Taurine, an essential β-amino acid insulates against ketamine-induced experimental psychosis by enhancement of cholinergic neurotransmission, inhibition of oxidative/nitrergic imbalances, and suppression of COX-2/iNOS immunoreactions in mice

Ben‐Azu, Benneth; Adebayo, Olusegun G.; Jarikre, Theophilus Aghogho; Oyovwi, Mega O.; Edje, K.E.; Omogbiya, Itivere Adrian; Eduviere, Anthony T.; Moke, Emuesiri Goodies; Chijioke, Bienose S.; Odili, Onyebuchi S.; Omondiabge, Osemudiame P.; Oyovbaire, Aghogho; Esuku, Daniel T.; Ozah, Esther O.; Japhet, Kelvin

doi:10.1007/s11011-022-01075-5

Cited by 30 publications

(11 citation statements)

References 102 publications

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“…37 Of note, these brain regions have been majorly associated with the onset of complex symptoms of schizophrenia that the typical antipsychotics unable to treat. 32 In the current study, the preventive treatment with geraniol was found to lower the levels of 5-HT in the ST, PFC, and HC altered by ketamine. Here, we suggested that 5-HT2A may also be involved in the mechanism of action of geraniol on SCZ mice showing negative and probably cognitive symptoms, although this has not been elucidated using antagonist receptor interaction study.…”

Section: Discussionsupporting

confidence: 45%

“…The findings of this study show that ketamine (NMDAr antagonist)] induce neurobehavioral patterns in mice that are similar to human psychosis. 6,31,32 Ketamine also deranged neurochemical (DA, 5-HT, GAD, and AChE) and neurotrophic (BDNF) pathways in the striatum, prefrontal cortex, and hippocampus of mice. 4,9 However, the brain insults caused by these psychotomimetics were prevented by geraniol, a naturally occurring acyclic monoterpene with diverse pharmacological activities.…”

Section: Discussionmentioning

confidence: 99%

“…9 Notably, the 5-HTergic system is another system that has been linked to schizophrenia, particularly in the pathogenesis of its negative and cognitive symptoms. 32 According to clinical and preclinical studies, prolonged ketamine treatment interferes with the 5-THergic pathway by activating the expression of 5-HT2A in the frontal-parietal cortex as well as increasing the brain level of cortical and striatal 5-HT. 37 Of note, these brain regions have been majorly associated with the onset of complex symptoms of schizophrenia that the typical antipsychotics unable to treat.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that the ability of memory enhancing and antipsychotic drugs to improve the cognitive symptoms of schizophrenia is partly and clinically dependent on the extent of inhibition of AChE enzyme activity especially in cortical brains regions. 6,9,32 Therefore, the finding that geraniol inhibits ketamineinduced increased AChE activity, suggests potential ability to ameliorate the cognitive deficits common to schizophrenia disease.…”

Section: Discussionmentioning

confidence: 99%

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Preventive effects of geraniol in schizophrenia-like symptoms in mice models of psychosis

Uruaka

Georgewill²,

Georgewill³

2023

Int J Res Med Sci

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Background: The pathogenesis of schizophrenia has been linked to N-methyl-D-aspartate receptor (NMDAr) inhibition and DAr hyperfunction. Geraniol is a naturally occurring acyclic monoterpene with diverse pharmacological applications. We aimed to assess the effect of geraniol on schizophrenia-like symptoms, vis a vis its modulatory actions on neurochemicals in mice models of psychosis. Methods: In acute studies, male Swiss mice (n=5/group) were intraperitoneally treated with geraniol (25, 50 and 100 mg/kg), risperidone (0.5 mg/kg) or vehicle (10 ml/kg) prior to ketamine (KET) (10 mg/kg)-induced stereotypy and hyperlocomotion. In the chronic studies, mice (n=7/group) were exposed to 14 days interventions (geraniol or risperidone) following a preventive treatment with KET (20 mg/kg) from days 7-14 consecutively. The effects of treatments (e.g., geraniol or risperidone) alone and on KET-induced schizophrenia-like symptoms were investigated on the last day, 24 hours after treatments. Following that, neurochemical and neurotrophic alterations in the brain (striatum, prefrontal cortex, and hippocampus) tissues were investigated. Results: Intoxication with KET was associated with schizophrenia-like symptoms as evidenced by stereotypy behavior and hyperlocomotion. KET further induced hyperlocomotion, behavioral despair, and cognitive impairment in the chronic studies. It altered the levels of dopamine, 5-hydroxytrypamine, glutamic acid decarboxylase (GAD), acetylcholinesterase (AChE), and brain-derived neurotrophic factor (BDNF) in brain tissues. However, GER (50 and 100 mg/kg) administration significantly prevented the brain's insults caused by KET. Conclusions: Altogether, the findings support geraniol's neuroprotective activity while also adding to the body of knowledge that geraniol inhibits schizophrenia-like symptoms via modulation of neurochemical and neurotrophic pathways.

