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Article ; Online: Regulation of adult-born and mature neurons in stress response and antidepressant action in the dentate gyrus of the hippocampus.

Segi-Nishida, Eri / Suzuki, Kanzo

2022

Abstract: The dentate gyrus (DG) of the hippocampus has been implicated in the regulation of stress responses, and in the pathophysiology and treatment of depression. This review discusses the cellular changes caused by chronic stress and the cellular role of the ... ...

Abstract	The dentate gyrus (DG) of the hippocampus has been implicated in the regulation of stress responses, and in the pathophysiology and treatment of depression. This review discusses the cellular changes caused by chronic stress and the cellular role of the DG in stress-induced behavioral changes and its antidepressant-like effects. Regarding adult-born neurogenic processes in the DG, chronic stress, such as repeated social defeat, suppresses cell proliferation during and immediately after stress; however, this effect is transient. The subsequent differentiation and survival processes are differentially regulated depending on the timing and sensitivity of stress. The activation of young adult-born neurons during stress contributes to stress resilience, while the transient increase in the survival of adult-born neurons after the cessation of stress seems to promote stress susceptibility. In mature granule neurons, the predominant cells in the DG, synaptic plasticity is suppressed by chronic stress. However, a group of mature granule neurons is activated by chronic stress. Chronic antidepressant treatment can transform mature granule neurons to a phenotype resembling that of immature neurons, characterized as "dematuration". Adult-born neurons suppress the activation of mature granule neurons during stress, indicating that local neural interactions within the DG are important for the stress response. Elucidating the stress-associated context- and timing-dependent cellular changes and functions in the DG will provide insights into stress-related psychiatric diseases.
Language	English
Publishing date	2022-08-27
Publishing country	Ireland
Document type	Journal Article ; Review
ZDB-ID	605842-5
ISSN	1872-8111 ; 0168-0102 ; 0921-8696
ISSN (online)	1872-8111
ISSN	0168-0102 ; 0921-8696
DOI	10.1016/j.neures.2022.08.010
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Article ; Online: Hippocampal Inflammation and Gene Expression Changes in Peripheral Lipopolysaccharide Challenged Mice Showing Sickness and Anxiety-Like Behaviors.

Matsuura, Sumire / Nishimoto, Yuki / Endo, Akane / Shiraki, Hirono / Suzuki, Kanzo / Segi-Nishida, Eri

Biological & pharmaceutical bulletin

2023 Volume 46, Issue 9, Page(s) 1176–1183

Abstract: Neuroinflammation is often associated with the development of depressive and anxiety disorders. The hippocampus is one of the brain regions affected by inflammation that is associated with these symptoms. However, the mechanism of hippocampal ... ...

Abstract	Neuroinflammation is often associated with the development of depressive and anxiety disorders. The hippocampus is one of the brain regions affected by inflammation that is associated with these symptoms. However, the mechanism of hippocampal inflammation-induced emotional behavior remains unknown. The aim of this study was to clarify temporal changes in the neuroinflammatory responses in the hippocampus and the response of dentate gyrus (DG) neurons using peripheral lipopolysaccharide (LPS)-challenged mice. LPS administration induced anxiety-like activity in the elevated plus maze test and social interaction test after 24 h, at which time the mice had recovered from sickness behavior. We examined the hippocampal inflammation-related gene expression changes over time. The expression of interleukin-1β (Il1b) and tumor necrosis factor α (Tnfa) was rapidly enhanced and sustained until 24 h after LPS administration, whereas the expression of Il6 was transiently induced at approx. 6 h. IL-6-dependent downstream signaling of transducer and activator of transcription 3 (STAT3) was also activated approx. 3-6 h after LPS treatment. The expression of innate immune genes including interferon-induced transmembrane proteins such as interferon-induced transmembrane protein 1 (Ifitm1) and Ifitm3 and complement factors such as C1qa and C1qb started to increase approx. 6 h and showed sustained or further increase at 24 h. We also examined changes in the expression of several maturation markers in the DG and found that LPS enhanced the expression of calbindin 1 (Calb1), tryptophan-2,3-dioxigenase 2 (Tdo2), Il1rl, and neurotrophin-3 (Ntf3) at 24 h after LPS treatment. Collectively, these results demonstrate temporal changes of inflammation and gene expression in the hippocampus in LPS-induced sickness and anxiety-like behaviors.
MeSH term(s)	Animals ; Mice ; Lipopolysaccharides/toxicity ; Anxiety/chemically induced ; Anxiety/genetics ; Inflammation/chemically induced ; Inflammation/genetics ; Hippocampus ; Interferons ; Gene Expression
Chemical Substances	Lipopolysaccharides ; Interferons (9008-11-1)
Language	English
Publishing date	2023-09-03
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1150271-x
ISSN	1347-5215 ; 0918-6158
ISSN (online)	1347-5215
ISSN	0918-6158
DOI	10.1248/bpb.b22-00729
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Zs.A 1474: Show issues

