Oxytocin ameliorates KCC2 decrease induced by oral bacteria-derived LPS that affect rat primary cultured cells and PC-12 cells

Tomita, Kazuo; Yamanishi-Taira, Sayuri; Igarashi, Kento; Oogai, Yuichi; Kuwahara, Yoshikazu; Roudkenar, Mehryar Habibi; Roushandeh, Amaneh Mohammadi; Miyawaki, Shuichi; Kurimasa, Akihiro; Sato, Tomoaki

doi:10.1016/j.peptides.2021.170734

Cited by 8 publications

(10 citation statements)

References 51 publications

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“…130 Similarly, psychological stress and neuroinflammation during early prenatal development reduce KCC2 expression delaying the E/I GABA shift, which has been implicated in neurodevelopmental and psychiatric disorders. [133][134][135][136] Reduced KCC2 function also contributes to circadian rhythm disruption 137 and age-associated neurodegenerative diseases, such as Alzheimer's and Huntington's disease, through impairment of GABAergic inhibition. 136,138,139 As a result of alternative promoter usage, the Scl12a5 gene produces two proteins, KCC2a and KCC2b which differ in their N-termini.…”

Section: Potential Common Effectorsmentioning

confidence: 99%

Rett and Rett-related disorders: Common mechanisms for shared symptoms?

D’Mello

2023

Exp Biol Med (Maywood)

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Rett syndrome is a neurodevelopmental disorder caused by loss-of-function mutations in the methyl-CpG binding protein-2 (MeCP2) gene that is characterized by epilepsy, intellectual disability, autistic features, speech deficits, and sleep and breathing abnormalities. Neurologically, patients with all three disorders display microcephaly, aberrant dendritic morphology, reduced spine density, and an imbalance of excitatory/inhibitory signaling. Loss-of-function mutations in the cyclin-dependent kinase-like 5 (CDKL5) and FOXG1 genes also cause similar behavioral and neurobiological defects and were referred to as congenital or variant Rett syndrome. The relatively recent realization that CDKL5 deficiency disorder (CDD), FOXG1 syndrome, and Rett syndrome are distinct neurodevelopmental disorders with some distinctive features have resulted in separate focus being placed on each disorder with the assumption that distinct molecular mechanisms underlie their pathogenesis. However, given that many of the core symptoms and neurological features are shared, it is likely that the disorders share some critical molecular underpinnings. This review discusses the possibility that deregulation of common molecules in neurons and astrocytes plays a central role in key behavioral and neurological abnormalities in all three disorders. These include KCC2, a chloride transporter, vGlut1, a vesicular glutamate transporter, GluD1, an orphan-glutamate receptor subunit, and PSD-95, a postsynaptic scaffolding protein. We propose that reduced expression or activity of KCC2, vGlut1, PSD-95, and AKT, along with increased expression of GluD1, is involved in the excitatory/inhibitory that represents a key aspect in all three disorders. In addition, astrocyte-derived brain-derived neurotrophic factor (BDNF), insulin-like growth factor 1 (IGF-1), and inflammatory cytokines likely affect the expression and functioning of these molecules resulting in disease-associated abnormalities.

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Section: Potential Common Effectorsmentioning

confidence: 99%

Rett and Rett-related disorders: Common mechanisms for shared symptoms?

D’Mello

2023

Exp Biol Med (Maywood)

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“…Western blotting was performed as described previously [32] with slight modi cation. Brie y, frozen samples were extracted in lysis buffer (50 mM Tris-HCl pH 7.5, 150 mM NaCl, 1% Nonidet P-40, 0.1% sodium deoxycholate, 1 mM sodium uoride, 1 mM sodium vanadate, and 1 mM phenylmethylsulfonyl uoride: PMSF).…”

Section: Western Blot Analysismentioning

confidence: 99%

Glycogen Synthase Kinase-3 Inhibitors Block Morphine-Induced Locomotor Activation, Straub Tail, and Depression of Rearing in Mice Via a Possible Central Action