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Preventive effects of geraniol in schizophrenia-like symptoms in mice models of psychosis

Uruaka

Georgewill²,

Georgewill³

2023

Int J Res Med Sci

View full text Add to dashboard Cite

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“…As more data illustrate the biological timeline and mechanisms of the disease, SCZ is increasingly painted as both a neurodevelopmental disease and a disease of accelerated aging. The conceptualization of SCZ as a neurodevelopmental disorder demonstrates the complexity of the disease as a whole ( Murray and Lewis, 1987 ; Keshavan and Paus, 2015 ; Murray et al, 2017 ; Ben-Azu et al, 2022 ). Whereas SCZ symptomatology most often emerges in late adolescence, phenotypic alterations can arise much earlier in childhood before the onset of symptomatology into adulthood ( Woodberry et al, 2008 ; Sørensen et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Emerging epigenetic dynamics in gut-microglia brain axis: experimental and clinical implications for accelerated brain aging in schizophrenia

Ben-Azu

VanderZwaag

et al. 2023

Front. Cell. Neurosci.

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Brain aging, which involves a progressive loss of neuronal functions, has been reported to be premature in probands affected by schizophrenia (SCZ). Evidence shows that SCZ and accelerated aging are linked to changes in epigenetic clocks. Recent cross-sectional magnetic resonance imaging analyses have uncovered reduced brain reserves and connectivity in patients with SCZ compared to typically aging individuals. These data may indicate early abnormalities of neuronal function following cyto-architectural alterations in SCZ. The current mechanistic knowledge on brain aging, epigenetic changes, and their neuropsychiatric disease association remains incomplete. With this review, we explore and summarize evidence that the dynamics of gut-resident bacteria can modulate molecular brain function and contribute to age-related neurodegenerative disorders. It is known that environmental factors such as mode of birth, dietary habits, stress, pollution, and infections can modulate the microbiota system to regulate intrinsic neuronal activity and brain reserves through the vagus nerve and enteric nervous system. Microbiota-derived molecules can trigger continuous activation of the microglial sensome, groups of receptors and proteins that permit microglia to remodel the brain neurochemistry based on complex environmental activities. This remodeling causes aberrant brain plasticity as early as fetal developmental stages, and after the onset of first-episode psychosis. In the central nervous system, microglia, the resident immune surveillance cells, are involved in neurogenesis, phagocytosis of synapses and neurological dysfunction. Here, we review recent emerging experimental and clinical evidence regarding the gut-brain microglia axis involvement in SCZ pathology and etiology, the hypothesis of brain reserve and accelerated aging induced by dietary habits, stress, pollution, infections, and other factors. We also include in our review the possibilities and consequences of gut dysbiosis activities on microglial function and dysfunction, together with the effects of antipsychotics on the gut microbiome: therapeutic and adverse effects, role of fecal microbiota transplant and psychobiotics on microglial sensomes, brain reserves and SCZ-derived accelerated aging. We end the review with suggestions that may be applicable to the clinical setting. For example, we propose that psychobiotics might contribute to antipsychotic-induced therapeutic benefits or adverse effects, as well as reduce the aging process through the gut-brain microglia axis. Overall, we hope that this review will help increase the understanding of SCZ pathogenesis as related to chronobiology and the gut microbiome, as well as reveal new concepts that will serve as novel treatment targets for SCZ.

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D-ribose-L-cysteine exhibits restorative neurobehavioral functions through modulation of neurochemical activities and inhibition oxido-inflammatory perturbations in rats exposed to polychlorinated biphenyl

Oyovwi,

Ben-Azu,

Falajiki

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Taurine, an essential β-amino acid insulates against ketamine-induced experimental psychosis by enhancement of cholinergic neurotransmission, inhibition of oxidative/nitrergic imbalances, and suppression of COX-2/iNOS immunoreactions in mice

Cited by 30 publications

References 102 publications

Preventive effects of geraniol in schizophrenia-like symptoms in mice models of psychosis

Preventive effects of geraniol in schizophrenia-like symptoms in mice models of psychosis

Emerging epigenetic dynamics in gut-microglia brain axis: experimental and clinical implications for accelerated brain aging in schizophrenia

D-ribose-L-cysteine exhibits restorative neurobehavioral functions through modulation of neurochemical activities and inhibition oxido-inflammatory perturbations in rats exposed to polychlorinated biphenyl

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