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Article ; Online: KNT-127, a selective delta opioid receptor agonist, shows beneficial effects in the hippocampal dentate gyrus of a chronic vicarious social defeat stress mouse model.

Yoshioka, Toshinori / Yamada, Daisuke / Segi-Nishida, Eri / Nagase, Hiroshi / Saitoh, Akiyoshi

Neuropharmacology

2023 Volume 232, Page(s) 109511

Abstract: Delta opioid receptors (DOPs) play an important role in depression and other mood disorders. However, little is known about the underlying physiological mechanisms. The hypothalamic-pituitary-adrenal axis, adult hippocampal neurogenesis, and ... ...

Abstract	Delta opioid receptors (DOPs) play an important role in depression and other mood disorders. However, little is known about the underlying physiological mechanisms. The hypothalamic-pituitary-adrenal axis, adult hippocampal neurogenesis, and neuroinflammation are regarded as key pathophysiological factors in depression. In this study, we investigated the influence of DOP activation on those factors in a valid animal model of depression, chronic vicarious social defeat stress (cVSDS) mice. cVSDS mice (male C57BL/6J mice) were produced following a 10-day exposure to witness of social defeat stress, and each evaluation was performed more than 28 days after the stress period. Repeated administrations to cVSDS mice with a selective DOP agonist, KNT-127, both during (10 days) and after (28 days) the stress period respectively improved their decreased social interaction behaviors and increased serum corticosterone levels. When administered during the stress period, KNT-127 suppressed decreases in the hippocampal newborn neuron survival rate in cVSDS mice. Moreover, in both administration paradigms, KNT-127 reduced the number of Iba-1- and CD11b-positive cells in the subgranular zone and the granule cell layer of the hippocampal dentate gyrus, indicating a suppression of cVSDS-induced microglial overactivation. These results suggest that KNT-127 acts over the hypothalamic-pituitary-adrenal axis and regulates neurogenesis and neuroinflammation resulting in anti-stress effects, and the antidepressant-like effects of the DOP agonist are implicated in the suppression of the neuroinflammation. This study presents a new finding on the effects of repeated DOP activations on the pathophysiological states of depression.
MeSH term(s)	Male ; Mice ; Animals ; Receptors, Opioid, delta/agonists ; Social Defeat ; Hypothalamo-Hypophyseal System/metabolism ; Neuroinflammatory Diseases ; Mice, Inbred C57BL ; Pituitary-Adrenal System/metabolism ; Analgesics, Opioid/pharmacology ; Hippocampus ; Dentate Gyrus/metabolism ; Stress, Psychological/drug therapy ; Neurogenesis ; Depression/drug therapy
Chemical Substances	KNT 127 ; Receptors, Opioid, delta ; Analgesics, Opioid
Language	English
Publishing date	2023-03-30
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.2023.109511
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Article ; Online: Search for factors contributing to resistance to the electroconvulsive seizure treatment model using adrenocorticotrophic hormone-treated mice.

Kobayashi, Yurika / Segi-Nishida, Eri

Pharmacology, biochemistry, and behavior

2019 Volume 186, Page(s) 172767

Abstract: Approximately one third of patients with depression remain treatment resistant with existing antidepressants, suggesting that the currently-available antidepressants cannot induce appropriate responses in the brains of all patients. Long-term exposure to ...

