title: Nardostachys jatamansi Targets BDNF-TrkB to Alleviate Ketamine-Induced Schizophrenia-Like Symptoms in Rats.
abstract: OBJECTIVE
  Schizophrenia, a common neurological disorder appearing in the late teens or early adulthood, is characterized by disorganized thinking, behaviour, and perception of emotions. Aberrant N-methyl-D-aspartate (NMDA) receptor-mediated synaptic plasticity is a major pathological event here due to dysfunction of dopamine and glutamate transmission at NMDA receptors. De-regulated brain-derived neurotrophic factor (BDNF), i.e., its signalling through the tropomyosin receptor kinase B (TrkB) receptor, is a major feature of schizophrenia. With recent global awareness of traditional plant medicines in reducing side effects, the aim of our study was to evaluate the efficacy of the ethanolic root extract of a herb belonging to the Valerianacea family, Nardostachys jatamansi, against ketamine-induced schizophrenia-like model in rats.
  
  
  METHODS
  The effect of the N. jatamansi drug (oral dosage of 500 mg/kg body weight for 14 days) in ketamine-administered male Wistar albino rats (30 mg/kg body weight for 5 days) on modulating behaviour and the level of neurotransmitters like dopamine and glutamate was studied in whole-brain homogenates, and its influence on BDNF and TrkB levels in 2 relevant brain regions, the hippocampus and prefrontal cortex, was assessed.
  
  
  RESULTS
  We observed that N. jatamansi treatment exhibited encouraging results in the modulation of ketamine-induced schizophrenia-like behaviours, principally the positive symptoms. Our drug both significantly upregulated the glutamate level and downregulated the dopamine level in whole-brain homogenates and retained the normal levels of BDNF (in the hippocampus but not in the prefrontal cortex) and TrkB (in both hippocampus and prefrontal cortex) induced by ketamine in rats.
  
  
  CONCLUSIONS
  These findings suggest a neuroprotective effect of the ethanolic root extract of N. jatamansi against ketamine-induced schizophrenia-like symptoms in rats; possibly, regarding its effect on TrkB signalling. Further research is warranted in the treatment of schizophrenic symptoms.
authors.affiliation: Department of Biochemistry, University of Madras, Chennai, India.
authors.forename: Anjali
authors.initials: A
authors.lastname: Janardhanan
authors.forename: Anjana
authors.initials: A
authors.lastname: Sadanand
authors.forename: Arambakkam Janardhanam
authors.initials: AJ
authors.lastname: Vanisree
mesh_terms: D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000378:metabolism; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D007649:Ketamine; D008297:Male; D032404:Nardostachys / Q000737:chemistry*; D008517:Phytotherapy / Q000379:methods*; D010936:Plant Extracts / Q000737:chemistry / Q000627:therapeutic use*; D018517:Plant Roots / Q000737:chemistry; D051381:Rats; D020813:Receptor, trkB / Q000378:metabolism*; D012559:Schizophrenia / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D010936:Plant Extracts; D018698:Glutamic Acid; D007649:Ketamine; D020813:Receptor, trkB; D004298:Dopamine