Cyclic Adenosine Monophosphate–Independent Tyrosine Phosphorylation of NR2B Mediates Cocaine-Induced Extracellular Signal-Regulated Kinase Activation

TL;DR: The role of the DA system in drug addiction and food motivation is focused on, with an overview of the role of D1 and D2 receptors in the control of reward-associated behaviors.

TL;DR: These findings establish synaptic potentiation selectively in D1R-MSNs as a mechanism underlying a core component of addiction, probably by creating an imbalance between distinct populations of MSNs in the nucleus accumbens, and provide proof of principle that reversal of cocaine-evoked synaptic plasticity can treat behavioural alterations caused by addictive drugs.

TL;DR: The emergence of a circuit model for addiction will open the door for novel therapies, such as deep brain stimulation, and to establish links of causality with drug-adaptive behaviors.

TL;DR: In the striatum, dopamine D1 receptors are preferentially expressed in striatonigral neurons, and increase the neuronal excitability, leading to the increase in GABAergic inhibitory output to substantia nigra pars reticulata.

TL;DR: Progress in identifying candidate mechanisms of addiction is reviewed, including molecular and cellular mechanisms that underlie long-term associative memories in several forebrain circuits (involving the ventral and dorsal striatum and prefrontal cortex) that receive input from midbrain dopamine neurons.

TL;DR: A large-scale screen is described to create an atlas of CNS gene expression at the cellular level, and to provide a library of verified bacterial artificial chromosome vectors and transgenic mouse lines that offer experimental access to CNS regions, cell classes and pathways.

TL;DR: There has been considerable progress in identifying the mechanisms that contribute to long-lived neural and behavioural plasticity related to addiction, including drug-induced changes in gene transcription, in RNA and protein processing, and in synaptic structure.

TL;DR: It is found that application of amyloid-β promoted endocytosis of NMDA receptors in cortical neurons, indicating a new mechanism by which amyloids-β can cause synaptic dysfunction and contribute to Alzheimer disease pathology.