@misc{kruyer_parilla-carerro_powell_brandt_gutwinski_angelis_chalhoub_amato_2020, 
  title={Accumbens D2-MSN hyperactivity drives behavioral supersensitivity}, 
  DOI={10.1101/2020.11.12.380667}, 
  abstractNote={<jats:p>Antipsychotic-induced behavioral supersensitivity is a problematic consequence of long-term treatment with antipsychotic drugs and is characterized by emergence of refractory symptoms and dyskinesias. The underlying mechanisms are unknown, and no rational approaches exist to prevent or reverse antipsychotic-induced supersensitivity. Here we describe major adaptations impacting populations of striatal medium spiny neurons (MSNs) during the development of behavioral supersensitivity and reveal a prominent role played by D2 receptor expressing MSNs. We show that enhanced D2-MSN activity underlies several symptoms spanning from psychostimulant sensitization, to antipsychotic treatment resistance and drug addiction. Our data warn against severe adverse events following antipsychotic treatment discontinuation and offer insight that may inform therapeutic approaches to overcome antipsychotic-induced supersensitivity.</jats:p>}, 
  publisher={Cold Spring Harbor Laboratory}, 
  author={Kruyer, Anna and Parilla-Carerro, Jeffrey and Powell, Courtney and Brandt, Lasse and Gutwinski, Stefan and Angelis, Ariana and Chalhoub, Reda and Amato, Davide}, 
  year={2020}, 
  month={Nov}
  }