LIVIVO - Search results -

Search results

Result 1 - 10 of total 24

Search options

Article ; Online: [NOX1/NADPH Oxidase Facilitates Repetitive Behaviors by Enhancing D

Asaoka, Nozomi

Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan

2022 Volume 142, Issue 11, Page(s) 1137–1143

Abstract: Repetitive behavior, a form of compulsivity, is a component of several neuropsychiatric disorders, including obsessive-compulsive disorder and addiction. Dysfunction of dopaminergic modulation in the striatum is thought to be a key neural mechanism ... ...

Abstract	Repetitive behavior, a form of compulsivity, is a component of several neuropsychiatric disorders, including obsessive-compulsive disorder and addiction. Dysfunction of dopaminergic modulation in the striatum is thought to be a key neural mechanism underlying compulsive behavior repetition; however, the mechanistic links between dopaminergic abnormalities and compulsivity remain unclear. This review discusses our recent work demonstrating the contribution of the NOX1 isoform of the superoxide-producing enzyme, nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), to compulsive-like repetitive behavior in mice that received repeated stimulation of D
MeSH term(s)	Mice ; Animals ; NADPH Oxidases/metabolism ; NADPH Oxidase 1 ; Superoxides ; Neurons/metabolism ; Gene Expression
Chemical Substances	NADPH Oxidases (EC 1.6.3.-) ; NADPH Oxidase 1 (EC 1.6.3.-) ; Superoxides (11062-77-4)
Language	Japanese
Publishing date	2022-11-03
Publishing country	Japan
Document type	Review ; English Abstract ; Journal Article
ZDB-ID	200514-1
ISSN	1347-5231 ; 0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
ISSN (online)	1347-5231
ISSN	0031-6903 ; 0372-7750 ; 0919-2085 ; 0919-2131
DOI	10.1248/yakushi.22-00125
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 643: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Amelioration of obsessive-compulsive disorder by intracellular acidification of cortical neurons with a proton pump inhibitor.

Hatakama, Hikari / Asaoka, Nozomi / Nagayasu, Kazuki / Shirakawa, Hisashi / Kaneko, Shuji

Translational psychiatry

2024 Volume 14, Issue 1, Page(s) 27

Abstract: Obsessive-compulsive disorder (OCD) is a highly prevalent neuropsychiatric disorder poorly controlled with pharmacological treatment because of the wide variation in symptom patterns. We analysed real-world data on adverse self-reports and insurance ... ...

Abstract	Obsessive-compulsive disorder (OCD) is a highly prevalent neuropsychiatric disorder poorly controlled with pharmacological treatment because of the wide variation in symptom patterns. We analysed real-world data on adverse self-reports and insurance claims to identify a novel therapeutic target for OCD. We found that dopamine D
MeSH term(s)	Mice ; Animals ; Quinpirole/pharmacology ; Proton Pump Inhibitors/pharmacology ; Proton Pump Inhibitors/therapeutic use ; Obsessive-Compulsive Disorder/drug therapy ; Obsessive-Compulsive Disorder/etiology ; Neurons ; Hydrogen-Ion Concentration
Chemical Substances	Quinpirole (20OP60125T) ; Proton Pump Inhibitors
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-024-02731-3
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Enhancement of adenosine A

Nagaoka, Koki / Asaoka, Nozomi / Nagayasu, Kazuki / Shirakawa, Hisashi / Kaneko, Shuji

Frontiers in neuroscience

2023 Volume 16, Page(s) 1082375

Abstract: Repeated administration of dopamine ... ...

Abstract	Repeated administration of dopamine D
Language	English
Publishing date	2023-01-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.1082375
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: A selective serotonin reuptake inhibitor ameliorates obsessive-compulsive disorder-like perseverative behavior by attenuating 5-HT

Hatakama, Hikari / Asaoka, Nozomi / Nagayasu, Kazuki / Shirakawa, Hisashi / Kaneko, Shuji

Neuropharmacology

2021 Volume 206, Page(s) 108926

Abstract: Perseveration is a characteristic of patients with obsessive-compulsive disorder (OCD). Clinically, neuronal activity in the lateral orbitofrontal cortex (OFC) is increased in OCD patients. Successful treatment with selective serotonin reuptake ... ...

