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Article: [Preface].

Ago, Yukio / Mouri, Akihiro

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2023 Volume 158, Issue 3, Page(s) 228

Language	Japanese
Publishing date	2023-04-28
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.22151
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Article ; Online: Chronic social defeat stress induces anxiety-like behaviors via downregulation of serotonin transporter in the prefrontal serotonergic system in mice.

Araki, Ryota / Kita, Ayami / Ago, Yukio / Yabe, Takeshi

Neurochemistry international

2024 Volume 174, Page(s) 105682

Abstract: The serotonergic (5-HTergic) system is closely involved in the pathophysiology of mood and anxiety disorders and the responsibility of this system may differ for each symptom. In this study, we examined the relationship between the dysfunction of the 5- ... ...

Abstract	The serotonergic (5-HTergic) system is closely involved in the pathophysiology of mood and anxiety disorders and the responsibility of this system may differ for each symptom. In this study, we examined the relationship between the dysfunction of the 5-HTergic system and abnormal behaviors in the social defeat stress model, an animal model of mood and anxiety disorders and in mice with knockdown of Slc6a4, the gene encoding SERT. Monoamine content, serotonin (5-HT) release, 5-HT uptake, 5-HT transporter (SERT) protein levels, and behaviors were investigated in mice subjected to chronic social defeat stress and in mice with knockdown of Slc6a4, in 5-HTergic neurons projecting to the prefrontal cortex (PFC). Furthermore, DNA methylation of Slc6a4 was examined in mice subjected to chronic social defeat stress. Increased turnover, increased extracellular basal levels, decreased release and decreased uptake of 5-HT, and decreased SERT protein levels were observed in the PFC of the stressed mice. The decreased 5-HT uptake correlated with anxiety-like behavior characterized by decreased time spent in the open arms of the elevated plus maze. DNA methylation was increased in the CpG island of Slc6a4 in 5-HTergic neurons projecting to the PFC of the stressed mice. Similar to the stressed mice, mice with Slc6a4 knockdown in 5-HTergic neurons projecting to the PFC also showed decreased release and uptake of 5-HT in the PFC and increased anxiety-like behavior. Chronic stress may induce anxiety due to dysfunction in the prefrontal 5-HTergic system via decreased SERT expression in the PFC.
MeSH term(s)	Mice ; Animals ; Serotonin Plasma Membrane Transport Proteins/genetics ; Serotonin Plasma Membrane Transport Proteins/metabolism ; Serotonin/metabolism ; Down-Regulation ; Social Defeat ; Anxiety ; Prefrontal Cortex/metabolism
Chemical Substances	Serotonin Plasma Membrane Transport Proteins ; Serotonin (333DO1RDJY)
Language	English
Publishing date	2024-02-01
Publishing country	England
Document type	Journal Article
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2024.105682
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Article: [Development of the vasoactive intestinal peptide receptor 2 (VIPR2) antagonist peptide for the treatment of schizophrenia].

Ago, Yukio / Asano, Satoshi / Sakamoto, Kotaro

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2023 Volume 158, Issue 3, Page(s) 242–245

Abstract: Schizophrenia affects approximately 24 million people worldwide. Existing medications for the treatment of schizophrenia work primarily by improving positive symptoms such as agitation, hallucinations, delusions, and aggression. They possess common ... ...

Abstract	Schizophrenia affects approximately 24 million people worldwide. Existing medications for the treatment of schizophrenia work primarily by improving positive symptoms such as agitation, hallucinations, delusions, and aggression. They possess common mechanism of action (MOA), blocking to neurotransmitter receptors such as dopamine, serotonin, and adrenaline receptors. Although multiple agents are available for the treatment of schizophrenia, the majority do not address negative symptoms or cognitive dysfunction. In other cases, patients have drug-related adverse effects. The vasoactive intestinal peptide receptor 2 (VIPR2, also known as VPAC2 receptor) might be an attractive drug target for the treatment of schizophrenia because both clinical and preclinical studies have demonstrated a strong link between high expression/overactivation of VIPR2 and schizophrenia. Despite these backgrounds, the proof-of-concept of VIPR2 inhibitors has not been examined clinically. A reason might be that VIPR2 belongs to class-B GPCRs, and the discovery of small-molecule drugs against class-B GPCRs is generally difficult. We have developed a bicyclic peptide KS-133, which shows VIPR2 antagonist activity and suppresses cognitive decline in a mouse model relevant to schizophrenia. KS-133 has a different MOA from current therapeutic drugs and exhibits high selectivity for VIPR2 and potent inhibitory activity against a single-target molecule. Therefore, it may contribute to both the development of a novel drug candidate for the treatment of psychiatric disorders such as schizophrenia and acceleration of basic studies on VIPR2.
MeSH term(s)	Mice ; Animals ; Receptors, Vasoactive Intestinal Peptide, Type II ; Schizophrenia/drug therapy ; Vasoactive Intestinal Peptide/pharmacology ; Vasoactive Intestinal Peptide/therapeutic use
Chemical Substances	Receptors, Vasoactive Intestinal Peptide, Type II ; Vasoactive Intestinal Peptide (37221-79-7) ; Vipr2 protein, mouse
Language	Japanese
Publishing date	2023-03-29
Publishing country	Japan
Document type	English Abstract ; Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.22146
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Article ; Online: Roles of the monoaminergic system in the antidepressant effects of ketamine and its metabolites.

