Bipolar Disorder Animal Models
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. (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.
Information to Be Confirmed
Delivery Standard
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.
Inquiry
