alcohol Dependence

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Background Methamphetamine’s behavioral effects have been attributed to its interaction with monoamine transporters; however, methamphetamine also has affinity for sigma receptors. Method The present study investigated the effect of the sigma receptor agonist SA 4503 and the sigma receptor antagonists BD-1047 and BD-1063 on methamphetamine-evoked [3H] dopamine release from preloaded rat striatal slices. The effect of SA 4503 on methamphetamine-induced hyperactivity and on the discriminative stimulus properties of methamphetamine also was determined. Results SA 4503 attenuated methamphetamine-evoked [3H]dopamine release in a concentration-dependent manner. BD-1047 and BD-1063 did not affect release. SA 4503 dose-dependently potentiated and attenuated methamphetamine-induced hyperactivity. SA 4503 pretreatment augmented the stimulus properties of methamphetamine. Conclusions Our findings indicate that SA 4503 both enhances and inhibits methamphetamine’s effects and that sigma receptors are involved in the neurochemical, locomotor stimulatory and discriminative stimulus properties of methamphetamine.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

The sigma receptor agonist SA4503 both attenuates and enhances the effects of methamphetamine

Rodvelt

Oelrichs

Blount

et al. 2011

Drug and Alcohol Dependence

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“…Thus, σ1R agonists promote and antagonists reduce the activity of NMDARs, and these effects have been documented in electrophysiological studies as changes in NMDAR currents ( 36 , 68 ) and variations in the PKC-mediated phosphorylation of NR1 subunits ( 26 , 27 ). These profiles of neurosteroids on NMDAR activity when coupled with the opioid-mediated activation of MOR most likely contribute to the regulation of their analgesic effects.…”

Section: Discussionmentioning

confidence: 99%

The σ1 Receptor Engages the Redox-Regulated HINT1 Protein to Bring Opioid Analgesia Under NMDA Receptor Negative Control

Rodríguez-Muñoz

Sánchez‐Blázquez

Herrero-Labrador

et al. 2015

Antioxidants & Redox Signaling

191

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Aims: The in vivo pharmacology of the sigma 1 receptor (σ1R) is certainly complex; however, σ1R antagonists are of therapeutic interest, because they enhance mu-opioid receptor (MOR)-mediated antinociception and reduce neuropathic pain. Thus, we investigated whether the σ1R is involved in the negative control that glutamate N-methyl-d-aspartate acid receptors (NMDARs) exert on opioid antinociception. Results: The MOR C terminus carries the histidine triad nucleotide-binding protein 1 (HINT1) coupled to the regulator of G-protein signaling RGSZ2-neural nitric oxide synthase assembly. Activated MORs stimulate the production of nitric oxide (NO), and the redox zinc switch RGSZ2 converts this signal into free zinc ions that are required to recruit the redox sensor PKCγ to HINT1 proteins. Then, PKCγ impairs HINT1-RGSZ2 association and enables σ1R-NR1 interaction with MOR-HINT1 complexes to restrain opioid signaling. The inhibition of NOS or the absence of σ1Rs prevents HINT1-PKCγ interaction, and MOR-NMDAR cross-regulation fails. The σ1R antagonists transitorily remove the binding of σ1Rs to NR1 subunits, facilitate the entrance of negative regulators of NMDARs, likely Ca2+-CaM, and prevent NR1 interaction with HINT1, thereby impairing the negative feedback of glutamate on opioid analgesia. Innovation: A redox-regulated process situates MOR signaling under NMDAR control, and in this context, the σ1R binds to the cytosolic C terminal region of the NMDAR NR1 subunit. Conclusion: The σ1R antagonists enhance opioid analgesia in naïve mice by releasing MORs from the negative influence of NMDARs, and they also reset antinociception in morphine tolerant animals. Moreover, σ1R antagonists alleviate neuropathic pain, probably by driving the inhibition of up-regulated NMDARs. Antioxid. Redox Signal. 22, 799–818.

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“…The membrane potentials were corrected for the liquid‐junction potential between the pipette and artificial cerebrospinal fluid by adjusting the pipette offset (Heka Electronics, Lambrecht, Germany) at the beginning of the experiments. Whole‐cell currents were induced by brief application of 50 μ m NMDA with admixture of 10 μ m glycine using a U‐shaped tube pre‐positioned near the cell, as previously described (Yamazaki et al . 2002).…”

Section: Methodsmentioning

confidence: 99%

Embryonic stem cell‐derived neuron models of Parkinson's disease exhibit delayed neuronal death

Yamashita

Nakamura

Takahashi

et al. 2006

Journal of Neurochemistry

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Establishment of a Parkinson's disease (PD) neuron model was attempted with mouse embryonic stem (ES) cells. ES cell lines over-expressing mouse nuclear receptor-related 1 (Nurr1), together with human wild-type and alanine 30 fi proline (A30P) and alanine 53 fi threonine (A53T) mutant a-synuclein were established and subjected to differentiation into dopaminergic neurons. The ES cell-derived dopaminergic neurons expressing wild-type or mutant a-synuclein exhibited the fundamental characteristics consistent with dopaminergic neurons in the substantia nigra. The ES cell-derived PD model neurons exhibited increased susceptibility to oxidative stress, proteasome inhibition, and mitochondrial inhibition. Cell viability of PD model neurons and the control neurons was similar until 28 days after differentiation. Nonetheless, after that time, PD model neurons gradually began to undergo neuronal death over the course of 1 month, showing cytoplasmic aggregate formation and an increase of insoluble a-synuclein protein. Such delayed neuronal death was observed in a mutant a-synuclein protein level-dependent manner, which was slightly inhibited by a c-jun N-terminal kinase inhibitor and a caspase inhibitor. Such cell death was not observed when the same ES cell lines were differentiated into oligodendrocytes. The ES cellderived PD model neurons are considered as prospective candidates for a new prototype modelling PD that would allow better investigation of the underlying neurodegenerative pathophysiology. Keywords: a-synuclein, dopaminergic neuron, embryonic stem cell, neuronal death, oligodendrocyte, Parkinson's disease. Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by rigidity, bradykinesia, gait disturbance, and resting tremour. The pathological hallmarks of PD are selective loss of dopaminergic neurons in the substantia nigra pars compacta (SNc) in the midbrain and the presence of Lewy bodies in the remaining neurons. Most cases of PD occur sporadically, with the cause and pathogenesis of the disease remaining unknown; mitochondrial dysfunction, oxidative damage, endoplasmic reticulum stress, failure of the ubiquitin-proteasome system (UPS), environmental factors, and genetic predisposition might all be involved (Hattori and Mizuno 2004).A Mendelian inheritance pattern (familial form) is observed in approximately 5% of PD patients. Identification

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Inhibition by sigma receptor ligand, MS-377, of N -methyl- D -aspartate-induced currents in dopamine neurons of the rat ventral tegmental area

Abstract: The results suggest that MS-377, as well as other sigma receptor ligands, indirectly acts on the sigma receptor to inhibit glutaminergic transmission mediated by NMDA receptor/ion channel complex in VTA dopamine neurons, thereby inhibiting dopamine release in target VTA areas.

Cited by 11 publications

References 27 publications

The sigma receptor agonist SA4503 both attenuates and enhances the effects of methamphetamine

The sigma receptor agonist SA4503 both attenuates and enhances the effects of methamphetamine

The σ1 Receptor Engages the Redox-Regulated HINT1 Protein to Bring Opioid Analgesia Under NMDA Receptor Negative Control

Embryonic stem cell‐derived neuron models of Parkinson's disease exhibit delayed neuronal death

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