Neonatal 6-hydroxydopamine-induced hypo/hyperactivity: Blockade by Dopamine reuptake Inhibitors and effect of acute D-amphetamine
Tóm tắt
Five experiments were performed to assess the changes in motor activity resulting from neonatal administration of 6-hydroxydopamine (6-OHDA) on Days 1 or 2 postnatal, at doses of either 75 or 100 μg in a volume of 10 μl vehicle, following pretreatment with either GBR 12909 (40 mg/kg, s.c.) or amphonelic acid (4.0 mg/kg, s.c.) or saline. Motor activity was measured either over 60-min test periods on five consecutive days of testing or at 12-min intervals within a single 60-min test session. The initial extent of locomotor hyperactivity was dependent upon the neonatal dose of 6-OHDA: the 100 μg, but not 75 μg, dose induced marked hyperactivity from test day 1 onwards whereas the 75 μg dose did so from test day 3 onwards. The initial hypoactivity for rearing behaviour was observed for both doses of 6-OHDA: this hypoactivity was altered over successive test days so that by test day 5 an hyperactivity by the 75 μg, but not 100 μg, was observed. Pretreatment with either GBR 12909 or amphonelic acid abolished the effects of both doses of 6-OHDA. In the within 60-min test session procedure, 6-OHDA treated rats (both 75 and 100 μg) showed initial hyperactivity for locomotion that intensified, in relation to the other groups, over each 12-min interval and initial hypoactivity for rearing that developed into hyperactivity over each 12-min interval. Pretreatment with either GBR 12909 or amphonelic acid again abolished the effects of both doses of 6-OHDA (75 and 100 μg) rats, compared to the control groups in all four experiments. In Experiment V, a low dose of D-amphetamine abolished the hyperactivity of 6-OHDA (75μg) treated rats whereas a higher dose did so only transiently. Pretreatment with GBR 12909 abolished these effects. These findings underline the neuropharmacological utility of the neonatal 6-OHDA treatment for studying brain receptor system adaptive changes underlying the respective functional alterations and as a possible laboratory model for clinical disorders.
Tài liệu tham khảo
Archer, T. (1989) “Neurotoxin-induced cognitive and motor activity modifications: a catecholamine connection,” In: Sagvolden, T. and Archer, T., eds, Attention Deficit Disorder: Clinical and Basic Research (LEA, Hillsdale, NJ), pp 287–322.
Archer, T. and Fredriksson, A. (1992) “Functional changes implicating dopaminergic systems following perinatal treatments”, Dev. Pharmacol. Ther. 18, 201–222.
Archert, T. and Fredriksson, A. (2000) “Effects of α-adrenoceptor agonists in chronic morphine administered DSP 4-treated rats: evidence for functional cross-sensitization”, Neurotoxicity Res. 2, 1–22.
Archer, T., Jonsson, G. and Ross, S.B. (1984) “A parametric study of the effects of the noradrenaline neurotoxin DSP4 on avoidance acquisition and noradrenaline neurones in the CNS of the rat”, Br. J. Pharmacol. 82, 249–257.
Archer, T., Fredriksson, A., Jonsson, G., Lewander, T., Mohammed, A.K., Ross, S.B. and Söderberg, U. (1986) “Central noradrenaline depletion antagonizes aspects of d-amphetamine-induced hyperactivity in the rat”, Psychopharmacology (Berl.) 88, 141–146.
Archer, T., Danysz, W., Fredriksson, A., Jonsson, G., Luthman, J., Sundström, E. and Teiling, A. (1988) “Neonatal 6-hydroxydopamine-induced dopamine depletions: motor activity and performance in maze learning”, Pharmacol. Biochem. Behav. 31, 357–364.
Archer, T., Beninger, R.J., Järbe, T.U.C. and Seiden, L.S. (1990) “Latent tearning in a radial arm maze following neonatal dopamine depletion”, Behav. Pharmacol. 1, 191–199.
Breese, G.R. and Traylor, T.D. (1972) “Developmental characteristics of brain catecholamines and tyrosine hydroxylase in the rat: effects of 6-hydroxydopamine”, Br. J. Pharmacol. 44, 210–222.
Breese, G.R., Napier, T.C. and Mueller, R.A. (1985) “Dopamine agonist-induced locomotor activity in rats treated with 6-hydroxydopamine at differing ages: functional supersensitivity of D-1 dopamine receptors in neonatally lesioned rats”, J. Pharmacol. Exp. Ther. 234, 447–455.
Buonamici, M., Caccia, C., Carpentieri, M., Pegrassi, L., Rossi, A.C. and Di Chiara, G. (1986) “D-1 receptor supersensitivity in the rat striatum after unilateral 6-hydroxydopamine lesions”, Eur. J. Pharmacol. 126, 347–348.
Creese, I. and Iversen, S.D. (1973) “Blockade of amphetamine-induced motor stimulation and stereotypy in the adult rat following neonatal treatment with 6-hydroxydopamine”, Brain Res. 55, 369–382.
Eastgate, S.M., Wright, J.J. and Werry, J.S. (1978) “Behavioural effects of methylphenidate in 6-hydroxydopamine-treated neonatal rats”, Psychopharmacology 58, 157–159.
Erinoff, L., MacPhail, R.C., Heller, A. and Seiden, L.S. (1979) “Age dependent effects of 6-hydroxydopamine on locomotor activity inthe rat”, Brain Res. 164, 195–205.