Abstract	Approximately one third of patients with depression remain treatment resistant with existing antidepressants, suggesting that the currently-available antidepressants cannot induce appropriate responses in the brains of all patients. Long-term exposure to adrenocorticotrophic hormone (ACTH) has been proposed as a model that mimics at least some aspects of clinical treatment-resistant depression in rodents. The purpose of this study was to explore potential causes of antidepressant treatment resistance using the chronic ACTH-treated mouse model. We subjected ACTH-treated mice to a rodent model of electroconvulsive therapy, i.e., electroconvulsive seizure (ECS), which induces various molecular and cellular changes, including in gene expression and adult neurogenesis in the hippocampus. First, behavioral effect of repeated ECS in the forced swim test (FST) was examined. In our experimental setting, ACTH-treated mice showed resistance to the antidepressant-like effect of ECS in the FST. We then examined which cellular and molecular changes induced by ECS were attenuated by ACTH administration. Chronic ACTH treatment suppressed the increase of gene expression such as of Bdnf, Npy, and Drd1 induced by ECS in the hippocampus. In contrast, there was no difference in ECS-induced promotion of the early neurogenetic process in the hippocampus between ACTH-treated and control mice. Our results suggest the possibility that impaired neuromodulation and monoamine signaling in the hippocampus are among the factors contributing to antidepressant treatment resistance.
MeSH term(s)	Adrenocorticotropic Hormone/administration & dosage ; Adrenocorticotropic Hormone/pharmacology ; Animals ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/genetics ; Electroconvulsive Therapy ; Male ; Mice ; Models, Biological ; Neurogenesis ; Neuropeptide Y/genetics ; RNA, Messenger/metabolism ; Receptors, Dopamine D1/genetics
Chemical Substances	Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; Neuropeptide Y ; RNA, Messenger ; Receptors, Dopamine D1 ; Adrenocorticotropic Hormone (9002-60-2)
Language	English
Publishing date	2019-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	191042-5
ISSN	1873-5177 ; 0091-3057
ISSN (online)	1873-5177
ISSN	0091-3057
DOI	10.1016/j.pbb.2019.172767
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Zs.A 1060: Show issues

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Article: The Effect of Serotonin-Targeting Antidepressants on Neurogenesis and Neuronal Maturation of the Hippocampus Mediated via 5-HT1A and 5-HT4 Receptors.

Segi-Nishida, Eri

Frontiers in cellular neuroscience

2017 Volume 11, Page(s) 142

Abstract: Antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs) specifically increase serotonin (5-HT) levels in the synaptic cleft and are widely used to treat mood and anxiety disorders. There are 14 established subtypes of 5-HT receptors ... ...

Abstract	Antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs) specifically increase serotonin (5-HT) levels in the synaptic cleft and are widely used to treat mood and anxiety disorders. There are 14 established subtypes of 5-HT receptors in rodents, each of which has regionally different expression patterns. Many preclinical studies have suggested that the hippocampus, which contains abundant 5-HT1A and 5-HT4 receptor subtypes in the dentate gyrus (DG), is critically involved in the mechanisms of action of antidepressants. This review article will analyze studies demonstrating regulation of hippocampal functions and hippocampus-dependent behaviors by SSRIs and similar serotonergic agents. Multiple studies indicate that 5-HT1A and 5-HT4 receptor signaling in the DG contributes to SSRI-mediated promotion of neurogenesis and increased neurotrophic factors expression. Chronic SSRI treatment causes functions and phenotypes of mature granule cells (GCs) to revert to immature-like phenotypes defined as a "dematured" state in the DG, and to increase monoamine reactivity at the dentate-to-CA3 synapses, via 5-HT4 receptor signaling. Behavioral studies demonstrate that the 5-HT1A receptors on mature GCs are critical for expression of antidepressant effects in the forced swim test and in novelty suppressed feeding; such studies also note that 5-HT4 receptors mediate neurogenesis-dependent antidepressant activity in, for example, novelty-suppressed feeding. Despite their limitations, the collective results of these studies describe a potential new mechanism of action, in which 5-HT1A and 5-HT4 receptor signaling, either independently or cooperatively, modulates the function of the hippocampal DG at multiple levels, any of which could play a critical role in the antidepressant actions of 5-HT-enhancing drugs.
Language	English
Publishing date	2017-05-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2017.00142
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Article ; Online: Electroconvulsive seizures lead to lipolytic-induced gene expression changes in mediobasal hypothalamus and decreased white adipose tissue mass.

