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Schizophrenia is a devastating disorder for the afflicted people and very costly for the society. Therapy is not solved and preclinical testing requires animal models. Several studies suggested that vasopressin is important in schizophrenia. Patients have lower plasma vasopressin levels, which was normalized after antipsychotic treatment. Prepulse inhibition (PPI) is reduced in unmedicated schizophrenic patients, which correlates with the degree of thought disorder. Therefore the vasopressin-deficient Brattleboro rat might be an appropriate model. Indeed, they have a number of cognitive and behavioral abnormalities that are analogous to those seen in schizophrenia patients. Beside the reduced PPI, their object, as well as social discrimination abilities are also poor. In connection with social communication deficit pups emit less ultrasound upon maternal separation. EEG analysis showed circadian rhythm alterations in vasopressin-deficient rats; they spent more time awake during their inactive phase. After antipsychotic treatment all of these changes was normalized. Although these alterations might be observable in other mental disorders, but all data together and the response to antipsychotic treatment suggest that Brattleboro rats are unique model of schizophrenia having a natural (nonpharmacological) deficit in all above mentioned tests.
Vasopressin (AVP) has fundamental role in the regulation of the hypothalamo-pituitary-adrenal axis, the main target of stress and adaptation. Its role is especially important during chronic load, which can induce anxiety and depression. The importance of AVP in stress and related mood disorders were studied in spontaneously mutated AVP-defi cient Brattleboro rats (di/di). AVP was confi rmed to be a prominent regulator of the adrenocorticotrop hormone secretion in wide range of stresses. Accompanied corticosterone elevation was reduced in di/di rats just occasionally and remained elevated longer. Endogenous AVP acts as a paracrine signal to facilitate the return of plasma corticosterone to basal levels. Behavioral studies confi rmed that di/di animals were less anxious in the defensive withdrawal test and revealed lower depressive indeces during forced swimming. Thus, AVP-antagonists are promising targets for drug development
The hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei are activated by body salt-fluid variations. Stimulation of 2-adrenoceptors by an agonist-xylazine (XYL) activates oxytocinergic but not vasopressinergic magnocellular neurons. In this study, tyrosine hydroxylase (TH), corticoliberine (CRH), and neuropeptide Y (NPY) magnocellular phenotypes, were analysed in response to 2-adrenoceptor manipulations and sustained hyperosmolality in vasopressin deficient homozygous Brattleboro (di/di) rats. Saline (0.9% NaCl, 0.1 ml/100g/bw), XYL (10 mg/kg/bw), atipamezole (ATIP, 2-adrenoceptors antagonist, 1 mg/kg/bw), and ATIP 5 min later followed by XYL, were applied intraperitoneally. Presence of immunolabeled Fos peptide signalized the neuronal activity. Ninety minutes after injections, the rats were anesthesized and sacrificed by transcardial perfusion with fixative. Coronal sections of 30 µm thickness double immunolabeled with Fos/neuropeptide were evaluated under light microscope. Under basal conditions, di/di in comparison with control Long Evans rats, displayed significantly higher number of TH, CRH, and NPY immunoreactive neurons in the SON and PVN (except NPY cells in PVN) and more than 90%, 75%, and 86% of TH, NPY, and CRH neurons, respectively, displayed also Fos signal in the SON. XYL did not further increase the number of Fos in the PVN and SON and ATIP failed to reduce the stimulatory effect of hypertonic saline in all neuronal phenotypes studied. Our data indicate that hyperosmotic conditions significantly influence the activity of TH, CRH, and NPY magnocellular neuronal phenotypes, but 2-adrenoceptors do not play substantial role in their regulation during osmotic challenge induced by AVP deficiency.
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