**2.1 Animal models in schizophrenia (SCZ)**

Schizophrenia (SCZ) is a severe brain disorder, characterized by a set of positive and negative symptoms and cognitive disorders, which are the basis for the clinical diagnosis of individuals who needs to present at least two or more of those symptoms, according to the DSM. SCZ is one of the most debilitating mental disorders, affecting about 21 million people worldwide. The antipsychotics used to treat SCZ patients can soften the development of the disorder, and this pharmacological treatment was the basis for the most accepted theory to explain the neurobiology of SCZ, as noticed by the alterations in the dopamine transmission. In addition, several other theories have been suggested soon after, as for instance, the serotoninergic, glutamatergic, GABAergic, and the neurodevelopmental susceptibility hypothesis, among others [20]. However, none of these theories had allowed the characterization of the etiology or the identification of strong biomarker for the diagnosis of SCZ. Many efforts are being made to characterize a model for SCZ, but there is a great difficulty in reproduce endophenotypes that frame all the groups of symptoms related to this disease, or which allow associating all risk factors that are already known. Below, we exemplify some of these models, and for a more detailed review of SCZ models can be found elsewhere [21].

Most of the models are based on the theory of neurotransmitter imbalance, and they are induced by the disruption of these pathways, other models explore changes in the levels of expression of candidate genes involved in the processes of SCZ susceptibility. It should be considered that SCZ is a multifactorial disorder, and thus, the genetic component should be evaluated in addition to changes in the environment, as in contrast to the models based on genetic alterations, there are those taking into account the environmental changes, such as the prenatal insults, which impose changes in the neurodevelopment processes. Some of these models are exemplified in **Table 2**.

All of these models show behavioral and molecular changes that can be associated with SCZ.
