CONCLUSÃO GERAL

Por fim, pode-se concluir que as alterações dos níveis de citocinas pró-inflamatórias dosadas no estriado de ratos, podem participar no desenvolvimento dos MMV induzidos por haloperidol. No entanto, os resultados devem ser analisados com cautela, uma vez que também foi observado alteração de citocinas para os animais também tratados com risperidona. Além disso, o tratamento com ambos os antipsicóticos não induziram qualquer alteração em parâmetros oxidativos/antioxidantes, nem em parâmetros dopaminérgicos avaliados no córtex cerebral desses animais, podendo essa estrutura cerebral não estar intimamente ligada ao desenvolvimento de alterações motoras.

AGGARWAL, B.B. The role of TNF and its family members in inflammation and cancer: lessons from gene deletion. Curr. Drug. Targets. Inflamm. Allergy., v. 1, p. 327–341, 2000.

AGGARWAL, B.B. Tumor necrosis factors receptor associated signallingmolecules and their role in activation of apoptosis, JNK and NF-κB. Ann. Rheum. Dis., v. 59, p. i6–i16, 2000.

AGHAJANIAN, G.K.; MAREK, G.J. Serotonin model of schizophrenia: emerging role of glutamate mechanisms. Brain. Res. Rev., v. 31, p. 302-12, 2000.

ALLISON, D.B.; MACKELL, J.A.; MCDONNELL, D.D. The impact of weight gain on quality of life among persons with schizophrenia. Psychiatr. Serv., v. 54, p. 565-567. 2003.

AMARA, S.G. SONDERS, M.S. Neurotransmitter transporters as molecular targets for addictive drugs. Drug. Alcohol. Depend., v. 51, p. 87–96, 1998.

ANDREASSEN, O.A.; JORGENSEN, H.A. Neurotoxicity associated with

neurolepticinduced oral dyskinesias in rats Implications for tardive dyskinesia. Prog.

Neurobiol., v. 61, p. 525–541, 2000.

ARNT, J.; SKARSFELDT, T. Do novel antipsychotics have similar pharmacological characteristics? A review of the evidence. Neuropsychopharmacology, v. 18, p. 63-101, 1998.

BALE, T. L. et al. Early life programming and neurodevelopmental disorders. Biol.

Psychiatry., v. 68, p. 314-9, 2011.

BALIJEPALLI, S. et al. Protein thiol oxidation by haloperidol results in inhibition of mitochondrial complex I in brain regions: comparison with atypical antipsychotics.

Neurochem. Int., v. 38, p. 425– 35, 2001.

BARBEAU, A. L-DOPA and juvenile Huntington’s disease. Lancet, v. 2, p. 1066, 1969a.

BARBEAU, A. L-DOPA therapy in Parkinson’s disease. Canad. Med. Ass. J., v. 101, p. 791-800, 1969b.

BEHL, C. et al. Haloperidol-induced cell death-mechanism and protection with vitamin E in vitro. Neuroreport., v. 7, p. 360-364, 1995.

BEHL, C. et al. Oxidative stress resistant cells are protected against haloperidol toxicity.

Brain. Res., v. 717, p. 193-195, 1996.

BELFORTE, J. E. Postnatal NMDA receptor ablation in corticolimbic interneurons confers schizophrenia-like phenotypes. Nature. Neurosci., v. 13, p. 76-83, 2011.

BILBO, S.D.; SCHWARZ, J.M. Early-life programming of later-life brain and behavior: a critical role for the immune system. Front. Behav. Neurosci., v. 3, p. 14, 2009.

BILBO, S.D.; SCHWARZ, J.M. The immune system and developmental programming of brain and behavior. Front. Neuroendocrinol. v. 33, p. 267–286, 2012.

BISHNOI, M.; CHOPRA, K.; KULKARNI, S.K. Differential striatal levels of TNF-alpha, NFkappaB p65 subunit and dopamine with chronic typical and atypical neuroleptic treatment: role in orofacial dyskinesia. Prog. Neuropsychopharmacol. Biol. Psychiatry., v. 32, p. 1473-8, 2008.

BLOKHINA, O.; FAGERSTEDT, K.V. Oxidative metabolism, ROS and NO under oxygen deprivation. Plant. Physiol. Bio. Chem., 48, p. 359–73, 2010.

BONIZZI, G. et al. Reactive oxygen intermediate-dependent NF-κB activation by interleukin- 1β requires 5-lipoxygenase or NADPH oxidase activity. Mol. Cell. Biol., v. 10, p. 1950-1960, 1999.

BORTOLATO, M.; CHEN, K.; SHIH, J.C. Monoamine oxidase inactivation: from pathophysiology to therapeutics. Adv. Drug. Deliv. Rev., v. 60, p. 1527–1533, 2008.

BOWIE, A.G.; MOYNAGH, P.N.; O’NEILL, L.A. Lipid peroxidation is involved in the activation of NF-κB by tumor necrosis factor but interleukin-1 in the human endothelial cell line ECV304. J. Biol. Chem., v. 272, p. 25941-25950, 1997.

