Abstract
In three experiments, male Wistar rats (250–350 g) were injected (SC) daily with the D1-type dopamine receptor agonist, SKF 38393 (0.0, 4.0, 8.0, or 16.0 mg/kg), the D2-type dopamine receptor agonist, quinpirole (0.0, 0.3, or 3.0 mg/kg), and/or the D1-type dopamine receptor antagonist, SCH 23390 (0.0 or 0.5 mg/kg) for 8–10 days. After each daily injection, the rats were tested for locomotor activity in photocell arenas for 20 min. Following this subchronic pretreatment, all rats were challenged with the mixed dopamine receptor agonist apomorphine (1.0 mg/kg, SC) and tested for locomotor activity. SKF 38393 treatments produced a dose-dependent decrease in locomotor activity which did not significantly change across days. Quinpirole also depressed locomotor activity when first injected, but this quinpirole-induced inhibition of activity progressively decreased across days. When subsequently challenged with apomorphine, rats in both the SKF 38393 and the quinpirole pretreatment groups displayed greater locomotor activity than rats pretreated with only vehicle. Although SCH 23390 pretreatments did not affect subsequent sensitivity to apomorphine, SCH 23390 completely blocked the effect of quinpirole. These results suggest that although repeated D1 receptor stimulation may be sufficient to induce behavioral sensitization to apomorphine, D2 receptor stimulation also contributes to the effect.
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References
Braun AR, Chase TN (1988) Behavioral effects of chronic exposure to selective D-1 and D-2 dopamine receptor agonists. Eur J Pharmacol 147:441–451
Clark D, White FJ (1987) Review: D1 dopamine receptor — the search for a function: a critical evaluation of the D1/D2 dopamine receptor classification and its functional implications. Synapse 1:347–388
Criswell H, Mueller RA, Breese GR (1989) Priming of D1-dopamine responses: long lasting behavioral supersensitivity to a D1-dopamine agonist following repeated administration to 6-OHDA-lesioned rats. J Neurosci 9:125–133
Diana M, Young SJ, Groves PM (1991) Modulation of dopaminergic terminal excitability by D-1 selective agents: further characterization. Neuroscience 42:441–449
Drukarch B, Stoof JC (1990) D-2 dopamine autoreceptor selective drugs: do they really exist? Life Sci 47:361–376
Hirabayasi M, Saito T, Tadokoro S (1991) Differential sensitization to ambulation-increasing effect of metamphetamine after repeated administration to mice in activity cages of different sizes. Jpn J Pharmacol 57:91–97
Henry DJ, White FJ (1991) Repeated cocaine administration causes persistent enhancement of D1 dopamine receptor sensitivity within the rat nucleus accumbens. J Pharmacol Exp Ther 258:882–890
Henry DJ, Greene MA, White FJ (1989) Electrophysiological effects of cocaine in the mesoaccumbens dopamine system: repeated administration. J Pharmacol Exp Ther 251:833–839
Hoffman DC, Wise RA (1992) Locomotor-activating effects of the D2 agonist bromocriptine show environment-specific sensitization following repeated injections. Psychopharmacology 107:277–284
Horger BA, Schenk S (1991) Sensitization to cocaine's reinforcing and motor activating effects: different response to quinpirole preexposure. Soc Neurosci Abstr 17:683
Kalivas PW, Weber B (1988) Amphetamine injection into the ventral mesencephalon sensitizes rats to peripheral amphetamine and cocaine. J Pharmacol Exp Ther 245:1095–1101
Kuczenski R, Leith NJ (1981) Chronic amphetamine: is dopamine a link in or a mediator of the development of tolerance and reverse tolerance? Pharmacol Biochem Behav 15:405–413
Lynch M (1991) Dissociation of autoreceptor activation and behavioral consequences of low-dose apomorphine treatment. Prog Neuropsychopharmacol Biol Psychiatry 15:689–698
Mattingly BA, Gotsick JE (1989) Conditioning and experiential factors affecting the development of sensitization to apomorphine. Behav Neurosci 103:1311–1317
