Positron emission tomography with fluorodeoxyglucose-F18 in an animal model of mania

Hougland, M. Tyler; Gao, Yonglin; Herman, Laura; Ng, Chin K.; Lei, Zhenmin; El‐Mallakh, Rif S.

doi:10.1016/j.pscychresns.2008.01.004

Cited by 11 publications

(5 citation statements)

References 22 publications

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“…In the ouabain-induced rat model of bipolar mania, PET imaging suggests reduced cerebral glucose metabolism, and is prevented by pre-treatment with lithium which concurs with similar decreases in cerebral metabolism noted in BPD patients [ 61 ]. Furthermore, lithium prevented stress-induced alterations in the amygdala by preventing increases in dendritic branching of pyramidal neurons in this structure [ 62 ].…”

Section: The Neuroanatomy and Neurocircuitry Of Psychiatric Illnessmentioning

confidence: 92%

A Review of Biomarkers in Mood and Psychotic Disorders: A Dissection of Clinical vs. Preclinical Correlates

Brand¹,

Möller²,

Harvey

2015

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Despite significant research efforts aimed at understanding the neurobiological underpinnings of mood (depression, bipolar disorder) and psychotic disorders, the diagnosis and evaluation of treatment of these disorders are still based solely on relatively subjective assessment of symptoms as well as psychometric evaluations. Therefore, biological markers aimed at improving the current classification of psychotic and mood-related disorders, and that will enable patients to be stratified on a biological basis into more homogeneous clinically distinct subgroups, are urgently needed. The attainment of this goal can be facilitated by identifying biomarkers that accurately reflect pathophysiologic processes in these disorders. This review postulates that the field of psychotic and mood disorder research has advanced sufficiently to develop biochemical hypotheses of the etiopathology of the particular illness and to target the same for more effective disease modifying therapy. This implies that a "one-size fits all" paradigm in the treatment of psychotic and mood disorders is not a viable approach, but that a customized regime based on individual biological abnormalities would pave the way forward to more effective treatment. In reviewing the clinical and preclinical literature, this paper discusses the most highly regarded pathophysiologic processes in mood and psychotic disorders, thereby providing a scaffold for the selection of suitable biomarkers for future studies in this field, to develope biomarker panels, as well as to improve diagnosis and to customize treatment regimens for better therapeutic outcomes.

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Section: The Neuroanatomy and Neurocircuitry Of Psychiatric Illnessmentioning

confidence: 92%

A Review of Biomarkers in Mood and Psychotic Disorders: A Dissection of Clinical vs. Preclinical Correlates

Brand¹,

Möller²,

Harvey

2015

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“…The average standardized uptake value (SUV) of each ROI was obtained for analysis as described previously (Chen et al, 2014; Ono et al, 2012). The average SUV of the tongue was used as a reference point for each scan (Hougland et al, 2008) because glycine is abundant in the brain, and MK-801 evidently increased the overall brain activity, including in the cerebellum. The normalized SUV was calculated after each scan using the following formula: SUV target ROI (FDG) /SUV tongue (FDG) as an index of the brain metabolic change in each ROI after treatment.…”

Section: Methodsmentioning

confidence: 99%

Therapeutic potential and underlying mechanism of sarcosine (N-methylglycine) in N-methyl-D-aspartate (NMDA) receptor hypofunction models of schizophrenia