Abstract	Perseveration is a characteristic of patients with obsessive-compulsive disorder (OCD). Clinically, neuronal activity in the lateral orbitofrontal cortex (OFC) is increased in OCD patients. Successful treatment with selective serotonin reuptake inhibitors (SSRIs) reduces activity in the lateral OFC of OCD patients, but the precise mechanisms underlying this effect are unclear. Previously, we reported that repeated injection of the dopamine D
MeSH term(s)	Animals ; Behavior, Animal/drug effects ; Disease Models, Animal ; Interneurons/drug effects ; Mice ; Obsessive-Compulsive Disorder/drug therapy ; Prefrontal Cortex/drug effects ; Pyramidal Cells/drug effects ; Receptor, Serotonin, 5-HT2C/drug effects ; Reversal Learning/drug effects ; Serotonin 5-HT2 Receptor Agonists/pharmacology ; Serotonin 5-HT2 Receptor Antagonists/pharmacology ; Serotonin Uptake Inhibitors/pharmacology ; Signal Transduction/drug effects
Chemical Substances	Receptor, Serotonin, 5-HT2C ; Serotonin 5-HT2 Receptor Agonists ; Serotonin 5-HT2 Receptor Antagonists ; Serotonin Uptake Inhibitors
Language	English
Publishing date	2021-12-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2021.108926
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ui I Zs.242: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Infection-induced extracellular vesicles evoke neuronal transcriptional and epigenetic changes.

Tedford, Ellen / Badya, Norhidayah Binti / Laing, Conor / Asaoka, Nozomi / Kaneko, Shuji / Filippi, Beatrice Maria / McConkey, Glenn Alan

Scientific reports

2023 Volume 13, Issue 1, Page(s) 6913

Abstract: Infection with the protozoan Toxoplasma gondii induces changes in neurotransmission, neuroinflammation, and behavior, yet it remains elusive how these changes come about. In this study we investigated how norepinephrine levels are altered by infection. ... ...

Abstract	Infection with the protozoan Toxoplasma gondii induces changes in neurotransmission, neuroinflammation, and behavior, yet it remains elusive how these changes come about. In this study we investigated how norepinephrine levels are altered by infection. TINEV (Toxoplasma-induced neuronal extracellular vesicles) isolated from infected noradrenergic cells down-regulated dopamine ß-hydroxylase (DBH) gene expression in human and rodent cells. Here we report that intracerebral injection of TINEVs into the brain is sufficient to induce DBH down-regulation and distrupt catecholaminergic signalling. Further, TINEV treatment induced hypermethylation upstream of the DBH gene. An antisense lncRNA to DBH was found in purified TINEV preparations. Paracrine signalling to induce transcriptional gene silencing and DNA methylation may be a common mode to regulate neurologic function.
MeSH term(s)	Humans ; Norepinephrine ; Dopamine/metabolism ; Neurons/metabolism ; Epigenesis, Genetic ; Extracellular Vesicles/metabolism
Chemical Substances	Norepinephrine (X4W3ENH1CV) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2023-04-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-34074-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: NOX1/NADPH Oxidase Promotes Synaptic Facilitation Induced by Repeated D

Asaoka, Nozomi / Ibi, Masakazu / Hatakama, Hikari / Nagaoka, Koki / Iwata, Kazumi / Matsumoto, Misaki / Katsuyama, Masato / Kaneko, Shuji / Yabe-Nishimura, Chihiro

The Journal of neuroscience : the official journal of the Society for Neuroscience

2021 Volume 41, Issue 12, Page(s) 2780–2794

Abstract: Repetitive behavior is a widely observed neuropsychiatric symptom. Abnormal dopaminergic signaling in the striatum is one of the factors associated with behavioral repetition; however, the molecular mechanisms underlying the induction of repetitive ... ...