Mattingly BA, Rowlett JK (1989) Effects of repeated apomorphine and haloperidol treatments on subsequent sensitivity to apomorphine. Pharmacol Biochem Behav 34:345–347
Mattingly BA, Gotsick JE, Salamanca K (1988) Latent sensitization to apomorphine following repeated low doses. Behav Neurosci 102:553–558
Mattingly BA, Rowlett JK, Graff JT, Hatton BJ (1991) Effects of selective D-1 and D-2 dopamine antagonists on the development of behavioral sensitization to apomorphine. Psychopharmacology 105:501–507
Mattingly BA, Hart T, Lim K, Perkins C (1992) Role of dopamine receptor subtypes in the development of cocaine-induced behavioral sensitization. Soc Neurosci Abstr 18:901
Muller P, Seeman P (1979) Presynaptic subsensitivity as a possible basis for sensitivity by long-term dopamine mimetics. Eur J Pharmacol 55:149–158
Niesewander JL, Lucki I, McGonigle P (1991) Behavioral and neurochemical effects of chronic administration of reserpine and SKF-39383 in rats. J Pharmacol Exp Ther 257:850–860
Peris J, Zahniser NR (1989) Persistent augmented dopamine release after acute cocaine requires dopamine receptor activation. Pharmacol Biochem Behav 32:71–76
Radhakishun FS, Van Ree JM (1987) The hypomotility elicited by small doses of apomorphine seems exclusively mediated by dopaminergic systems in the nucleus accumbens. Eur J Pharmacol 136:41–47
Rebec GV, Lee EH (1982) Differential subsensitivity of dopaminergic and neostriatal neurons to apomorphine with long term treatment. Brain Res 250:188–192
Robinson TE, Becker JB (1986) Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis. Brain Res Rev 11:157–198
Rowlett JK, Mattingly BA, Bardo MT (1991) Neurochemical and behavioral effects of acute and chronic treatment with apomorphine in rats. Neuropharmacology 30:191–197
Skirboll LR, Grace AA, Bunney BS (1979) Dopamine auto-and postsynaptic receptors: electrophysiological evidence for differential sensitivity to dopamine agonists. Science 206:80–82
Stahle L, Ungerstedt U (1989) Yawning and suppression of exploration in amphetamine-treated rats: incompatibility with the autoreceptor hypothesis. Psychopharmacology 97:553–560
Stahle L, Ungerstedt U (1990) Yawning and suppression of exploration induced by dopamine agonists: no relation to extracellular striatal levels of dopamine. Pharmacol Biochem Behav 35:201–209
Stewart J, Vezina P (1989) Microinjections of Sch-23390 into the ventral tegmental area and substantia nigra pars reticulata attenuate the development of sensitization to the locomotor activating effects of systemic amphetamine. Brain Res 495:401–416
Ujike H, Akiyama K, Nishikawa H, Onoune T, Otsuki S (1991) Lasting increase in D1 dopamine receptors in the lateral part of the substantia nigra pars reticulata after subchronic methamphetamine administration. Brain Res 540:159–163
Vezina P, Stewart J (1989) The effect of dopamine receptor blockade on the development of sensitization to the locomotor activating effects of amphetamine and morphine. Brain Res 499:108–120
Vezina P, Blanc G, Glowinski J, Tassin JP (1991) Opposed behavioral outputs of increased dopamine transmission in prefrontocortical and subcortical areas: a role for the cortical d-1 dopamine receptor. Eur J Neurosci 3:1001–1007
White FJ, Hu XT, Brooderson RJ (1990) Repeated stimulation of dopamine D-1 receptors enhances the effects of dopamine receptor agonists. Eur J Pharmacol 191:497–499
Wolf ME, Roth RH (1987) Dopamine autoreceptors. In: Creese I, Fraser CM (eds) Dopamine receptors. Liss, New York, pp 45–96
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Portions of this paper were presented at the 1991 Society for Neuroscience meetings, New Orleans, La, USA.
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Mattingly, B.A., Rowlett, J.K. & Lovell, G. Effects of daily SKF 38393, quinpirole, and SCH 23390 treatments on locomotor activity and subsequent sensitivity to apomorphine. Psychopharmacology 110, 320–326 (1993). https://doi.org/10.1007/BF02251287
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DOI: https://doi.org/10.1007/BF02251287