The Circuitry Mediating Cocaine-Induced Reinstatement of Drug-Seeking Behavior

By K. McFarland, Peter W. Kalivas. Journal of Neuroscience, 2001

914 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/471d465e3b760f2c735cb3998066702e05eb0d80

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Peter W. Kalivas
2. G. Koob
3. Nora D. Volkow
4. Barry J. Everitt
5. Kent C. Berridge
6. Y. Shaham
7. M. Le Moal
8. J. Steketee

In Cognitive Neuroscience

1. Peter W. Kalivas
2. G. Koob
3. Nora D. Volkow
4. Barry J. Everitt
5. Y. Shaham
6. J. Steketee
7. J. Peters
8. M. Wolf

Citations in the corpus

• Neurobiology of Relapse to Heroin and Cocaine Seeking: A Review (2002, background): “In agreement with this idea, McFarland and Kalivas (2001) recently found that infusions of fluphenazine into the medial prefrontal cortex (mPFC) attenuate cocaine-induced reinstatement.”
• Drug Wanting: Behavioral Sensitization and Relapse to Drug-Seeking Behavior (2011, background): “For example, ibotenate lesions of the mPFC, which encompasses both the prelimbic and infralimbic regions, disrupted the induction of sensitization to cocaine and amphetamine (Wolf et al., 1995; Cador et al., 1999; Li et al., 1999).”
• Psychomotor Stimulant Addiction: A Neural Systems Perspective (2002, background): “1) was established, and the medial PFC, not the striatum, was identified as the primary site at which DA receptor blockade prevented the relapse-inducing effects of cocaine (McFarland and Kalivas, 2001).”
• Drug Addiction as a Pathology of Staged Neuroplasticity (2008, background): “Thus, extinction training engages brain regions involved in more declarative and emotional processing in drug-seeking behavior (McFarland and Kalivas, 2001; See, 2002; McFarland et al, 2004), implying the assertion of executive behavioral modulation.”
• Neurocircuitry of Addiction (2009, background): “Much evidence from animal studies suggests that druginduced reinstatement is localized to the medial prefrontal cortex/nucleus accumbens/ventral pallidum circuit mediated by the neurotransmitter glutamate (McFarland and Kalivas, 2001).”
• The neural basis of addiction: a pathology of motivation and choice. (2005, methodology): “For example, cue-primed drug seeking requires involvement of the basolateral amygdala (66–68), while stress- and drug-primed drug seeking do not (29, 55, 69).”
• The reinstatement model of drug relapse: history, methodology and major findings (2003, background): “On the other hand, McFarland and Kalivas (2001) found that reversible inactivation of the NAc core, but not shell, blocks cocaine-induced reinstatement.”
• Brain circuitry and the reinstatement of cocaine-seeking behavior (2003, background): “In contrast to cue-primed reinstatement, inactivation of neither the basolateral nor central amygdala nuclei inhibited cocaine-primed reinstatement (Grimm and See 2000; McFarland and Kalivas 2001).”
• Prefrontal Glutamate Release into the Core of the Nucleus Accumbens Mediates Cocaine-Induced Reinstatement of Drug-Seeking Behavior (2003, background): “…drug-seeking behavior, because transient inhibition of the PFCd with GABA agonists or TTX prevent cocaine-, stress-, and cue-primed reinstatement (McFarland and Kalivas, 2001; Capriles et al., 2002; McLaughlin and See, 2003), and the microinjection of either cocaine or dopamine into the PFCd…”
• Addiction and the brain antireward system. (2008, background): “Most evidence from animal studies suggests that drug-induced reinstatement is by the medial prefrontal cortex/nucleus accumbens/glutamatergic circuit modulated by dopamine in the frontal cortex (McFarland & Kalivas 2001).”
• Extinction circuits for fear and addiction overlap in prefrontal cortex. (2009, methodology): “…be critical for cocaine relapse, triggered by multiple forms of relapse-inducing stimuli, including cocaine-paired cues, cocaine itself, and stress (McFarland and Kalivas 2001; Capriles et al. 2003; McLaughlin and See 2003; McFarland et al. 2004; Di Pietro et al. 2006; but see Di Ciano et al.…”
• Neuroadaptations in cystine-glutamate exchange underlie cocaine relapse (2003, background): “, and a variety of data indicate that corticolimbic circuitry, including the glutamatergic projection from the prefrontal cortex to the nucleus accumbens, mediates reinstatement in experimental animals and craving in cocaine addict”