Schizophrenia Animal Models
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. (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 |
| Gestational MAM (GD17) |
Normal acquisition, but impaired re-learning in the Morris water maze, impaired extra-dimensional shift in attentional set-shifting task. |
Reduced PFc and hippocampal size, enlarged ventricals, reduced hippocampal soma size and neuropil; enhanced nAcc DA release; spontaneously hyperactive VTA DA neurones; decreased PFc parvalbumin GABA interneurones |
| Post-weaning social isolation |
Deficit in novel object recognition, no effect on acquisition of spatial learning by impaired reversal learning in water maze, extra-dimensional shift in the attentional set-shifting task and fear-motivated conditioned emotional response. |
Reduced PFc volume; reduced dendritic spine density, cytoskeletal alteration and loss of parvalbumin-containing interneurones and reelin in the hippocampus; reduced PFc D1 binding, no change in striatal D2 density, but increased proportion of striatal D2High; increased spontaneously active VTA DA neurones |
| 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
Delivery Standard
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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