Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons

By Mark A. Ungless, Jennifer L. Whistler, R. Malenka, A. Bonci. Nature, 2001

1,135 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/906fc16253279d7033498e40a388b125eba690e9

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Citations in the corpus

NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012, background): “For example, a single dose of a drug of abuse such as cocaine enhances excitatory transmission onto dopamine neurons of the ventral tegmental area (Ungless et al. 2001).”
Burst timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons: A putative cellular substrate for reward learning (2009, positive): “classical and experience-dependent synaptic plasticity in midbrain DA neurons (Bellone and Luscher, 2006; Bonci and Malenka, 1999; Chen et al., 2008; Hyman et al., 2006; Kauer, 2004; Liu et al., 2005; Mameli et al., 2007; Pu et al., 2006; Saal et al., 2003; Stuber et al., 2008; Thomas and Malenka, 2”
Alcoholism: a systems approach from molecular physiology to addictive behavior. (2009, background): “Some key publications on druginduced adaptations in the mesolimbic system have revealed that glutamatergic synapses on DA neurons in the VTA, in particular, undergo plastic changes following administration of drugs of abuse including ethanol (414, 501).”
The reinstatement model of drug relapse: history, methodology and major findings (2003, background): “For example, cocaine can induce LTP in the VTA (Ungless et al. 2001) and LTD in the NAc (Thomas et al. 2001).”
Drug Wanting: Behavioral Sensitization and Relapse to Drug-Seeking Behavior (2011, background): “…1993) as a result of decreased autoreceptor sensitivity (White and Wang, 1984; Henry et al., 1989), which can act on D1 receptors to enhance glutamate release from mPFC projecting neurons and to induce LTP in dopamine neurons (Kalivas and Duffy, 1995; Ungless et al., 2001; Saal et al., 2003).”
Psychomotor Stimulant Addiction: A Neural Systems Perspective (2002, background): “A transient increase in excitatory drive to VTA DA neurons occurs shortly after discontinuing stimulant administration (for review, see Wolf, 1998), suggesting that plasticity at synapses between glutamatergic afferents and VTA DA neurons is responsible for driving downstream changes related to sens”
Adolescent cortical development: a critical period of vulnerability for addiction. (2007, background): “This plasticity was also demonstrated in other limbic regions that are believed to be involved in drug addiction, including amygdala (Ungless et al., 2001), VTA (Thomas et al.”
Reward and aversion in a heterogeneous midbrain dopamine system (2013, background): “Thus, it is not surprising that an important research topic over the last decade has been to elucidate how motivational stimuli, stress, and drugs of abuse induce adaptations of VTA DA neuron excitatory inputs, which drive spiking of VTA DA neurons (Argilli et al., 2008; Bellone and Luscher, 2006; B”
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling (2011, background): “This conclusion is based on the observations that systemic administration of an NMDAR antagonist blocks the plasticity (Ungless et al., 2001), as does ablation of the critical NMDAR subunit NR1 selectively in DA neurons (Engblom et al.”
Addiction and the brain antireward system. (2008, background): “59 :2 9- 53 .”