Abstract	Repetitive behavior is a widely observed neuropsychiatric symptom. Abnormal dopaminergic signaling in the striatum is one of the factors associated with behavioral repetition; however, the molecular mechanisms underlying the induction of repetitive behavior remain unclear. Here, we demonstrated that the NOX1 isoform of the superoxide-producing enzyme NADPH oxidase regulated repetitive behavior in mice by facilitating excitatory synaptic inputs in the central striatum (CS). In male C57Bl/6J mice, repeated stimulation of D
MeSH term(s)	Animals ; Cells, Cultured ; Compulsive Behavior/chemically induced ; Compulsive Behavior/metabolism ; Compulsive Behavior/psychology ; Dopamine Agonists/pharmacology ; Dopamine Agonists/toxicity ; Locomotion/drug effects ; Locomotion/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 1/antagonists & inhibitors ; NADPH Oxidase 1/biosynthesis ; NADPH Oxidases/antagonists & inhibitors ; NADPH Oxidases/biosynthesis ; Pyrazolones/pharmacology ; Pyridones/pharmacology ; Receptors, Dopamine D2/agonists ; Receptors, Dopamine D2/biosynthesis ; Synapses/drug effects ; Synapses/metabolism
Chemical Substances	Dopamine Agonists ; Pyrazolones ; Pyridones ; Receptors, Dopamine D2 ; setanaxib (45II35329V) ; NADPH Oxidase 1 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; NOX1 protein, mouse (EC 1.6.3.-)
Language	English
Publishing date	2021-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.2121-20.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 1668: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: NOX1/NADPH oxidase affects the development of autism-like behaviors in a maternal immune activation model.

Zhang, Xueqing / Ibi, Masakazu / Haga, Ryu / Iwata, Kazumi / Matsumoto, Misaki / Asaoka, Nozomi / Liu, Junjie / Katsuyama, Masato / Yabe-Nishimura, Chihiro

Biochemical and biophysical research communications

2020 Volume 534, Page(s) 59–66

Abstract: Autism spectrum disorder (ASD) is a neurodevelopmental disorder caused by genetic and environmental factors. Among the environmental factors, maternal infection is known as one of the principal risk factors for ASD. On the other hand, postmortem studies ... ...

Abstract	Autism spectrum disorder (ASD) is a neurodevelopmental disorder caused by genetic and environmental factors. Among the environmental factors, maternal infection is known as one of the principal risk factors for ASD. On the other hand, postmortem studies suggested the relationship of oxidative stress with ASD etiology. However, the role of oxidative stress in the development of ASD remains unclear. Here, we report the involvement of NOX1/NADPH oxidase, an enzyme generating reactive oxygen species (ROS), in behavioral and anatomical abnormalities in a maternal immune activation (MIA) model. In the MIA model of gestational polyinosinic-polycytidylic acid (poly(I:C)) exposure, increased serum levels of IL-6 were observed in both wild-type (WT) and Nox1-deficient mice (Nox1KO). Following the comparable induction of MIA in the two genotypes, impairment of social preference and defects in motor coordination were observed in WT offspring but not in offspring deficient in Nox1. MIA up-regulated NOX1 mRNA in the cerebral cortex and cerebellum of the fetus but not in the adult offspring. Although the development of cortical neurons was unaffected by MIA in either genotype, the dropout of Purkinje cells in lobule VII of MIA-affected offspring was significantly ameliorated in Nox1KO. Taken together, these results suggested that NOX1/NADPH oxidase plays an essential role in some behavioral phenotypes observed in ASD, possibly by promoting the loss of Purkinje cells in the cerebellum.
MeSH term(s)	Animals ; Autism Spectrum Disorder/etiology ; Autism Spectrum Disorder/immunology ; Behavior, Animal/physiology ; Cerebellum/embryology ; Cerebral Cortex/embryology ; Disease Models, Animal ; Female ; Gene Expression Regulation, Developmental ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; NADPH Oxidase 1/genetics ; NADPH Oxidase 1/metabolism ; Poly I-C/immunology ; Poly I-C/pharmacology ; Pregnancy ; Purkinje Cells/pathology ; Mice
Chemical Substances	NADPH Oxidase 1 (EC 1.6.3.-) ; NOX1 protein, mouse (EC 1.6.3.-) ; Poly I-C (O84C90HH2L)
Language	English
Publishing date	2020-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.11.070
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 116: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Clioquinol inhibits dopamine-β-hydroxylase secretion and noradrenaline synthesis by affecting the redox status of ATOX1 and copper transport in human neuroblastoma SH-SY5Y cells.

