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Reinforcement: Neurochemical Substrates
2015, International Encyclopedia of the Social & Behavioral Sciences: Second EditionDisruption of endogenous opioid activity during instrumental learning enhances habit acquisition
2009, NeuroscienceCitation Excerpt :Although it has long been thought that the endogenous opioid system is important for hedonic tone (Narayanan et al., 2004; Skoubis et al., 2005), here we show that opioid processes are critical for the acquisition of normal goal-directed control of actions. Indeed, blockade of opioid receptors acutely has previously been shown to negatively impact sucrose (Cleary et al., 1996) and self-stimulation (Trujillo et al., 1989) reward in progressive ratio tests. Similarly, mu opioid receptor (Papaleo et al., 2007), beta-endorphin- and enkephalin-knockout mice also show reduced responding for a food reward on a progressive ratio schedule (Hayward et al., 2002).
Excitability and gap junction-mediated mechanisms in nucleus accumbens regulate self-stimulation reward in rats
2009, NeuroscienceCitation Excerpt :Two studies used these antagonists but they were injected intraperitoneally, and thus the effects observed in these studies were attributed to the blockade of peripheral and central opiate receptors. Like in our study, these experiments demonstrated that blockade of opiate receptors results in less self-stimulation (Trujillo et al., 1989a,b). The dopaminergic innervation of the Acb from the ventral tegmental area is an important modulator of the activity in the Acb, and of interest is the dopaminergic modulation of GJC in the striatum, and other brain areas as well (Cepeda et al., 1989; O'Donnell and Grace, 1993; Perez Velazquez et al., 1997).
Biological substrates of reward and aversion: A nucleus accumbens activity hypothesis
2009, NeuropharmacologyCitation Excerpt :The combination of these findings suggests that while dopamine may contribute to reward-related inhibition of NAc firing, there must be other factors that can drive it as well. Although there has been much less investigation of other potential contributors, additional candidates include the release of acetylcholine and the activation of μ-opioid receptors in the NAc, both of which have been shown to occur under rewarding conditions (Trujillo et al., 1989; West and Wise, 1988; Mark et al., 1992; Imperato et al., 1992; Guix et al., 1992; Bodnar et al., 1995; Kelley et al., 1996) and both of which have the ability to inhibit NAc firing (McCarthy et al., 1977; Hakan and Henriksen, 1989; de Rover et al., 2002). Another newer line of electrophysiological evidence supporting the inhibition–reward hypothesis comes from experiments in which molecular approaches have been used to manipulate the excitable properties of NAc neurons.
Effect of naltrexone during extinction of alcohol-reinforced responding and during repeated cue-conditioned reinstatement sessions in a cue exposure style treatment
2008, AlcoholCitation Excerpt :First, the literature indicates that rats are able to maintain considerable rates of responding for food or fluid after naloxone or NTX doses as high as 30 mg/kg (Sanger and McCarthy, 1982; Schindler et al., 1990; Williams, 2007). In rats responding for electrical brain stimulation, latency to respond was also unaffected by naloxone or NTX doses as high as 20 mg/kg (Trujillo et al., 1989a; 1989b). Second, a direct measurement of ambulatory activity alone shows no effect of naloxone doses up to 10 mg/kg (Timar et al., 2005) and NTX 30 mg/kg has conflicting effects where horizontal activity is reduced but a measure of ambulatory activity is unaffected (Schaefer and Michael, 1985).
Effects of naloxone on rewarding and aversive brain sites
2003, Behavioural Brain Research
A preliminary report of this work was presented at the 1984 Society for Neuroscience Meeting in Anaheim, California72.