Bipolar Disorder Animal Models

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Ace Therapeutics, as a drug discovery and development partner, has a mature animal model research and development platform. We are committed to providing bipolar disorder animal models to help researchers further understand the environmental, biological and genetic etiological factors of bipolar disorder.

Introduction of Bipolar Disorder Animal Models

Bipolar disorder (BD), originally called manic-depressive disorder, is a devastating neuropsychiatric disorder. The main feature of BD is mood cycles of episodes of depression (such as helplessness, decreased energy and activity, and anhedonia) and mania (such as increased energy and hyperactivity, decreased need for sleep, decreased impulsivity, anxiety, and depression). BD affects more than 1% of the world's population and is the leading cause of disability. The use of animal models is critical to expanding our understanding of various aspects of human biology. Rodents play a leading role in the field of neuropsychiatric disease modeling because they offer a unique combination of traits, such as molecular mechanisms conserved with humans, a relatively fast life cycle, advanced genetics, and a wealth of well-characterized behaviors.

Fig. 1 Validities of psychiatric disorders. Fig. 1 Validities of psychiatric disorders. (Samira S, et al.,2021)

Animal Modeling Services for Bipolar Disorder

Ace Therapeutics has many years of experience in mental disease research and a mature animal research and development platform. We can provide some pharmacological, environmental and genetic animal models for the study of BD. Most of these models can summarize the symptoms related to mania. Our models are capable of assessing more complex behaviors in more detail with higher specificity, reducing the gap between human and animal behavior, and possessing good face and predictive validity.

Information on animal models of BD we provide:

Table 1 Pharmacological and environmental mouse models of BD.

Manipulation	Symptoms	Features
Ouabain	Hyperactivity, spatial learning deficits	Increased levels of oxidative stress, changes in BDNF levels
D2 receptor stimulation	Hyperactivity	Increased dopaminergic signaling
Sleep deprivation	Hyperactivity, insomnia, aggressive behavior, hypersexuality, increased stereotypy, cognitive deficits, circadian rhythm disruption	Acute circadian rhythm and sleep changes can precipitate mania in humans. PKC signaling is altered.
Resident-intruder paradigm	Increased aggression	Stress is associated with changes in mood state

Table 2 Genetic mouse models of BD.

Manipulation	Symptoms	Features
ClockΔ19 mutant	Reduced anxiety, depression Increased impulsivity, reward-seeking Hyperactivity Impaired decision-making, sensorimotor gating disrupted circadian rhythms (phase and amplitude) and sleep	CLOCK polymorphisms, disrupted phase coherence, synchronization, and communication of cortico-striatal circuitry, hyperdopaminergia and altered glutamatergic neurotransmission
GSK-3β OX	Hyperactivity Reduced depression	GSK-3β polymorphisms, reduced expression human bipolar DLPFC and temporal cortex, disrupted downstream targets of GSK-3β, hyperdopaminergia
DAT-KD	Hyperactivity (reduced spatial) increased goal-directed behavior repetitive locomotor patterns impaired decision-making	DAT polymorphisms, impaired DAT function, hyperdopaminergia
SHANK3-OX	Hyperactivity Hypersensitivity to reward stimuli Elevated acoustic startle response Impaired sensorimotor gating Reduced depression Altered circadian rhythm behavior	SHANK3 polymorphisms, variants predict treatment in patients with bipolar depression, imbalance between excitatory and inhibitory neurotransmission, altered dopaminergic and glutamatergic signaling
ANK3 disruptions	Hyperactivity Reduced anxiety Altered circadian activity rhythms Increased reward-seeking Stress-induced anxiety, anhedonia	Potential regulation of β-catenin and Wnt signaling pathways
Myshkin mutant	Hyperactivity Impaired sensorimotor gating Disrupted sleep homeostasis Altered circadian rhythm behavior	ATP1A3 polymorphisms, NA+K+ATPase a3 sodium pump dysfunction, multiple isoforms associated with bipolar disorder, altered ERK signaling and downstream effectors, such as BDNF, DISC1, GluR6, RASGRP1, and EGFR
Black Swiss	Hyperactivity Reduced anxiety and depression Elevated sucrose preference	Genetic heterogeneity, reduced β-catenin expression in various brain regions
Madison	Hyperactivity Reduced anxiety and depression Increased sexual behavior Disrupted circadian rhythm behaviors	Genetic heterogeneity, abnormal expression patterns of numerous genes associated with bipolar disorder
DBP-KO	Abnormal circadian rhythm behaviors Disrupted sleep homeostasis Reduced activity Mania-like behaviors induced by chronic stress or acute sleep deprivation include hyperactivity, increased drug-taking	Gene locus mapped near coding region for Dbp, ranked highly among candidate genes for bipolar disorder

Note: Our service list is constantly updated and improved. Please contact us via email for more latest information and related information.

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Information to Be Confirmed

Ace Therapeutics can not only provide preclinical animal models simulating human BD, but also combine pharmacological, environmental and genetic methods to help you further understand the environmental, biological and genetic etiological factors of BD. Please tell us your project requirements, we will provide you with a comprehensive service from solution to report. If you have any questions, please feel free to make an inquiry.

References

Logan RW, McClung CA. Animal models of bipolar mania: The past, present and future. Neuroscience. 2016, 321:163-188.
Samira S, et al. Chapter 9 - The evolution of animal models for bipolar disorder. Neurobiology of Bipolar Disorder. 2021, 109-115.

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