Katsuyama, Masato / Kimura, En / Ibi, Masakazu / Iwata, Kazumi / Matsumoto, Misaki / Asaoka, Nozomi / Yabe-Nishimura, Chihiro

Archives of toxicology

2020 Volume 95, Issue 1, Page(s) 135–148

Abstract: Clioquinol (5-chloro-7-indo-8-quinolinol), a chelator and ionophore of copper/zinc, was extensively used as an amebicide to treat indigestion and diarrhea in the mid-1900s. However, it was withdrawn from the market in Japan because its use was ... ...

Abstract	Clioquinol (5-chloro-7-indo-8-quinolinol), a chelator and ionophore of copper/zinc, was extensively used as an amebicide to treat indigestion and diarrhea in the mid-1900s. However, it was withdrawn from the market in Japan because its use was epidemiologically linked to an increase in the incidence of subacute myelo-optic neuropathy (SMON). SMON is characterized by the subacute onset of sensory and motor disturbances in the lower extremities with occasional visual impairments, which are preceded by abdominal symptoms. Although pathological studies demonstrated axonopathy of the spinal cord and optic nerves, the underlying mechanisms of clioquinol toxicity have not been elucidated in detail. In the present study, a reporter assay revealed that clioquinol (20-50 µM) activated metal response element-dependent transcription in human neuroblastoma SH-SY5Y cells. Clioquinol significantly increased the cellular level of zinc within 1 h, suggesting zinc influx due to its ionophore effects. On the other hand, clioquinol (20-50 µM) significantly increased the cellular level of copper within 24 h. Clioquinol (50 µM) induced the oxidation of the copper chaperone antioxidant 1 (ATOX1), suggesting its inactivation and inhibition of copper transport. The secretion of dopamine-β-hydroxylase (DBH) and lysyl oxidase, both of which are copper-dependent enzymes, was altered by clioquinol (20-50 µM). Noradrenaline levels were reduced by clioquinol (20-50 µM). Disruption of the ATOX1 gene suppressed the secretion of DBH. This study suggested that the disturbance of cellular copper transport by the inactivation of ATOX1 is one of the mechanisms involved in clioquinol-induced neurotoxicity in SMON.
MeSH term(s)	Cell Line, Tumor ; Clioquinol/toxicity ; Copper/metabolism ; Copper Transport Proteins/genetics ; Copper Transport Proteins/metabolism ; Dopamine beta-Hydroxylase/metabolism ; Humans ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Neurons/drug effects ; Neurons/enzymology ; Norepinephrine/biosynthesis ; Oxidation-Reduction ; Protein-Lysine 6-Oxidase/metabolism ; Secretory Pathway ; Toxic Optic Neuropathy/enzymology ; Toxic Optic Neuropathy/etiology ; Zinc/metabolism
Chemical Substances	ATOX1 protein, human ; Copper Transport Proteins ; Molecular Chaperones ; Copper (789U1901C5) ; Clioquinol (7BHQ856EJ5) ; Dopamine beta-Hydroxylase (EC 1.14.17.1) ; LOX protein, human (EC 1.4.3.13) ; Protein-Lysine 6-Oxidase (EC 1.4.3.13) ; Zinc (J41CSQ7QDS) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2020-10-09
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	124992-7
ISSN	1432-0738 ; 0340-5761
ISSN (online)	1432-0738
ISSN	0340-5761
DOI	10.1007/s00204-020-02894-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uf I Zs.90: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Neurotropin inhibits neuronal activity through potentiation of sustained K

Kawai, Hiroyuki / Asaoka, Nozomi / Miyake, Takahito / Nagayasu, Kazuki / Nakagawa, Takayuki / Shirakawa, Hisashi / Kaneko, Shuji

Journal of pharmacological sciences

2018 Volume 137, Issue 3, Page(s) 313–316

Abstract: Neurotropin (NTP) is a Japanese analgesic agent for treating neuropathic pain; however, its method of action remains unclear. This study examined the effects of NTP on the activity of small dorsal root ganglion (DRG) neurons using whole-cell patch clamp ... ...

