Schizophrenia is the most serious psychiatric disorder and has an extremely high rate of disability. The onset of the illness can severely affect the individual's thoughts, feelings and behaviors, thereby impairing normal life.
Our company applies our expertise to the research of mechanisms and therapies for psychotic disorders. We are committed to providing a variety of rational and effective behavioral tests for evaluating animal models of schizophrenia, thereby saving time and achieving desirable results for our clients' innovative project researches.
Schizophrenia is caused by a series of neurodevelopmental problems and has a psychologically underlying mental disorder. Symptoms usually manifest as behavioral abnormalities and decreased cognitive function. With the development of the disease, it gradually affects the thinking, emotions, behavior, language and perception of the individual and other aspects. At present, the exact cause of schizophrenia is unknown, but researches have shown that genetic factors, abnormalities in brain function and structure in combination with environmental factors contribute to the development of the disease.
Fig. 1 Potential triggers of schizophrenia.
Animal models well simulate the etiology, brain pathology and behavioral abnormalities associated with human schizophrenia. Our company offers the most comprehensive approach to animal modeling for building schizophrenia models.
Neurodevelopmental models involve the administration of neonatal brain damage (especially disruption of hippocampal development), fetal viral infection or disruption of normal neuronal development in animals. These models are often used to screen new drugs.
Developmental Models | Description |
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Methylazomethanol (MAM) model | MAM is an antimitotic and antiproliferative agent that affects the proliferation of neuroblastoma cells. MAM administration to pregnant rats resulted in abnormalities in brain structure and function as well as decreased memory, reduced social interaction and increased anxiety in their offspring. |
Maternal immune activation (MIA) model | Maternal immune activation in pregnant rodents is usually triggered by drugs such as virus-mimicking polyinosinic acid - polycytidylic acid (poly I:C), and their offspring exhibit neurodevelopmental disorders as well as behavioral abnormalities. |
Drug-induced Models | Description |
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Dopamine enhancer | Repeated intermittent administration of dopamine enhancers to rodents induces cognitive dysfunction in animals. |
Non-competitive NMDA receptor antagonist | Application of these agents to rodents can lead to hypermobility, reduced socialization, and cognitive deficits, among other behaviors. |
Other drug models | It usually involves injecting drugs into specific brain regions of the animal to mimic the known pathophysiology associated with schizophrenia. |
Genetic models usually involve genes associated with an increased risk of schizophrenia. Most of these genes are associated with neuronal plasticity, glutamate or dopamine function, and proteins related to synaptogenesis.
Genetic Models | Behavioral Methods |
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DISC1 model | A synaptic protein, involved in early developmental expression, is involved in neuronal development. |
22q11.2 model | Mice with 22q11.2 deletion exhibit deficits in fear conditioning, impaired spatial memory, and delayed mismatch placement tasks. |
NRG1 and ErbB4 model | Mutations in NRG1 and its receptor ErbB4 gene in mice exhibit behavioral phenotypes, increased activity and exploration, and working memory deficits. |
Dysbindin model | A protein associated with excitatory synaptic transmission, Dysbindin mutant mice exhibit behaviors consistent with a schizophrenia-like phenotype, including ADHD, learning and memory deficits, and increased impulsive and compulsive behavior. |
Reelin model | Involved in synaptogenesis and plasticity, deletion of 1 allele of the gene encoding reelin in mice causes them to exhibit schizophrenia-like pathology and behavioral changes such as social interaction, cognitive deficits, and changes in motor responses. |
Models that usually have good face validity, predictive validity and construct validity are essential for disease research. Our company is committed to providing scientifically reliable models of schizophrenia by providing sound behavioral assessment methods based on our clients' research demands.
Behavior Categories | Description |
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Motor activity | Viability in response to novel environments, stress or pharmacological challenges (dopamine enhancers, NMDA receptor antagonists) is quantified. |
Sucrose preference | Preference for sweetened water over unsweetened water is measured. |
Social interaction | Time spent in close proximity or direct contact with an unfamiliar or less familiar animal. |
Latent inhibition (attentional processes, cognitive symptoms) | A classical conditioning procedure whereby previously unreinforced stimuli are slower (less efficient) in generating a conditioned response than novel stimuli. |
Memory (cognitive symptoms) | Many tests have been validated to measure various aspects of working memory, declarative memory, recognition memory (visual, spatial, and olfactory domains), and conditioning. |
Reasoning and problem solving (cognitive symptoms) | Tests of behavioral flexibility in response to dynamic environments include set shifting and reversal learning. |
Prepulse inhibition (sensorimotor deficits) | A reduction in the acoustic startle response is typically observed if the startling stimulus is preceded close in time by a low-intensity prepulse. |
Anxiety-like behavior | Patterns of exploration in environments such as the elevated plus maze, open field, or light-dark box. |
Our company is committed to combining our specialized experimental platform and extensive scientific knowledge to jointly provide effective research models for the development of the field of neuroscience. If you are interested, please contact us and describe your specific research, and we will be happy to assist you.