Takefusa, Marika / Kubo, Yuki / Ohno, Marie / Segi-Nishida, Eri

Neuropsychopharmacology reports

2021 Volume 41, Issue 1, Page(s) 56–64

Abstract: Aims: Electroconvulsive seizure (ECS) therapy is highly effective in the treatment of several psychiatric disorders, including depression. Past studies have shown that the rodent model of ECS reveals the activation of multiple brain regions including ... ...

Abstract	Aims: Electroconvulsive seizure (ECS) therapy is highly effective in the treatment of several psychiatric disorders, including depression. Past studies have shown that the rodent model of ECS reveals the activation of multiple brain regions including the hypothalamus, suggesting that this method of brain stimulation broadly regulates central neuronal function, which results in peripheral function. The ventromedial nucleus of the hypothalamus (VMH) plays an important role in feeding and energy homeostasis. Our previous study showed that ECS increases the expression of anorexigenic factors in the VMH and has an anorexigenic effect in a mouse model. Since the VMH is also suggested to play a critical role in the peripheral lipid metabolism of white adipose tissue (WAT), we hypothesized that ECS alters lipid metabolism via activation of the VMH. Methods and results: Here, we demonstrate that repeated ECS suppresses the fat mass of epididymal WAT and significantly increases the expression levels of lipolytic and brown adipose tissue markers such as Adrb3, Hsl/Lipe, and Ppargc1a. In the VMH, ECS increased the expression of multiple genes, notably Bdnf, Adcyap1, and Crhr2, which are not only anorexigenic factors but are also modulators of lipid metabolism. Furthermore, gold-thioglucose-induced hypothalamic lesions affecting the VMH abolished the effect of ECS on the WAT, indicating that hypothalamus activation is required for the phenotypic changes seen in the epididymal WAT. Conclusion: Our data demonstrates a new effect of ECS on the lipid metabolism of WAT via induction of hypothalamic activity involving the VMH.
MeSH term(s)	Adipose Tissue, White/metabolism ; Animals ; Behavior, Animal/physiology ; Electroshock ; Epididymis/metabolism ; Gene Expression/genetics ; Hypothalamus, Middle/metabolism ; Hypothalamus, Middle/pathology ; Lipid Metabolism/physiology ; Lipolysis/genetics ; Locomotion/physiology ; Male ; Mice ; Weight Gain/physiology
Language	English
Publishing date	2021-01-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2574-173X
ISSN (online)	2574-173X
DOI	10.1002/npr2.12156
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Article: Overexpression of NT-3 in the hippocampus suppresses the early phase of the adult neurogenic process.

Kasakura, Nanami / Murata, Yuka / Shindo, Asuka / Kitaoka, Shiho / Furuyashiki, Tomoyuki / Suzuki, Kanzo / Segi-Nishida, Eri

Frontiers in neuroscience

2023 Volume 17, Page(s) 1178555

Abstract: The dentate gyrus (DG) of the hippocampus regulates stress-related emotional behaviors and ensures neurogenesis throughout life. Neurotrophin-3 (NT-3) is a neurotrophic factor that regulates neuronal differentiation, survival, and synaptic formation in ... ...