Abstract	Neurotropin (NTP) is a Japanese analgesic agent for treating neuropathic pain; however, its method of action remains unclear. This study examined the effects of NTP on the activity of small dorsal root ganglion (DRG) neurons using whole-cell patch clamp recordings. After 3 days of treatment, NTP decreased current injection-induced firing activity of cultured DRG neurons by raising the current threshold for action potential generation. Additionally, NTP increased the sustained component of voltage-gated potassium (K
MeSH term(s)	Action Potentials/drug effects ; Analgesics/pharmacology ; Animals ; Cells, Cultured ; Ganglia, Spinal/cytology ; Male ; Neurons/metabolism ; Patch-Clamp Techniques ; Polysaccharides/pharmacology ; Potassium Channels, Voltage-Gated/metabolism ; Rats, Wistar ; Time Factors
Chemical Substances	Analgesics ; Polysaccharides ; Potassium Channels, Voltage-Gated ; neurotropin (57657-35-9)
Language	English
Publishing date	2018-05-31
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2018.05.005
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 237: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Striatal TRPV1 activation by acetaminophen ameliorates dopamine D2 receptor antagonist-induced orofacial dyskinesia.

Nagaoka, Koki / Nagashima, Takuya / Asaoka, Nozomi / Yamamoto, Hiroki / Toda, Chihiro / Kayanuma, Gen / Siswanto, Soni / Funahashi, Yasuhiro / Kuroda, Keisuke / Kaibuchi, Kozo / Mori, Yasuo / Nagayasu, Kazuki / Shirakawa, Hisashi / Kaneko, Shuji

JCI insight

2021 Volume 6, Issue 10

Abstract: Antipsychotics often cause tardive dyskinesia, an adverse symptom of involuntary hyperkinetic movements. Analysis of the US Food and Drug Administration Adverse Event Reporting System and JMDC insurance claims revealed that acetaminophen prevented the ... ...

Abstract	Antipsychotics often cause tardive dyskinesia, an adverse symptom of involuntary hyperkinetic movements. Analysis of the US Food and Drug Administration Adverse Event Reporting System and JMDC insurance claims revealed that acetaminophen prevented the dyskinesia induced by dopamine D2 receptor antagonists. In vivo experiments further showed that a 21-day treatment with haloperidol increased the number of vacuous chewing movements (VCMs) in rats, an effect that was inhibited by oral acetaminophen treatment or intracerebroventricular injection of N-(4-hydroxyphenyl)-arachidonylamide (AM404), an acetaminophen metabolite that acts as an activator of the transient receptor potential vanilloid 1 (TRPV1). In mice, haloperidol-induced VCMs were also mitigated by treatment with AM404 applied to the dorsal striatum, an effect not seen in TRPV1-deficient mice. Acetaminophen prevented the haloperidol-induced decrease in the number of c-Fos+preproenkephalin+ striatal neurons in wild-type mice but not in TRPV1-deficient mice. Finally, chemogenetic stimulation of indirect pathway medium spiny neurons in the dorsal striatum decreased haloperidol-induced VCMs. These results suggest that acetaminophen activates the indirect pathway neurons by activating TRPV1 channels via AM404.
MeSH term(s)	Acetaminophen/pharmacology ; Acetaminophen/therapeutic use ; Animals ; Disease Models, Animal ; Dopamine D2 Receptor Antagonists/adverse effects ; Dyskinesia, Drug-Induced/drug therapy ; Dyskinesia, Drug-Induced/etiology ; Male ; Mice ; Mice, Inbred C57BL ; Rats ; Rats, Wistar ; TRPV Cation Channels/drug effects ; TRPV Cation Channels/metabolism
Chemical Substances	Dopamine D2 Receptor Antagonists ; TRPV Cation Channels ; TRPV1 protein, mouse ; Trpv1 protein, rat ; Acetaminophen (362O9ITL9D)
Language	English
Publishing date	2021-05-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.145632
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED