Schizophrenia 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 promote the rapid and efficient completion of projects according to the specific requirements of customers.

Introduction of Schizophrenia Animal Models

Schizophrenia is a chronic debilitating neuropsychiatric disease, affecting approximately 1% of the global population. Symptoms are divided into three categories: positive (including auditory and visual hallucinations, delusions, conceptual confusion and thinking disorders), negative (blunted emotions, social withdrawal, anhedonia, anoria, poor thought, and verbal content) and cognitive dysfunction (including impaired executive function, working memory and attention). Preclinical animal models of psychiatric disorders allow faster monitoring of disease progress than humans, allow invasive research on structural and molecular changes in the course of disease development, and allow relatively easy testing of potential therapeutic drugs.

Fig. 1 Different approaches to construct animal models for neuropsychiatric disorders studies. Fig. 1 Different approaches to construct animal models for neuropsychiatric disorders studies. (Nani JV, et al., 2019)

Animal Modeling Services for Schizophrenia

Ace Therapeutics has developed more than 20 different animal models of schizophrenia based on 4 induction methods (developmental, drug-induced, lesion and genetic manipulation). These models are very valuable preclinical tools that can be used to help you study schizophrenia neurobiological basis of the disease. Our animal model R&D platform can help you rapidly monitor schizophrenia disease progression and invasively monitor the structural and molecular changes that underlie the cause of the disease, accelerating the development of new therapies.

Information on animal models of schizophrenia we provide:

Schizophrenia Models	Emulated Schizophrenia Characteristics	Structure and Neurochemistry
Ketamine-induced model	Ketamine is an NMDA receptor antagonist, and the compound is a derivative of PCP. In addition to eliciting positive symptoms, such as perceptual changes and delusions, ketamine also produces negative symptoms, including blunted affect and emotional withdrawal, when administered to experimental animals.	Ketamine binds to a variety of receptors, but principally acts at the NMDAR, and convergent genetic and molecular evidence point to NMDAR hypofunction in schizophrenia. Furthermore, NMDAR hypofunction can explain connectional and oscillatory abnormalities in schizophrenia in terms of both weakened excitation of inhibitory -aminobutyric acidergic (GABAergic) interneurons that synchronize cortical networks and disinhibition of principal cells.
Dizocilpine-induced model	Dizocilpine (also known as MK-801) is a noncompetitive NMDA receptor antagonist with a higher inhibitory potency than ketamine and PCP. Modeling with MK-801 has been shown to elicit both positive and negative symptoms associated with schizophrenia. In addition，it can mimic particular cognitive deficits such as behavioral inflexibility, impaired spatial memory, and social withdrawal.	Dizocilpine, as a noncompetitive NMDA receptor antagonist, interferes with the function of the glutamatergic system, leading to disturbances in glutamatergic signaling. At the same time, the activity of the dopamine system is altered, and an increase in dopamine release and hypersensitivity of dopamine D₂ receptors are observed. In addition, the GABA system was disturbed and synaptic plasticity was affected and involved abnormalities in inflammatory and immune factors.
PCP models	Deficits in novel object recognition, attentional set shifting and T-maze delayed alternation.	Reduced basal and stress-induced PFc DA and glutamate release; decreased synaptic spines on Fc neurones and cortical and hippocampal parvalbumin-positive neurones
DISC-1 knock-out	Impaired T-maze performance seen in most strains, impaired spatial working memory only seen in female CaMK-ΔC inducible mutants.	Reduced brain volume in most strains; enlarged lateral ventricles, reduced hippocampal and PFc dendritic density, structure and complexity in some strains; reduced hippocampal parvalbumin immunoreactivity in some, but not all mutants
Neuregulin1 and ErbB4 knock-out	Impaired contextual fear and mismatched negativity performance in some mutants.	Increased lateral ventricles and reduced hippocampal spine density; reduction in functional forebrain NMDA receptors
Dysbindin knock-out	Increased acquisition of T-maze task, impaired spatial reference memory and novel object recognition performance.	Hyperexcitability of PFc pyramidal neurones; altered synaptic structure and formation; elevated HVA/DA ratio in cortico-limbic regions
Reelin knock-out	Few memory deficits reported, normal reversal learning and inhibitory control, normal MWM performance, some learning deficits in acquisition of operant tasks.	Increased neuronal packing and decreased dendritic spine density in PFc and hippocampal neurones.

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

Model species (rat or mouse or other species).

The weight and age of the animal are required or not.

Male and female requirements.

Specific plan for model construction.

Customers need to provide experimental materials (treatment drugs) and detailed experimental information (experimental animal grouping, drug treatment does and treatment time).

Delivery Standard

Original photos of experiments
Complete experimental report (including experimental materials,expermental steps, experimental results,etc.

Ace Therapeutics provides customized services for animal models of schizophrenia. We aim to help you study the neurobiological basis of schizophrenia and identify new drug targets. 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

Jones CA, et al. Animal Models of Schizophrenia. Br J Pharmacol. 2011, 164(4):1162-1194.
Nani JV, et al. Animal Models in Psychiatric Disorder Studies. Animal Models in Medicine and Biology, edited by Eva Tvrdá, Sarat Yenisetti, IntechOpen, 2019, 10.5772/intechopen.89034.

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