et al. 2019

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Background: Compelling animal and clinical studies support the N-methyl-D-aspartate receptor (NMDAR) hypofunction hypothesis of schizophrenia and suggest promising pharmacological agents to ameliorate negative and cognitive symptoms of schizophrenia, including sarcosine, a glycine transporter-1 inhibitor. Aims and methods: It is imperative to evaluate the therapeutic potential of sarcosine in animal models, which provide indispensable tools for testing drug effects in detail and elucidating the underlying mechanisms. In this study, a series of seven experiments was conducted to investigate the effect of sarcosine in ameliorating behavioral deficits and the underlying mechanism in pharmacological (i.e., MK-801-induced) and genetic (i.e., serine racemase-null mutant (SR−/−) mice) NMDAR hypofunction models. Results: In Experiment 1, the acute administration of 500/1000 mg/kg sarcosine (i.p.) had no adverse effects on motor function and serum biochemical responses. In Experiments 2–4, sarcosine significantly alleviated MK-801-induced (0.2 mg/kg) brain abnormalities and behavioral deficits in MK-801-induced and SR−/− mouse models. In Experiment 5, the injection of sarcosine enhanced CSF levels of glycine and serine in rat brain. In Experiments 6–7, we show for the first time that sarcosine facilitated NMDAR-mediated hippocampal field excitatory postsynaptic potentials and influenced the movement of surface NMDARs at extrasynaptic sites. Conclusions: Sarcosine effectively regulated the surface trafficking of NMDARs, NMDAR-evoked electrophysiological activity, brain glycine levels and MK-801-induced abnormalities in the brain, which contributed to the amelioration of behavioral deficits in mouse models of NMDAR hypofunction.

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“…Despite these findings pertaining to the amphetamine model, animal models in which the sodium pump is rendered dysfunctional, either by using ICV injections of ouabain [70][71][72], or by knocking down the α [73] or α3 [74][75][76] isoforms of the sodium pump, fulfill all three validity criteria for an animal model of a psychiatric illness [13]. These models mimic the abnormalities documented in bipolar patients, including reduced sodium pump activity, increased intracellular sodium [13], and CNS hypometabolism [77]. Importantly, these are the only animal models in which the same abnormality can produce both manic-like behaviors [71] and depressive-type behaviors [78]; thus, they are the best models we have of BD [13].…”

Section: Role Of Exogenous Cs and Ecs In Animal Models Of Mood Disordersmentioning

confidence: 99%

Endogenous Cardiac Steroids in Bipolar Disorder: State of the Art

El‐Mallakh

Sampath²,

Horesh³

et al. 2022

IJMS

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Bipolar disorder (BD) is a severe psychiatric illness with a poor prognosis and problematic, suboptimal, treatments. Treatments, borne of an understanding of the pathoetiologic mechanisms, need to be developed in order to improve outcomes. Dysregulation of cationic homeostasis is the most reproducible aspect of BD pathophysiology. Correction of ionic balance is the universal mechanism of action of all mood stabilizing medications. Endogenous sodium pump modulators (collectively known as endogenous cardiac steroids, ECS) are steroids which are synthesized in and released from the adrenal gland and brain. These compounds, by activating or inhibiting Na+, K+-ATPase activity and activating intracellular signaling cascades, have numerous effects on cell survival, vascular tone homeostasis, inflammation, and neuronal activity. For the past twenty years we have addressed the hypothesis that the Na+, K+-ATPase-ECS system may be involved in the etiology of BD. This is a focused review that presents a comprehensive model pertaining to the role of ECS in the etiology of BD. We propose that alterations in ECS metabolism in the brain cause numerous biochemical changes that underlie brain dysfunction and mood symptoms. This is based on both animal models and translational human results. There are data that demonstrate that excess ECS induce abnormal mood and activity in animals, while a specific removal of ECS with antibodies normalizes mood. There are also data indicating that circulating levels of ECS are lower in manic individuals, and that patients with BD are unable to upregulate synthesis of ECS under conditions that increase their elaboration in non-psychiatric controls. There is strong evidence for the involvement of ion dysregulation and ECS function in bipolar illness. Additional research is required to fully characterize these abnormalities and define future clinical directions.

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Positron emission tomography with fluorodeoxyglucose-F18 in an animal model of mania

Cited by 11 publications

References 22 publications

A Review of Biomarkers in Mood and Psychotic Disorders: A Dissection of Clinical vs. Preclinical Correlates

A Review of Biomarkers in Mood and Psychotic Disorders: A Dissection of Clinical vs. Preclinical Correlates

Therapeutic potential and underlying mechanism of sarcosine (N-methylglycine) in N-methyl-D-aspartate (NMDA) receptor hypofunction models of schizophrenia

Endogenous Cardiac Steroids in Bipolar Disorder: State of the Art

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