Abstract
Central administration of 6-hydroxydopamine (6-OHDA) to adult or neonatal rats destroys dopamine-containing neurons, produces a variety of behavioral deficits (Breese et al., 1973; Smith et al., 1973) and enhances behavioral responses to dopamine agonists (Ungerstedt, 1971; Schoenfeld and Uretsky, 1972; Hollister et al., 1974; 1979; Setler et al. 1978; Kilts et al. 1979). In spite of the common biochemical deficiency observed in neonatally and adult-lesioned rats, Breese et al. (1984 a,b) reported that certain behavioral responses to L-DOPA or apomorphine in adult-6-OHDA-treated rats (Breese et al., 1970) differ from those observed in rats lesioned as neonates and tested with dopamine agonists as adults (Breese et al., 1972; Smith et al., 1973). For example, neonatally 6-OHDA-lesioned rats exhibit self-mutilation behavior (SMB) after treatment with dopamine agonists which do not elicit this response in adult-6-OHDA treated rats (Breese et al., 1984b).
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Breese, G.R., Mueller, R.A., Napier, T.C., Duncan, G.E. (1986). Neurobiology of D1 Dopamine Receptors after Neonatal-6-OHDA Treatment: Relevance to Lesch-Nyhan Disease. In: Breese, G.R., Creese, I. (eds) Neurobiology of Central D1-Dopamine Receptors. Advances in Experimental Medicine and Biology, vol 204. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5191-7_13
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DOI: https://doi.org/10.1007/978-1-4684-5191-7_13
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