Abstract	The dentate gyrus (DG) of the hippocampus regulates stress-related emotional behaviors and ensures neurogenesis throughout life. Neurotrophin-3 (NT-3) is a neurotrophic factor that regulates neuronal differentiation, survival, and synaptic formation in both the peripheral and central nervous systems. NT-3 is expressed in the adult DG of the hippocampus; several chronic stress conditions enhance NT-3 expression in rodents. However, functional modulation of the adult DG by NT-3 signaling remains unclear. To directly investigate the impact of NT-3 on DG function, NT-3 was overexpressed in the hippocampal ventral DG by an adeno-associated virus carrying NT-3 (AAV-NT-3). Four weeks following the AAV-NT-3 injection, high NT-3 expression was observed in the ventral DG. We examined the influence of NT-3 overexpression on the neuronal responses and neurogenic processes in the ventral DG. NT-3 overexpression significantly increased the expression of the mature DG neuronal marker calbindin and immediate early genes, such as
Language	English
Publishing date	2023-07-27
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.2023.1178555
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Article: Double function of MFSD2A transporter at the blood-brain barrier.

Segi-Nishida, Eri

Nihon yakurigaku zasshi. Folia pharmacologica Japonica

2014 Volume 144, Issue 5, Page(s) 253

Language	Japanese
Publishing date	2014
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.144.253
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Zs.A 439: Show issues

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Article ; Online: Noradrenaline activation of hippocampal dopamine D

Kobayashi, Katsunori / Shikano, Kisako / Kuroiwa, Mahomi / Horikawa, Mio / Ito, Wakana / Nishi, Akinori / Segi-Nishida, Eri / Suzuki, Hidenori

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 33, Page(s) e2117903119

Abstract: ... Dopamine ... ...

Abstract	Dopamine D
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Dentate Gyrus/metabolism ; Depressive Disorder/metabolism ; Dopamine/metabolism ; Dopaminergic Neurons/metabolism ; Mice ; Norepinephrine/metabolism ; Norepinephrine/pharmacology ; Receptors, Dopamine D1/metabolism
Chemical Substances	Antidepressive Agents ; Receptors, Dopamine D1 ; Dopamine (VTD58H1Z2X) ; Norepinephrine (X4W3ENH1CV)
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2117903119
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Zs.A 1148: Show issues

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Article ; Online: Chronic vicarious social defeat stress attenuates new-born neuronal cell survival in mouse hippocampus.

Yoshioka, Toshinori / Yamada, Daisuke / Kobayashi, Riho / Segi-Nishida, Eri / Saitoh, Akiyoshi

Behavioural brain research

2021 Volume 416, Page(s) 113536

Abstract: Increasing evidence has shown that adult hippocampal neurogenesis is closely related to the pathophysiological condition of depressive disorders. Recently, chronic social defeat stress paradigms have been regarded as important animal models of depression, ...

Abstract	Increasing evidence has shown that adult hippocampal neurogenesis is closely related to the pathophysiological condition of depressive disorders. Recently, chronic social defeat stress paradigms have been regarded as important animal models of depression, accompanied with neural plastic changes in the hippocampus. However, little is known about influences of non-physical stress on neurogenesis. In the present study, we focused on the chronic vicarious social defeat stress paradigm and examined the effect of psychological stress on mouse hippocampal neurogenesis. Immediately after the chronic psychological stress, the cell survival rate in the dentate gyrus of the hippocampus was significantly diminished without modifying the cell proliferation rate. The decreased ratio in cell survival persisted for 4 weeks after the stress-loading period, while the differentiation and maturity of new-born neurons were identical to control groups. Furthermore, treatment with the chronic antidepressant fluoxetine reversed the social behavioral deficits and promoted new-born neurons survival. These results demonstrate that emotional stress in the vicarious social defeat stress paradigm influences neuronal cell survival in the hippocampus, which reinforces its validity as an animal model of depression.
MeSH term(s)	Animals ; Antidepressive Agents/pharmacology ; Cell Survival/drug effects ; Disease Models, Animal ; Fluoxetine/antagonists & inhibitors ; Fluoxetine/pharmacology ; Hippocampus/drug effects ; Male ; Mice ; Neurogenesis/drug effects ; Neurogenesis/physiology ; Neurons/physiology ; Social Defeat
Chemical Substances	Antidepressive Agents ; Fluoxetine (01K63SUP8D)
Language	English
Publishing date	2021-08-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2021.113536
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