Neuroleptics block high- but not low-dose heroin place preferences: Further evidence for a two-system model of motivation.

Abstract

We thank Francis Harrington for help with the early experiments.

Voluntary Consumption of Amphetamine, Cocaine, Ethanol and Morphine by Rats as Influenced by a Preceding Period of Forced Drug Intake and Clozapine

“…Here, the increase could be explained as compensation for the subjective loss of the rewarding effects of both drugs due to the receptor blockade caused by clozapine [34]. This agrees with other studies showing the involvement of the dopaminergic system in the rewarding effects of these drugs [10,35,36].…”

Opioid-induced rewards, locomotion, and dopamine activation: A proposed model for control by mesopontine and rostromedial tegmental neurons

“…In contrast to the effects described above in drug-naïve animals, PPTg lesions do not block the acquisition of morphine CPP in opioid dependent/withdrawn rats and do not affect established heroin self-administration (Bechara and van der Kooy, 1989; Bechara et al, 1992; Nader & van der Kooy, 1997; Nader et al, 1994; Olmstead et al, 1998). PPTg lesions using a toxin designed to target PPTg cholinergic neurons (Clark et al, 2007), also do not affect established heroin self-administration (Steidl et al, 2014).…”

“…PPTg or LDTg excitotoxic lesions also block morphine-induced locomotion or stereotypy (Bechara and van der Kooy, 1992; Forster et al, 2002a; Miller et al, 2002; Olmstead and Franklin, 1994a). PPTg excitotoxic lesions block the acquisition of morphine or heroin CPP and the acquisition of heroin self-administration in drug-naïve rats (Bechara et al, 1992; Nader and van der Kooy, 1997; Nader et al, 1994; Olmstead and Franklin, 1993; 1994b; Olmstead et al, 1998; Vargas-Perez et al, 2007). …”

“…Accordingly, the PPTg has been suggested to be part of a DA-independent mechanism, likely involving its descending projections (Heinmiller et al, 2009), important for opioid reward in drug-naïve animals (Bechara et al, 1998; Nader et al, 1997; Ting-A-Kee and van der Kooy, 2012). Dorsal tegmental outputs become less important for opioid CPP and self-administration after opioid dependence and withdrawal while DA output becomes more important (Bechara and van der Kooy, 1989; Bechara et al, 1998; 1992; Laviolette and van der Kooy, 2001; Laviolette et al, 2004; Nader and van der Kooy; 1997; Nader et al, 1997; 1994; Vargas-Perez et al, 2009; 2007; Ting-A-Kee and van der Kooy, 2012). Importantly, the effects of LDTg lesions on opioid reward in drug-experienced animals have not been tested.…”

Blockade of muscarinic acetylcholine receptors in the ventral tegmental area prevents acquisition of food-rewarded operant responding in rats

“…PPN lesions have been shown to prevent the acquisition of conditioned place preference (CPP) to food, opiates, and amphetamine van der Kooy 1989, 1992;Franklin 1993, 1994), but failed to block the CPP effect after conditioning sessions van der Kooy 1989, 1992;Nader et al 1994). PPN lesions have also been shown to disrupt acquisition of a brain-stimulation maintained lever-pressing task; however, responding for self-stimulation was also impaired in animals lesioned after acquisition (Lepore and Franklin 1996).…”