Effect of quinpirole on timing behaviour in the free-operant psychophysical procedure: evidence for the involvement of D2 dopamine receptors

Abstract

Results suggest that quinpirole reduced T (50) via an action at D(2) receptors. D(1)-like and D(2)-like receptors may mediate behaviourally similar but pharmacologically distinct effects on timing behaviour.

Systemic Administration of 8-OH-DPAT and Eticlopride, but not SCH23390, Alters Loss-Chasing Behavior in the Rat

“…This raises the possibility that 8-OH-DPAT diminished chasing behavior by disturbing our rats' ability to use delays-to-reward to regulate the balance between chase and quit responding. However, while eticlopride blocks the underestimation of time intervals induced by the D 2 receptor agonist, quinpirole, it has no effect on its own at doses comparable to those used here (Cheung et al, 2007). Therefore, this and our own data suggest that D 2 receptor activity influences risk-seeking choices when attempting to avoid delays-to-reward independently of any effects upon timing-based behaviors.…”

Evidence for the sensitivity of operant timing behaviour to stimulation of D1 dopamine receptors

“…There is, however, a well established literature on functional interactions between D 1 -like and D 2 -like receptors, which shows that the two receptor types can act synergistically, antagonistically or independently in various behavioural and physiological functions (see Jackson and Westlind-Danielsson 1994). Although our results and those of Frederick and Allen (1996) and Cheung et al (2007) do not provide any evidence for functional interaction between D 1 -like and D 2 -like receptors in the case of temporal differentiation, it is not possible to rule out the possibility of such an interaction at this stage. Further experiments employing a broader range of agonists and antagonists, as well as combined treatment with D 1 -like and D 2 -like receptor agonists, may help to address this issue (Dreher and Jackson 1989).…”

“…a Absolute response rates. b Relative response rate on lever B. SKF-81297 displaced the psychometric function to the left; neither dose of haloperidol reversed this effect believed to entail D 2 -like receptor stimulation (Spyraki et al 1982;Velazquez Martinez et al 1995;Herrera and Velazquez Martinez 1997), and attenuate the effect of the direct D 2 -like receptor agonist quinpirole on T 50 in this schedule (Cheung et al 2007). The present results are similar to previous findings with d-amphetamine, whose ability to reduce T 50 in the freeoperant psychophysical procedure was reversed by SKF-83566 but not by haloperidol, implying D 1 -but not D 2 -like dopamine receptor involvement (Body et al 2006b;Cheung et al 2006).…”

“…The sensitivity of temporal differentiation to D 1 -like dopamine receptor stimulation is also supported by the finding that the D 1 -like receptor partial agonist SKF-38393 reduced peak time in the fixed-interval peak procedure (Frederick and Allen 1996). Interestingly, the D 2 -like dopamine receptor agonist quinpirole has also been found to reduce T 50 in the free-operant psychophysical procedure, an effect that was attenuated by D 2 -like receptor antagonists haloperidol, eticlopride and sulpiride, but not by SKF-83566, nor by the D 3 -receptor preferring antagonist nafadotride and D 4 receptor antagonist L-745870 (3-(4-[4-chlorophenyl]piperazin-1-yl)-methyl-1H-pyrrolo[2,3-b] pyridine trihydrochloride) (Cheung et al 2007). Taken together, these results are consistent with the notion that d-amphetamine, SKF-81297 and quinpirole may reduce T 50 in this schedule through two neuropharmacologically independent mechanisms, d-amphetamine and SKF-81297 via D 1 -like receptors, and quinpirole via D 2 -like receptors (probably D 2 rather than D 3 or D 4 receptors).…”

Acute Ethanol Potentiates the Clock‐Speed Enhancing Effects of Nicotine on Timing and Temporal Memory

“…This in turn would lead to indirect effects on clock speed depending upon the current level of DA activity in cortico‐striatal circuits (e.g., Cheng et al., 2006a, 2007a; Choi et al., 2006; Maldve et al., 2002; Matell and Meck, 2004; Matell et al., 2003; Rammsayer and Vogel, 1992; Rammsayer et al., 1989; Söderpalm et al., 2000). Alternatively, ethanol may potentiate nicotine‐induced effects on clock speed and temporal memory through its interaction with GABAergic, opioid, or serotonergic systems (e.g., Asgari et al., 2006; Body et al., 2005; Cheung et al., 2006, 2007; Chiang et al., 2000; Meck, 1996).…”