Ago, Yukio / Yokoyama, Rei / Asano, Satoshi / Hashimoto, Hitoshi

Neuropharmacology

2022 Volume 223, Page(s) 109313

Abstract: While the molecular target of (R,S)-ketamine (ketamine) is thought to be the NMDA receptor, subanesthetic doses of ketamine have been known to modulate monoaminergic neurotransmission in the central nervous system. Although the involvement of the ... ...

Abstract	While the molecular target of (R,S)-ketamine (ketamine) is thought to be the NMDA receptor, subanesthetic doses of ketamine have been known to modulate monoaminergic neurotransmission in the central nervous system. Although the involvement of the serotonergic system in the antidepressant effects of ketamine has been reported in most studies of this topic, some recent studies have reported that the dopaminergic system plays a key role in the effects of ketamine. Additionally, several lines of evidence suggest that the antidepressant-like effects of (R)-ketamine might be independent of the monoaminergic system. Ketamine metabolites also differ considerably in their ability to regulate monoamine neurotransmitters relative to (S)-ketamine and (R)-ketamine, while (2R,6R)-hydroxynorketamine might share common serotonergic signaling mechanisms with ketamine. In the current review, we summarize the effects of ketamine and its metabolites on monoamine neurotransmission in the brain and discuss the potential roles of the monoaminergic system in the mechanism of action of ketamine.
Language	English
Publishing date	2022-10-31
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2022.109313
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Article ; Online: AlphaFold version 2.0 elucidates the binding mechanism between VIPR2 and KS-133, and reveals an S-S bond (Cys

Sakamoto, Kotaro / Asano, Satoshi / Ago, Yukio / Hirokawa, Takatsugu

Biochemical and biophysical research communications

2022 Volume 636, Issue Pt 1, Page(s) 10–16

Abstract: The vasoactive intestinal peptide receptor 2 (VIPR2) has attracted attention as a drug target for the treatment of mental disorders, cancer, and immune diseases. In 2021, we identified the peptide KS-133 as a VIPR2-selective antagonist. In this study, we ...

Abstract	The vasoactive intestinal peptide receptor 2 (VIPR2) has attracted attention as a drug target for the treatment of mental disorders, cancer, and immune diseases. In 2021, we identified the peptide KS-133 as a VIPR2-selective antagonist. In this study, we aimed to elucidate the binding mechanism between VIPR2 and KS-133. To this end, VIPR2/KS-133 and VIPR2/vasoactive intestinal peptide (VIP) complex models were constructed through AlphaFold version 2.0 and molecular dynamic simulations. Our models revealed that: (i) both KS-133 and VIP have helical structures, (ii) the interaction residues on VIPR2 for both peptides are similar, and (iii) the orientation of their helices upon their binding to VIPR2 are different by ∼45°. Interestingly, in the process of constructing the aforementioned models, an S-S bond formation between Cys
MeSH term(s)	Humans ; Mice ; Animals ; Receptors, Vasoactive Intestinal Peptide, Type II ; Receptors, Vasoactive Intestinal Peptide/metabolism ; Vasoactive Intestinal Peptide/metabolism ; Cell Line
Chemical Substances	Receptors, Vasoactive Intestinal Peptide, Type II ; Receptors, Vasoactive Intestinal Peptide ; Vasoactive Intestinal Peptide (37221-79-7) ; VIPR2 protein, human ; Vipr2 protein, mouse
Language	English
Publishing date	2022-10-23
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.2022.10.071
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Article ; Online: Phospholipase C-related catalytically inactive protein enhances cisplatin-induced apoptotic cell death.

Asano, Satoshi / Maetani, Yuka / Ago, Yukio / Kanematsu, Takashi

European journal of pharmacology

2022 Volume 933, Page(s) 175273

Abstract: Cisplatin is one of the most widely used chemotherapeutic agents and induces caspase-9-mediated apoptosis. Here, we examined whether phospholipase C-related catalytically inactive protein (PRIP) enhances cisplatin-induced apoptosis of breast cancer cells. ...

