Matthew Wilkinson

TL;DR: This work used chromatin immunoprecipitation coupled with promoter microarray analysis to characterize genome-wide chromatin changes in the mouse nucleus accumbens, a crucial brain reward region, after repeated cocaine administration, and reveals several interesting principles of gene regulation by cocaine.

TL;DR: It is shown that chronic social defeat stress significantly increased the in vivo spontaneous firing rates and bursting events in susceptible mice but not in the resilient subgroup, and that the firing patterns of mesolimbic dopamine neurons in vivo mediate an individual's responses to chronic stress and antidepressant action.

TL;DR: It is found that plant phenological and physiological properties can be integrated in a robust index—the product of the length of CO2 uptake period and the seasonal maximal photosynthesis—to explain the GPP variability over space and time in response to climate extremes and during recovery after disturbance.

TL;DR: A direct role is established for NFκB pathways in the NAc to regulate structural and behavioral plasticity to cocaine and the ability of previous cocaine exposure to increase an animal's preference for cocaine.

TL;DR: The results demonstrate that chronic defeat stress causes widespread and long-lasting changes in gene regulation, including alterations in repressive histone methylation and in phospho-CREB (cAMP response element-binding protein) binding, in the mouse nucleus accumbens (NAc), a key brain reward region implicated in depression.