BRYDEN, K.E.; KOPALA, L.C. Body mass index increase of 58% associated with olanzapine. Am. J. Psychiatry., v. 156, p. 1835-1836, 1999.

BUSANELLO, A. et al. Resveratrol protects against a model of vacuous chewing movements induced by reserpine in mice. Behav. Pharmacol., 22, p. 71–75, 2011.

BUSANELLO, A. et al. Resveratrol reduces vacuous chewing movements induced by acute treatment with fluphenazine. Pharmacol. Biochem. Behav., v. 101, p. 307–310, 2012.

CADET, J.L.; LOHR, J.B.; JESTE, D.V. Free radicals and tardive dyskinesia. Trends.

Neurosci.,, v. 9, p. 107-108, 1986.

CADET, J.L.; KAHLER, L.A. Free radical mechanisms in schizophrenia and tardive dyskinesia. Neurosci. Biobehav. Rev., v. 18, p. 457-467, 1994.

CARLSSON, A. Biochemical implications of dopa-induced action on the central nervous system with particular reference to abnormal movements. In: L-DOPA and Parkinsonism. A. Bardeau, McDowell (Eds.), pp. 205-212, Davis, Philadelphia, 1970.

CARSON, M.J.; THRASH, J.C.; WALTER, B. The cellular response in neuroinflammation: The role of leukocytes, microglia and astrocytes in neuronal death and survival. Clin.

Neurosci. Res., v. 6, p. 237–245, 2006

CASEY, D.E. Tardive dyskinesia: reversible and irreversible. Psychopharmacology, v. 2, p. 88-97, 1985.

CASS, W.A.; GERHARDT, G.A. In vivo assessment of dopamine uptake in rat medial

prefrontal cortex: comparison with dorsal striatum and nucleus accumbens. J. Neurochem., v. 65, p. 201–207, 1995.

CHEW, M.L. et al. A model of anticholinergic activity of atypical antipsychotic medications.

Schizophr. Res., v. 88, p. 63-72, 2006.

CHOI, C. et al. Suppressive effects of genistein on oxidative stress and NF-κB activation in RAW 264.7 macrophages. Biosci. Biotechnol. Biochem., v. 67, p. 1916-1922, 2003.

COYLE, J.T.; PUTTFARCKEN, P. Oxidative stress glutamate and neurodegenerative disorders. Science, v. 262, p. 689-95, 1993.

CRANE, G.E. Persistent dyskinesia. Br. J. Psychiatry., v. 122, p. 395-405, 1973.

CREESE, I.; BURT, D.R.; SNYDER, S.H. Dopamine receptor binding predicts clinical and pharmacological potencies of antischizophrenic drugs. Science, v. 192, p. 481-483, 1976.

DADHEECH, G. et al. Evaluation of antioxidant deficit in schizophrenia. Indian. J.

Psychiatry., v. 50, p. 16-20, 2008.

DAVIS, K. L.; KAHN, R. S.; KO, G.; DAVIDSON, M. Dopamine in schizophrenia: a review and reconceptualization. Am. J. Psychiatry., v. 148, p. 1474-86, 1991.

DE KEYSER, K. Excitotoxic mechanisms may be involved in the pathophysiology of tardive dyskinesia. Clin. Neuropharmacol., v. 14, p. 562-565, 1991.

DE VRIES, E.F.; DIERCKX, R.A.; KLEIN, H.C. Nuclear imaging of inflammation in neurologic and psychiatric disorders. Curr. Clin. Pharmacol., v. 1, p. 229–242, 2006.

DINARELLO, C.A. Interleukin-1 in the pathogenesis and treatment of inflammatory diseases.

Blood, v. 117, p. 3720–3732, 2011.

DUNN, A.J.; WANG, J.; ANDO, T. Effects of cytokines on cerebral neurotransmission. Comparison with the effects of stress. Adv. Exp. Med. Biol., v. 461, p. 117–127, 1999.

ELKASHEF, A.M.; WYATT, R.J. Tardive dyskinesia: possible involvement of free radical and treatment with vitamin E. Schrizophr. Bull., v. 25, p. 731– 40, 1999.

ELLENBROEK, B.A. Treatment of schizophrenia: a clinical and preclinical evaluation of neuroleptic drugs. Pharmacol. Ther., v. 57, p. 1-78, 1993.

FACHINETTO, R. et al. Diphenyl diselenide decreases the prevalence of vacuous chewing movements induced by fluphenazine in rats. Psychopharmacology, v. 194, p. 423–432, 2007a.

FACHINETTO, R. et al. Valeriana officinalis does not alter the orofacial dyskinesia induced by haloperidol in rats: role of dopamine transporter. Prog. Neuropsychopharmacol. Biol.

FALUDI, G.; MIRNICS, K. Synaptic changes in the brain of subjects with schizophrenia. Int.