ISSN:
1432-2072
Keywords:
Key words U-50
;
488
;
Quinpirole
;
SKF 38393
;
AMPT
;
Kappa opioid
;
Dopamine
;
Ontogeny
;
Locomotor activity
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Treatment with a non-selective DA receptor agonist (i.e., NPA) has previously been shown to attenuate the kappa opioid mediated locomotor activity of preweanling rats. The purpose of the present study was to determine whether stimulation of D1-like or D2-like receptors is responsible for this behavioral effect and whether the critical DA receptors are located pre- or postsynaptically. To assess these questions, 17-day-old rats were injected with saline, the D2/D3 agonist quinpirole (0.1, 0.3, or 1.0 mg/kg, IP), or the D1 agonist SKF 38393 (7.5, 15, or 30 mg/kg, IP), 20 min after receiving the kappa opioid agonist U-50,488 (5 mg/kg, SC) or saline. Results showed that the locomotor activating effects of U-50,488 were blocked by the D2/D3, but not the D1, receptor agonist. To dissociate the effects of DA autoreceptors and postsynaptic receptors, 17-day-old rats were given α-methyl-dl-p-tyrosine (AMPT reduces endogenous DA stores) prior to U-50,488 or amphetamine (1.5 mg/kg, SC) treatment. Interestingly, AMPT (which reduced DA levels by more than 80%) fully attenuated amphetamine-induced locomotor activity, while having little effect on U-50,488-induced locomotion. In addition, quinpirole blocked the locomotor activating effects of U-50,488 in rats acutely depleted of DA. When considered together, these results indicate that kappa opioid stimulation enhances locomotor activity regardless of presynaptic DA levels. Similarly, quinpirole appears to attenuate U-50,488-induced locomotor activity by stimulating postsynaptic D2-like receptors, since the D2/D3 agonist inhibited kappa opioid mediated behavior independent of endogenous DA levels.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s002130050372
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