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    Investigação de sinais prodrômicos e possíveis tratamentos preventivos em um modelo animal de esquizofrenia: a linhagem de ratos shr
    (Universidade Federal de São Paulo (UNIFESP), 2013-11-27) Niigaki, Suzy Tamie [UNIFESP]; Abilio, Vanessa Costhek [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Schizophrenia is a severe mental disease which begins after puberty and early adulthood. The pharmacotherapy, characterized by the antipsychotic drugs, even being a useful treatment tool, still remains unsatisfactory. In this way the study of prodromic signs as well as the search for preventive treatments has become very relevant in the attempt to delay or even prevent the onset of the disease. In this context, we have recently proposed the Spontaneously Hypertensive Rats (SHR) as an animal model of Schizophrenia, as long as this strain presented (I) hyperlocomotion; (II) deficits in social behavior (SI); (III) deficits in the prepulse inhibition of startle (PPI) and (IV) contextual fear conditioning (CFC) deficits; furthermore, all these deficits seem to be specifically reverted by antipsychotics drugs and potentiated by proschizophrenic manipulations. In the first part of the project, we analyze these behavioral characteristics in juvenile SHR in order to compare possible prodromal signs in this strain. As a result, we have found that juvenile SHR presents deficits in SI, CFC and latent inhibition; but not in PPI, nor presents hyperlocomotion. These results are in line with the presence of social and cognitive deficits in prodromal phase of the schizophrenia as well as the absence of positive symptoms (here assigned to the hyperlocomotion) in this period. In the sequence, we evaluated the SHR throughout their development to the adult phase, revealing that these deficits persisted in the adulthood. In the second part of the project, we evaluated the effects of a preventive antipsychotic treatment and it results that each drug was able to prevent some behavioral deficits in adult SHR, but also impaired the control strain. In this way, clozapine altered PPI and CFC; quetiapine altered SI and PPI; risperidona altered PPI; while haloperidol altered PPI and promoted hyperlocomotion in both strain. None of the treatment produced extra-pyramidal collateral effects, nor altered sensibilization to methylphenidate. Finally, we evaluated the effects of an atypical antipsychotics combination treatment in two different designs: in the first treatment, we used the same dosage tested before, but in a shorter time interval (TTO A); on the other hand, in the second treatment we used lower doses with the same time interval (TTO B). As a result, both drug combination treatments attenuated the adult SHR hyperlocomotion. Moreover, TTO B reversed CFC deficits, but, as well as TTO A, deteriorated the control performance in CFC task. In this way, we suggest that early interventions may be useful to attenuate schizophrenia-like deficits in the adulthood; but it also may be harmful if administrated to individuals which may not convert to schizophrenic later on. Thus, more studies are needed in order to elaborate a preventive and safe treatment which can be feasible in clinical practice.