Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

Zhang, Cheng Gao; Kim, Sungjin

doi:10.1159/000107687

Cited by 44 publications

(23 citation statements)

References 48 publications

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“…Brain glycine content was significantly increased after hypoxia exposure in mice [71], as well as observed in our study. Activation of glycine receptors with taurine, which increased levels we also observed, may reduce anxiety [72] and thus influence FST behavior.…”

Section: Discussionmentioning

confidence: 86%

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Bogdanova

Abdullah

Kanekar

et al. 2014

Behavioural Brain Research

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Residing at high altitude may lead to reduced blood oxygen saturation in the brain and altered metabolism in frontal cortical brain areas, probably due to chronic hypobaric hypoxia. These changes may underlie the increased rates of depression and suicidal behavior that have been associated with life at higher altitudes. To test the hypothesis that hypobaric hypoxia is responsible for development of mood disorders due to alterations in neurochemistry, we assessed depression-like behavior in parallel to levels of brain metabolites in rats housed at simulated altitude. 32 female Sprague Dawley rats were housed either in a hypobaric hypoxia chamber at 10,000 ft of simulated altitude for 1 week or at local conditions (4500 ft of elevation in Salt Lake City, Utah). Depression-like behavior was assessed using the forced swim test (FST) and levels of neurometabolites were estimated by in vivo proton magnetic resonance spectroscopy in the frontal cortex, the striatum and the hippocampus at baseline and after a week of exposure to hypobaric hypoxia. After hypoxia exposure the animals demonstrated increased immobility behavior and shortened latency to immobility in the FST. Elevated ratios of myo-inositol, glutamate, and the sum of myo-inositol and glycine to total creatine were observed in the frontal cortex of hypoxia treated rats. A decrease in the ratio of alanine to total creatine was also noted. This study shows that hypoxia induced alterations in frontal lobe brain metabolites, aggravated depression-like behavior and might be a factor in increased rates of psychiatric disorders observed in populations living at high altitudes.

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Section: Discussionmentioning

confidence: 86%

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Bogdanova

Abdullah

Kanekar

et al. 2014

Behavioural Brain Research

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“…The activation of strychnine-sensitive GlyRs by taurine reduced anxiety in rodent models [274]. High micromolar concentrations of CBD are required to activate GlyRs and therefore GlyRs are not appropriate targets for CBD.…”

Section: Cbd Receptor Targets In Psychosismentioning

confidence: 99%

Molecular Targets of Cannabidiol in Neurological Disorders

Bih

Chen

Nunn³

et al. 2015

Neurotherapeutics

462

323

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Cannabis has a long history of anecdotal medicinal use and limited licensed medicinal use. Until recently, alleged clinical effects from anecdotal reports and the use of licensed cannabinoid medicines are most likely mediated by tetrahydrocannabinol by virtue of: 1) this cannabinoid being present in the most significant quantities in these preparations; and b) the proportion:potency relationship between tetrahydrocannabinol and other plant cannabinoids derived from cannabis. However, there has recently been considerable interest in the therapeutic potential for the plant cannabinoid, cannabidiol (CBD), in neurological disorders but the current evidence suggests that CBD does not directly interact with the endocannabinoid system except in vitro at supraphysiological concentrations. Thus, as further evidence for CBD's beneficial effects in neurological disease emerges, there remains an urgent need to establish the molecular targets through which it exerts its therapeutic effects. Here, we conducted a systematic search of the extant literature for original articles describing the molecular pharmacology of CBD. We critically appraised the results for the validity of the molecular targets proposed. Thereafter, we considered whether the molecular targets of CBD identified hold therapeutic potential in relevant neurological diseases. The molecular targets identified include numerous classical ion channels, receptors, transporters, and enzymes. Some CBD effects at these targets in in vitro assays only manifest at high concentrations, which may be difficult to achieve in vivo, particularly given CBD's relatively poor bioavailability. Moreover, several targets were asserted through experimental designs that demonstrate only correlation with a given target rather than a causal proof. When the molecular targets of CBD that were physiologically plausible were considered for their potential for exploitation in neurological therapeutics, the results were variable. In some cases, the targets identified had little or no established link to the diseases considered. In others, molecular targets of CBD were entirely consistent with those already actively exploited in relevant, clinically used, neurological treatments. Finally, CBD was found to act upon a number of targets that are linked to neurological therapeutics but that its actions were not consistent withmodulation of such targets that would derive a therapeutically beneficial outcome. Overall, we find that while >65 discrete molecular targets have been reported in the literature for CBD, a relatively limited number represent plausible targets for the drug's action in neurological disorders when judged by the criteria we set. We conclude that CBD is very unlikely to exert effects in neurological diseases through modulation of the endocannabinoid system. Moreover, a number of other molecular targets of CBD reported in the literature are unlikely to be of relevance owing to effects only being observed at supraphysiological concentrations. Of interest and after excludin...

