%0 Journal Article
%T Behavioral and antioxidant activity of a tosylbenz[g]indolamine derivative. A proposed better profile for a potential antipsychotic agent
%A Chara A Zika
%A Ioannis Nicolaou
%A Antonis Gavalas
%A George V Rekatas
%A Ekaterini Tani
%A Vassilis J Demopoulos
%J Annals of General Psychiatry
%D 2004
%I BioMed Central
%R 10.1186/1475-2832-3-1
%X Adult male Fischer-344 rats grouped as: i) Untreated rats: TPBIA was administered i.p. in various doses ii) Apomorphine-treated rats: were treated with apomorphine (1 mg kg-1, i.p.) 10 min after the administration of TPBIA. Afterwards the rats were placed individually in the activity cage and their motor behaviour was recorded for the next 30 min The antioxidant potential of TPBIA was investigated in the model of in vitro non enzymatic lipid peroxidation.i) In non-pretreated rats, TPBIA reduces the activity by 39 and 82% respectively, ii) In apomorphine pretreated rats, TPBIA reverses the hyperactivity and stereotype behaviour induced by apomorphine. Also TPBIA completely inhibits the peroxidation of rat liver microsome preparations at concentrations of 0.5, 0.25 and 0.1 mM.TPBIA exerts dopamine antagonistic activity in the central nervous system. In addition, its antioxidant effect is a desirable property, since TD has been partially attributed, to oxidative stress. Further research is needed to test whether TPBIA may be used as an antipsychotic agent.It is well established that compounds which interact with central dopamine receptors have therapeutic potential in the treatment of conditions like Parkinson's disease and psychotic disorders. For the later treatment, it is known that tardive dyskinesia (TD) is a major limitation of chronic antipsychotic drug therapy at least with older (typical) antipsychotics.There is increased awareness of the different ways in which this condition manifests itself and the variety of disabilities that TD produces. Although a substantial research has been stimulated to identify the underlying pathophysiological mechanisms of TD, they remain largely elusive. There are several hypotheses about the pathophysiology of TD (dopamine hypersensitivity, neurotoxicity, GABA insufficiency, noradrenergic dysfunction, structural abnormalities)[1], however the true mechanism remains unknown.The hypothesis of dopamine hypersensitivity proposes tha
%U http://www.annals-general-psychiatry.com/content/3/1/1