Synaptic plasticity and addiction

By J. Kauer, R. Malenka. Nature Reviews Neuroscience, 2007

1,365 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience

View Paper: https://www.semanticscholar.org/paper/0fca95aa265ea76ddab62a9631c378fa776ba0d3

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

Citations in the corpus

Alcoholism: a systems approach from molecular physiology to addictive behavior. (2009, background): “This is surprising in light of the fact that several other drugs of abuse act via glutamatergic input on the activity of midbrain DA neurons (148, 234) and, as such, clearly requires further research.”
Reward and aversion in a heterogeneous midbrain dopamine system (2013, background): “…on DA neurons projecting to the NAc medial shell but not synapses on DA neurons projecting to mPFC, as assayed by the ratio of AMPAR-mediated synaptic responses to NMDAR-mediated synaptic responses (see Kauer and Malenka, 2007 for discussion of the utility of this so-called AMPAR/NMDAR assay).”
Preventing Mental, Emotional, and Behavioral Disorders Among Young People: Progress and Possibilities (2009, background): “This exaggerated plasticity helps establish new, abnormal stimulus–response associations among the substance, the cues that accompany it, and the behavioral responses to those cues that define disorders of addiction (Kalivas and O’Brien, 2008; Kauer and Malenka, 2007).”
Neurocircuitry of Addiction (2009, background): “These dynamic changes may promote cellular excitation, which has been hypothesized to be an important substrate for sensitization and drug-related learning in the addictive state (Kauer and Malenka, 2007; Wolf et al, 2004).”
Memory engrams: Recalling the past and imagining the future (2020, background): “First, 1 day after training, hippocampal DG granule engram cells tagged during contextual fear conditioning showed greater synaptic strength [higher AMPA/NMDA ratio, which is a means of assessing basal strength of excitatory synapses by examining the relative expression of amino-3-hydroxy-5-methyl-4”
Dopamine signals for reward value and risk: basic and recent data (2010, background): “This burst response depends on the activation and plasticity of glutamatergic NMDA and AMPA receptors located on dopamine neurons [8-12].”
Addiction: Beyond dopamine reward circuitry (2011, background): “DA and Conditioning to Drug Cues The explanation may arise from the process of conditioning, which is one of the initial neuroadaptations that follow exposure to drugs and involves DA phasic signaling (predominantly D1Rs) and synaptic changes inNMDAandAMPA receptors (modulated by glutamate) (21, 22)”
Burst timing-dependent plasticity of NMDA receptor-mediated transmission in midbrain dopamine neurons: A putative cellular substrate for reward learning (2009, neutral): “Considering the important roles of these brain regions, in particular the nucleus accumbens, striatum and prefrontal cortices, in addiction (Day and Carelli, 2007; Everitt and Robbins, 2005; Hyman, 2005; Hyman et al., 2006a; Jones and Bonci, 2005; Kalivas and Volkow, 2005; Kauer and Malenka, 2007; M”
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling (2011, background): “…to addictive drugs and how these may contribute to addictionrelated behaviors in rodent models have been the subject of a number of recent reviews (Kauer and Malenka, 2007; Thomas et al., 2008; Russo et al., 2010; Kalivas et al., 2009; Schmidt and Pierce, 2010; Wolf and Ferrario, 2010; Bowers et…”
Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli (2011, positive): “This conclusion is based on the assumption that increases in the AMPAR/NMDAR ratio correlate with a net increase in synaptic strength (Ungless et al., 2001; Kauer and Malenka, 2007) and that this drives increased spiking activity in the DA cell subpopulation in vivo.”