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“…Previous work has highlighted imbalances in neural excitation and inhibition (E/I) in several brain areas in anxiety and mood disorders) and following stress exposure (Cordero et al, 2016;Hasler et al, 2010;Houtepen et al, 2017;Moghaddam, 2002;Popoli et al, 2012;Sandi, 2011 (Davison and Kaczmarek, 1971;El Idrissi and Trenkner, 2004;Jia et al, 2008). (Mezzomo et al, 2016;Zhang and Kim, 2007). Recently, a role for the nucleus accumbens (NAc), the main anatomical constituent of the ventral striatum (VS), is emerging in the context of anxiety (Gunaydin and Kreitzer, 2016;Levita et al, 2012) interconnected with the NAc function in behavioral adaptation (Haber and Behrens, 2014).…”

Section: Introductionmentioning

confidence: 99%

Nucleus accumbens neurochemistry in human anxiety: A 7 T¹H-MRS study

Strasser

Xin

Gruetter

et al. 2018

Preprint

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Individual differences in anxiety provide a differential predisposition to develop neuropsychiatric disorders. The neurochemical underpinnings of anxiety remain elusive, particularly in deep structures, such as the nucleus accumbens (NAc) whose involvement in anxiety is being increasingly recognized.We examined the associations between the neurochemical profile of human NAc metabolites involved in neural excitation and inhibition and inter-individual variation in temperamental and situational anxiety. Twenty-seven healthy 20-30 years-old human males were phenotyped with questionnaires for state and trait anxiety (State-Trait Anxiety Inventory, STAI), social anxiety (Liebowitz Social Anxiety Scale), depression (Beck Depression Inventory, BDI) and fatigue (Mental and Physical State Energy and Fatigue Scales, SEF). Using proton magnetic resonance spectroscopy ( 1 H-MRS) at 7 Tesla (7T), we measured metabolite levels for glutamate, glutamine, GABA and taurine in the NAc with. Salivary cortisol was also measured. Strikingly, trait anxiety was negatively associated with NAc taurine content. Perceived situational stress was negatively associated with NAc GABA, while positively with the Glu/GABA ratio. These findings were specific, as no correlation was observed between NAc taurine or GABA and other phenotypic variables examined (i.e., state anxiety, social anxiety, depression, or cortisol), except for a negative correlation between taurine and state physical fatigue. This first 7T study of NAc neurochemistry shows relevant metabolite associations with individual variation in anxiety traits and situational stress and state anxiety measurements. The novel identified association between NAc taurine levels and trait anxiety may pave the way for clinical studies aimed at identifying new treatments for anxiety and related disorders.

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Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

Cited by 44 publications

References 48 publications

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Molecular Targets of Cannabidiol in Neurological Disorders

Nucleus accumbens neurochemistry in human anxiety: A 7 T¹H-MRS study

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Taurine Induces Anti-Anxiety by Activating Strychnine-Sensitive Glycine Receptor in vivo

Cited by 44 publications

References 48 publications

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Neurochemical alterations in frontal cortex of the rat after one week of hypobaric hypoxia

Molecular Targets of Cannabidiol in Neurological Disorders

Nucleus accumbens neurochemistry in human anxiety: A 7 T1H-MRS study

Contact Info

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Nucleus accumbens neurochemistry in human anxiety: A 7 T¹H-MRS study