Fredriksson, A., Dahlgren, L., Danielsson, B.R., Eriksson, P., Dencker, L. and Archer, T. (1992) “Behavioural effects of neonatal metallic mercury exposure in rats”, Toxicology 74, 151–160.
Fredriksson, A., Schröder, N., Eriksson, P., Izquierdo, I. and Archer, T. (1999) “Neonatal iron exposure induces neurobehavioural dysfunctions in adult mice”, Toxicol. Appl. Pharmacol. 159, 25–30.
Fredriksson, A., Schröder, N., Eriksson, P., Izquierdo, I. and Archer, T. (2000) “Maze learning and motor activity deficits in adult mice induced by iron exposure during a critical post natal period”, Dev. Brain Res. 119, 65–74.
Jonsson, G., Hallman, H., Mefford, I. and Adams, R.N. (1980) “The use of liquid chromatography with electrochemical detection for the determination of adrenaline and other biogenic monoamines in the CNS”, In: Fuxe, K., Goldstein, M., Hökfelt, B. and Hökfelt, T., eds, Central Adrenaline Neurons (Pergamon Press, Oxford), pp. 59–71.
Kelly, P.H., Seviour, P.W. and Iversen, S.D. (1975) “Amphetamine and apomorphine responses in the rat following 6-OHDA lesions of the nucleus accumbens septi and corpus striatum”, Brain Res. 94, 507–522.
Keller, R., Oke, A., Mefford, I. and Adams, R.N. (1976) “Liquid chromatographic analysis of catecholamines—routine assay for regional brain mapping”, Life Sci. 19, 995–1004.
Kirk, R.E. (1995) Experimental Design: Procedures for the behavioural sciences Brooks/Cole, Belmont, CA).
Kostrzewa, R.M. (1995) “Dopamine receptor supersensitivity”, Neurosci. Biobehav. Rev. 19, 1–17.
Lewander, T. (1977) “Effects of amphetamine in animals”, In: Martin, W.R., eds, Drug Addictions II, Handbook of Experimental Pharmacology, (Springer, Berlin), pp. 33–264.
Luthman, J., Bolioli, B., Tsutsumi, T., Verhofstad, A. and Jonsson, G. (1987) “Sprouting of serotonin nerve terminals following selective lesions of nigro-striatal dopamine neurons in the neonatal rat”, Brain Res. Bull. 19, 269–274.
Luthman, J., Fredriksson, A., Sundström, E., Jonsson, G. and Archer, T. (1989a) “Selective lesion of central dopamine or noradrenaline neuron systems in the neonatal rat: motor behaviour and monoamine alterations at adult stage”, Brain Res. 33, 267–277.
Luthman, J., Fredriksson, A., Lewander, T., Jonsson, G. and Archer, T. (1989b) “Effects of d-amphetamine and methylphenidate on hyperactivity produced by neonatal 6-hydroxydopamine treatment”, Psychopharmacology 99, 550–557.
Luthman, J., Fredriksson, A., Plaznik, A. and Archer, T. (1991) “Ketanserin or mianserin treatment reverses hyperactivity in neonatally dopamine lesioned rats”, J. Psychopharmacol. 5, 418–425.
Luthman, J., Lindqvist, E. and Ögren, S.O. (1995) “Hyperactivity in neonatally dopamine-lesioned rats depends on residual activity in mesolimbic dopamine neurons”, J. Pharmacol. Biochem. Behav. 51, 159–163.
Luthman, J., Bassen, M., Fredriksson, A. and Archer, T. (1997) “Functional changes induced by neonatal 6-hydroxydopamine lesions: Effects of dose levels on behavioural parameters”, Behav. Brain Res. 82, 213–221.
Miller, F.E., Heffner, T.G., Kotake, C. and Seiden, L.S. (1981) “Magnitude and duration of hyperactivity following neonatal 6-hydroxydopamine is related to the extent of brain dopamine depletion”, Brain Res. 229, 123–132.
Pijnenburg, A.J.J. and Van Rossum, J.M. (1973) “Stimulation of locomotor activity following injection of dopamine into the nucleus accumbens”, J. Pharm. Pharmacol. 25, 1003–1005.
Rogers, D.C. and Dunnett, S.B. (1989) “Hypersensitivity to alphamethyl-p-tyrosine suggests that behavioural recovery of rats receiving neonatal 6-OHDA lesion is mediated by residual catecholamine neurons”, Neurosci. Lett. 102, 108–113.
Sokoloff, P., Andrieux, M., Besancon, R., Pilon, C., Martres, M.-P., Giros, B. and Schwartz, J.-C. (1992) “Pharmacology of human dopamine D3 receptor expressed in a mammalian cell line: comparison with D2 receptor”, Eur. J. Pharmacol. 225, 331–337.
Sorensen, C.A., Vayer, J.S. and Goldberg, C.S. (1977) “Amphetamine reduction of motor activity in rats after neonatal administration of 6-hydroxydopamine”, Biol. Psychiatry 12, 133–137.
Teicher, M.H., Barber, N.I., Reichheld, J.H., Baldessarini, R.J. and Finklestein, S.P. (1986) “Selective depletion of cerebral noradrenaline with 6-hydroxydopamine and GBR-12909 in neonatal rat”, Dev. Brain Res. 30, 124–128.