Dopamine release and metabolism in nucleus accumbens and striatum of morphine-tolerant and nontolerant rats
References (29)
- et al.
Persistence of chronic morphine effects upon activity in rats 8 months after ceasing the treatment
Neuropharmacology
(1975) - et al.
Long-term sensitization to the excitatory effects of morphine
Neuropharmacology
(1983) - et al.
Morphine-induced activation of A10 neurons in the rat
Brain Res.
(1983) - et al.
Interactions between ibogaine, a potential anti-addictive agent, and morphine: An in vivo microdialysis study
Eur. J. Pharmacol.
(1991) - et al.
Acute and prolonged effects of ibogaine on brain dopamine metabolism and morphine-induced locomotor activity in rats
Brain Res.
(1992) - et al.
Differential effect of morphine on dopaminergic neurons in frontal cortex and striatum of the rat
Life Sci.
(1976) - et al.
The effects of low doses of morphine on the activity of dopamine containing cells and on behavior
Life Sci.
(1982) - et al.
Conditioning and place-specific sensitization of increases in activity induced by morphine in the VTA
Pharmacol. Biochem. Behav.
(1984) - et al.
Regional rat brain levels of 3,4-dihydroxyphenylacetic acid and homovanillic acid: Concurrent fluorimetric measurement and influence of drugs
Eur. J. Pharmacol.
(1976) The role of reward pathways in the development of drug dependence
Pharmacol. Ther.
(1987)
Depression of mesolimbic dopamine transmission and sensitization to morphine during opiate abstinence
J. Neurochem.
Time-dose relationships for locomotor activity effects of morphine after acute or repeated treatments
Br. J. Pharmacol.
Inhibition of the development of tolerance to morphine in rats by drugs which inhibit ribonucleic acid or protein synthesis
Br. J. Pharmacol.
Opposite effects of mu and kappa opiate agonists on dopamine release in the nucleus accumbens and in the dorsal caudate of freely moving rats
J. Pharmacol. Exp. Ther.
Cited by (36)
Normalization of the H3K9me2/H3K14ac-ΔFosB pathway in the nucleus accumbens underlying the reversal of morphine-induced behavioural and synaptic plasticity by Compound 511
2023, PhytomedicineCitation Excerpt :Here, we employed two animal models of drug addiction, sensitization, and reinstatement, both of which were useful for assessing the impact of repeated drug exposure on neural function (Steketee and Kalivas, 2011). Consistent with shared increases in dopaminergic activity in the NAc, acute exposure to psychostimulants, opiates, and other abused substances causes a rapid increase in locomotor activity in rodents (Johnson and Glick, 1993; Kalivas and Duffy, 1990; Paulson and Robinson, 1995). It is noteworthy that Compound 511 failed to elicit any increase in spontaneous locomotor activity in the current study, which indicated that Compound 511 hardly caused an increase in dopamine release.
Captopril and losartan attenuate behavioural sensitization in mice chronically exposed to toluene
2022, Behavioural Brain ResearchCitation Excerpt :Systemic morphine-pretreated animals show enhanced locomotor activity after intra-accumbens administration of amphetamine or cocaine [76]. Moreover, long-term amphetamine, cocaine and morphine withdrawal (10–14 days) increases DA levels in the NAc [77–79]. In the present study, the Ang-(1–7)/Ang II ratio was significantly decreased in PFCx after toluene repeated-exposure (Fig. 4), but not in mice with a history of toluene exposure and treated with saline (Figs. 5 and 6), where animals were in a solvent-free period.
Sex differences in the discriminative stimulus characteristics of a morphine occasion setter in rats
2021, Pharmacology Biochemistry and BehaviorCitation Excerpt :Again, our plan to follow up while assessing estrous phase may provide additional insight into this intriguing pattern in sex differences. Another possible mechanism underlying these differences may involve sex-specific dopaminergic function, wherein females show enhanced striatal dopaminergic activity compared to males when mu-opioid receptor mediated increases in striatal dopamine release is induced by opioid administration (Johnson and Glick, 1993; Kalivas and Duffy, 1987; Manzanedo et al., 1999; Piepponen et al., 1999), so monitoring dopamine release during test trials should also be conducted. Finally, generalized behavioural activation could be reflected in both chamber activity as well as nose-pokes for sucrose.
Abuse potential and toxicity of the synthetic cathinones (i.e., “Bath salts”)
2020, Neuroscience and Biobehavioral ReviewsCitation Excerpt :It is often used as a surrogate for psychostimulants’ rewarding effects and abuse potential (Kalivas and Weber, 1988; Pierce and Kalivas, 1997), given the relationship of behavioral sensitization to striatal activity and elevated brain amines (primarily DA) in this area and the relationship of activity in this area to the incentive and motivational properties of drugs of abuse (see Robinson and Berridge, 2008). Interestingly, several studies suggest that enhanced DA transmission in the striatum and nucleus accumbens is associated with locomotor sensitization (Johnson and Glick, 1993; Kalivas and Duffy, 1990; Parsons and Justice, 1993; Robinson et al., 1988; Shoaib et al., 1994) and direct evidence for DA’s role in behavioral sensitization action comes from the fact that mice lacking DAT or D1 receptors fail to develop cocaine sensitization (Kelly et al., 2008; Mead et al., 2002; Morice et al., 2010; Xu et al., 1994; Yao et al., 2004). The relationship between the neurochemical consequences and the motor stimulating effects of synthetic cathinones has been investigated widely (see Table 1), but only a few studies have focused on behavioral sensitization with these compounds.
Reversal of oxycodone and hydrocodone tolerance by diazepam
2017, Brain ResearchCitation Excerpt :It has been theorized that both benzodiazepines and opioids produce a hyperpolarization of GABA interneurons which causes a reduction in the release of GABA which results in the disinhibition of dopaminergic neurons and an increase in extracellular dopamine in areas such as the striatum (Tan et al., 2011). The phenomenon of opioid-induced locomotion is due to mu opioid receptor-mediated increases in striatal dopamine (DA) release (Johnson and Glick, 1993; Kalivas and Duffy, 1987; Piepponen et al., 1999). GABAergic interneurons also play an important role in opioid antinociception (Lau et al., 2014).