Kitanaka

Kitanaka²,

Tomita

et al. 2023

Neurochem Res

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We investigated morphine-induced Straub's tail reaction (STR) in mice pretreated with or without glycogen synthase kinase-3 (GSK-3) inhibitors (SB216763 and AR-A014418) by using a newly modi ed, infrared beam sensor-based automated apparatus. Mice treated with a single injection of morphine (30 mg/kg, i.p.) showed a signi cant STR with a plateau level at a time point of 20 min after morphine challenge. Pretreatment of mice with SB216763 (5 mg/kg, s.c.) or AR-A014418 (3 mg/kg, i.p.) signi cantly inhibited morphine-induced STR and attenuated the duration of STR in a dose-dependent fashion. In the striatum and the nucleus accumbens, expression of pGSK-3β Tyr216 but not GSK3β or pGSK-3β Ser9 was slightly reduced after treatment with SB216763 (5 mg/kg, s.c.) in combination with/without morphine, indicating that the inhibitory effect of GSK-3 inhibitors on morphine-induced STR and hyperlocomotion might not depend on the direct blockade of GSK-3β function. In constipated mice after morphine challenge (30 mg/kg), the effect of GSK-3 inhibitors on gastrointestinal transit was examined to reveal whether the action of GSK-3 inhibitors on morphine effects was central and/or peripheral. Pretreatment with SB216763 (5 mg/kg) did not improve constipation in morphine-injected mice. The mechanism of action seems to be central but not peripheral, although the underlying subcellular mechanism of GSK-3 inhibitors is not clear. Our measurement system is a useful tool for investigating the excitatory effects of morphine in experimental animals.

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“…It has been reported that autism symptoms improved in clinical trials in which OXT was administered through the nasal mucosa [ 7 , 8 ]. OXT is also involved in anti-inflammation [ 9 ], glycogen synthase kinase-3β (GSK-3β) signaling [ 10 ], maintenance of plasma membrane potential [ 11 ], and the GABA switch by up-regulating K + -Cl - co-transporter 2 (KCC2) expression [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…Lipopolysaccharides (LPS) derived from the periodontal pathogen Porphyromonas gingivalis ( P. g LPS) induce inflammation and act as a stressor involved in the development of periodontal disease and systemic diseases, such as neuropsychiatric symptoms [ [13] , [14] , [15] ]. It has been reported that P. g LPS induce neuroinflammation by up-regulating IL-1β [ 11 ]. LPS derived from Escherichia coli causes depression-like behavior [ 16 ] and downregulates KCC2 in mice [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

“…P. g LPS treatment decreases the expression of KCC2, which is important for the maturation of the central nervous system. OXT treatment can attenuate or prevent the decreased KCC2 expression induced by P. g LPS [ 11 ]. Therefore, Kampo such as KKT may prevent the decreased KCC2 expression induced by LPS via the stress-protective effects of OXT.…”

Section: Introductionmentioning

confidence: 99%

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Kamishoyosan and Kamikihito protect against decreased KCC2 expression induced by the P. gingivalis lipopolysaccharide treatment in PC-12 cells and improve behavioral abnormalities in male mice

Tomita,

Oohara,

Igarashi

et al. 2023

Heliyon

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Oxytocin ameliorates KCC2 decrease induced by oral bacteria-derived LPS that affect rat primary cultured cells and PC-12 cells

Cited by 8 publications

References 51 publications

Rett and Rett-related disorders: Common mechanisms for shared symptoms?

Rett and Rett-related disorders: Common mechanisms for shared symptoms?

Glycogen Synthase Kinase-3 Inhibitors Block Morphine-Induced Locomotor Activation, Straub Tail, and Depression of Rearing in Mice Via a Possible Central Action

Kamishoyosan and Kamikihito protect against decreased KCC2 expression induced by the P. gingivalis lipopolysaccharide treatment in PC-12 cells and improve behavioral abnormalities in male mice

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