Lithium ameliorates sleep deprivation‐induced mania‐like behavior, hypothalamic‐pituitary‐adrenal (HPA) axis alterations, oxidative stress and elevations of cytokine concentrations in the brain and serum of mice

Valvassori, Samira S.; Resende, Wilson R.; Dal‐Pont, Gustavo C.; Sangaletti-Pereira, Heron; Gava, Fernanda F.; Peterle, Bruna R.; Carvalho, André F.; Varela, Roger B.; Dal‐Pizzol, Felipe; Quevedo, João

doi:10.1111/bdi.12503

Cited by 67 publications

(35 citation statements)

References 76 publications

(180 reference statements)

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“…Similarly, sleep deprivation protocols, usually obligating rodents to remain awake on a small platform surrounded by water for an extended period of time (72 h), have long been used to generate manic models 63 . The sleep-deprived animals indeed exhibit several manic-like behaviors, including locomotor hyperactivity, aggressive behavior, hypersexuality, and increased stereotypy, which could be normalized by treatment with lithium 63 , 64 .…”

Section: Animal Models Of Mania With E/i Synaptic Dysfunctionmentioning

confidence: 97%

Excitatory and inhibitory synaptic dysfunction in mania: an emerging hypothesis from animal model studies

et al. 2018

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Bipolar disorder (BD) is a common psychiatric disorder characterized by recurrent mood swings between depression and mania, and is associated with high treatment costs. The existence of manic episodes is the defining feature of BD, during which period, patients experience extreme elevation in activity, energy, and mood, with changes in sleep patterns that together severely impair their ability to function in daily life. Despite some limitations in recapitulating the complex features of human disease, several rodent models of mania have been generated and characterized, which have provided important insights toward understanding its underlying pathogenic mechanisms. Among the mechanisms, neuronal excitatory and inhibitory (E/I) synaptic dysfunction in some brain regions, including the frontal cortex, hippocampus, and striatum, is an emerging hypothesis explaining mania. In this review, we highlight recent studies of rodent manic models having impairments in the E/I synaptic development and function. We also summarize the molecular and functional changes of E/I synapses by some mood stabilizers that may contribute to the therapeutic efficacy of drugs. Furthermore, we discuss potential future directions in the study of this emerging hypothesis to better connect the outcomes of basic research to the treatment of patients with this devastating mental illness.

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Section: Animal Models Of Mania With E/i Synaptic Dysfunctionmentioning

confidence: 97%

Excitatory and inhibitory synaptic dysfunction in mania: an emerging hypothesis from animal model studies

et al. 2018

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“…Immune dysfunction in BD is supported by pre-clinical and clinical evidence showing elevated levels of proinflammatory cytokines, including interleukin-4 (IL-4), interleukin-1beta (IL-1b), interleukin-6 (IL-6), tumor necrosis factor (TNF)-alpha, soluble interleukin-2 receptor (sIL-2R), and soluble receptor of TNF-type 1 (STNFR1), among others, in patients compared to controls. [158][159][160][161][162][163][164] A recent systematic review has suggested an important role for acute inflammatory response during mania and depression, with the elevation in proinflammatory cytokines seemingly restored after remission of symptoms. 118 In addition, further findings in BD have also described significant negative associations between inflammatory markers and general cognitive abilities, as well as neuroanatomical alterations.…”

Section: Immune-inflammatory Imbalance and Kynurenine Pathwaymentioning

confidence: 99%

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Scaini

Valvassori

Diaz

et al. 2020

Braz. J. Psychiatry

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Bipolar disorder (BD) is a chronic mental illness characterized by changes in mood that alternate between mania and hypomania or between depression and mixed states, often associated with functional impairment. Although effective pharmacological and non-pharmacological treatments are available, several patients with BD remain symptomatic. The advance in the understanding of the neurobiology underlying BD could help in the identification of new therapeutic targets as well as biomarkers for early detection, prognosis, and response to treatment in BD. In this review, we discuss genetic, epigenetic, molecular, physiological and neuroimaging findings associated with the neurobiology of BD. Despite the advances in the pathophysiological knowledge of BD, the diagnosis and management of the disease are still essentially clinical. Given the complexity of the brain and the close relationship between environmental exposure and brain function, initiatives that incorporate genetic, epigenetic, molecular, physiological, clinical, environmental data, and brain imaging are necessary to produce information that can be translated into prevention and better outcomes for patients with BD.

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“…After the sleep deprivation period, the animals show mania-like behaviors such as insomnia, hyperactivity, aggression, stereotypy, and hypersexuality (as reviewed in [ 304 ]). Lithium and antipsychotics prevent some of the effects of sleep deprivation, indicating that the model has predictive validity [ 303 , 305 ].…”

Section: The Scn In Animal Models Of Mood Disordersmentioning

confidence: 99%

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

2017

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Circadian rhythm disturbances are a common symptom among individuals with mood disorders. The suprachiasmatic nucleus (SCN), in the ventral part of the anterior hypothalamus, orchestrates physiological and behavioral circadian rhythms. The SCN consists of self-sustaining oscillators and receives photic and nonphotic cues, which entrain the SCN to the external environment. In turn, through synaptic and hormonal mechanisms, the SCN can drive and synchronize circadian rhythms in extra-SCN brain regions and peripheral tissues. Thus, genetic or environmental perturbations of SCN rhythms could disrupt brain regions more closely related to mood regulation and cause mood disturbances. Here, we review clinical and preclinical studies that provide evidence both for and against a causal role for the SCN in mood disorders.

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Lithium ameliorates sleep deprivation‐induced mania‐like behavior, hypothalamic‐pituitary‐adrenal (HPA) axis alterations, oxidative stress and elevations of cytokine concentrations in the brain and serum of mice

Cited by 67 publications

References 76 publications

Excitatory and inhibitory synaptic dysfunction in mania: an emerging hypothesis from animal model studies

Excitatory and inhibitory synaptic dysfunction in mania: an emerging hypothesis from animal model studies

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Circadian Rhythm Disturbances in Mood Disorders: Insights into the Role of the Suprachiasmatic Nucleus

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