The GPR88 orphan G protein‐coupled receptor is expressed throughout the striatum, being preferentially localized in medium spiny neurons. It is also present in lower densities in frontal cortex and thalamus. Rare mutations in humans suggest a role in cognition and motor function, while common variants are associated with psychosis. Here we evaluate the influence of genetic deletion of GPR88 upon performance

Many neurodegenerative and neuropsychiatric diseases and other brain disorders are accompanied by impairments in high‐level cognitive functions including memory, attention, motivation, and decision‐making. Despite several decades of extensive research, neuroscience is little closer to discovering new treatments. Key impediments include the absence of validated and robust cognitive assessment tools

In the original publication of the article by Mineur et al. [1], the surname of the second was misspelled. The name of the second author should be Charlotte Ernstsen. This has since then be amended in the online version of the article.

Wellbeing, a key aspect of mental health, is moderately heritable with varying estimates reported from independent studies employing a variety of instruments. Recent genome‐wide association studies (GWAS) have enabled the construction of polygenic scores (PGS) for wellbeing, providing the opportunity for direct comparisons of the variance explained by PGS for different instruments commonly employed

Understanding the rules that govern neuronal dynamics throughout the brain to subserve behavior and cognition remains one of the biggest challenges in neuroscience research. Recent technical advances enable the recording of increasingly larger neuronal populations to produce increasingly more sophisticated datasets. Despite bold and important open‐science and data‐sharing policies, these datasets tend

Tryptophan hydroxylase‐1 (TPH1) is the rate‐limiting enzyme in serotonin biosynthesis, and allelic variations at the TPH1 locus have been implicated in the pathophysiology of depression. Using 1.5‐Tesla functional magnetic resonance imaging, we investigated the possible relationship between TPH1 A218C polymorphism and amygdala response to negative facial stimuli in twenty‐six right‐handed female subjects