{'fraction_non_alphanumeric': 0.020209059233449476, 'fraction_numerical': 0.017421602787456445, 'mean_word_length': 5.410714285714286, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
The expression of genes involved in glucose metabolism is affected by N‐methyl‐D‐aspartate receptor antagonism: A putative link between metabolism and an animal model of psychosis

Psychosis has been associated with glucose metabolism impairment. Here, we explored the gene expression of hexokinase 1 (Hk1) and glucose transporter 3 (GLUT3) after the administration of a subanesthetic or a subconvulsant dose of ketamine in rats, considered to provide an animal model of psychosis. Indeed, Hk1 and GLUT3 are crucially involved in the glucose utilization in brain tissues and have also been implicated in the pathophysiology of psychosis. Quantitative brain imaging of transcripts was used to evaluate Hk1 and GLUT3 mRNA in rat brain regions related to ketamine‐induced behavioral abnormalities. Hk1 transcript was significantly increased by 50 mg/kg ketamine in cortical and subcortical areas, whereas 12 mg/kg ketamine affected Hk1 expression in the auditory cortex only. GLUT3 expression was increased by 12 mg/kg ketamine in the frontal cortex and decreased by 50 mg/kg ketamine in subcortical areas. The results show that Hk1 and GLUT3 are extensively and differentially affected by ketamine dose, supporting the view that glucose metabolism and psychosis may be causally related and suggesting that these molecules may play a role in the pathophysiology of ketamine‐induced behavioral abnormalities. © 2012 Wiley Periodicals, Inc.