Abstract	Cisplatin is one of the most widely used chemotherapeutic agents and induces caspase-9-mediated apoptosis. Here, we examined whether phospholipase C-related catalytically inactive protein (PRIP) enhances cisplatin-induced apoptosis of breast cancer cells. PRIP depletion increased expression of X-linked inhibitor of apoptosis protein (XIAP) by inhibiting protein degradation, which is downstream of the phosphatidylinositol 3-kinase/AKT pathway and inhibits apoptotic signaling by blocking caspase-9 activation. Conversely, the viability of MCF-7 cells transfected with Prip1 was significantly lower than that of control cells in the presence of cisplatin. The number of apoptotic nuclei and expression levels of cleaved caspase-9 and downstream cleaved caspase-7 and poly-ADP ribose polymerase were greater in PRIP1-expressing MCF-7 cells treated with cisplatin than in control cells. XIAP was decreased by expression of pleckstrin homology domain of PRIP1 (PRIP1-PH domain) that blocked phosphatidylinositol 4,5 bisphosphate metabolism. In an orthotopic transplantation model, combined administration of PRIP1-PH domain-containing liposomes and cisplatin reduced the size of MCF-7 tumors compared with cisplatin alone. Our findings demonstrate that PRIP promotes XIAP degradation by inhibiting PI(3,4,5)P
MeSH term(s)	Adenosine Diphosphate Ribose ; Apoptosis ; Caspase 7/metabolism ; Caspase 9/metabolism ; Cell Line, Tumor ; Cisplatin/pharmacology ; Humans ; Liposomes ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositols ; Proto-Oncogene Proteins c-akt/metabolism ; Type C Phospholipases/metabolism ; X-Linked Inhibitor of Apoptosis Protein/genetics ; X-Linked Inhibitor of Apoptosis Protein/metabolism
Chemical Substances	Liposomes ; Phosphatidylinositols ; X-Linked Inhibitor of Apoptosis Protein ; Adenosine Diphosphate Ribose (20762-30-5) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Type C Phospholipases (EC 3.1.4.-) ; Caspase 7 (EC 3.4.22.-) ; Caspase 9 (EC 3.4.22.-) ; Cisplatin (Q20Q21Q62J)
Language	English
Publishing date	2022-09-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2022.175273
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Article: [Transitive inference task in mice using a touchscreen assay].

Ago, Yukio

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2014 Volume 144, Issue 1, Page(s) 45

MeSH term(s)	Animals ; Behavior, Animal ; Computers ; Disease Models, Animal ; Mice ; Translational Medical Research
Language	Japanese
Publishing date	2014-05-13
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.144.45
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Article: [Haploinsufficiency of the T-box transcription factor Tbr1].

Ago, Yukio

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2014 Volume 144, Issue 3, Page(s) 146

MeSH term(s)	Animals ; Haploinsufficiency ; Mice ; T-Box Domain Proteins/genetics
Chemical Substances	T-Box Domain Proteins ; Tbx1 protein, mouse
Language	Japanese
Publishing date	2014-05-13
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1097532-9
ISSN	1347-8397 ; 0015-5691
ISSN (online)	1347-8397
ISSN	0015-5691
DOI	10.1254/fpj.144.146
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Article: Probing the

Ago, Yukio / Asano, Satoshi / Hashimoto, Hitoshi / Waschek, James A

Frontiers in neuroscience

2021 Volume 15, Page(s) 717490

Abstract: Pituitary adenylate cyclase-activating polypeptide (PACAP, gene ... ...

Abstract	Pituitary adenylate cyclase-activating polypeptide (PACAP, gene name
Language	English
Publishing date	2021-07-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2021.717490
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Article: [Neurochemical basis for social encounter-induced hyperactivity in post-weaning isolation-reared mice].

Ago, Yukio

Nihon shinkei seishin yakurigaku zasshi = Japanese journal of psychopharmacology

2014 Volume 34, Issue 4, Page(s) 101–107

Abstract: Rearing rodents in social isolation from post-weaning causes abnormal behaviors in adulthood, such as hyper-locomotion, aggression, cognitive impairments, and depression- and anxiety-like behaviors. This social isolation is widely used as a model to ... ...

Abstract	Rearing rodents in social isolation from post-weaning causes abnormal behaviors in adulthood, such as hyper-locomotion, aggression, cognitive impairments, and depression- and anxiety-like behaviors. This social isolation is widely used as a model to study the effects of adverse early-life experiences on behavior and the neural mechanisms associated with neuropsychological development. Previous studies have shown abnormalities of dendritic spine density, synaptic protein levels and amine metabolism in the prefrontal cortex and hippocampus of isolation-reared animals, but the neurochemical basis for induction of abnormal behaviors is not known. We have established a novel methodology for assessing social interaction, focusing on the psychological stressor responsible for induction of abnormal behaviors as a transient environmental factor. This review summarizes the effect of a social encounter with an unfamiliar conspecific on behavior and neurochemistry in isolation-reared mice. The current analysis using the encounter response will provide new strategies to clarify the pathophysiology of psychiatric disorders including schizophrenia, depression and drug dependence.
MeSH term(s)	Animals ; Behavior, Animal ; Mice ; Psychomotor Agitation/psychology ; Social Behavior ; Social Isolation ; Stress, Psychological
Language	Japanese
Publishing date	2014-08
Publishing country	Japan
Document type	English Abstract ; Journal Article ; Review
ZDB-ID	1285665-4
ISSN	1340-2544
ISSN	1340-2544
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