Developmental pathology, dopamine, stress and schizophrenia.
Psychological stress is a contributing factor for a wide variety of neuropsychiatric diseases including substance use disorders, anxiety, depression and schizophrenia. However, it has not been conclusively determined how stress augments the symptoms of these diseases. Here we review evidence that the ventral hippocampus may be a site of convergence whereby a number of seemingly discrete risk factors, including stress, may interact to precipitate psychosis in schizophrenia. Specifically, aberrant hippocampal activity has been demonstrated to underlie both the elevated dopamine neuron activity and associated behavioral hyperactivity to dopamine agonists in a verified animal model of schizophrenia. In addition, stress, psychostimulant drug use, prenatal infection and select genetic polymorphisms all appear to augment ventral hippocampal function that may therefore exaggerate or precipitate psychotic symptoms. Such information is critical for our understanding into the pathology of psychiatric disease with the ultimate aim being the development of more effective therapeutics.
Lodge
Daniel J
DJ
Department of Pharmacology & Center for Biomedical Neuroscience, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, MC 7764, San Antonio, TX 78229, USA. LodgeD@uthscsa.edu
Grace
Anthony A
AA
D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000196:embryology* / Q000254:growth & development* / Q000503:physiopathology*; D006801:Humans; D009474:Neurons / Q000502:physiology; D012559:Schizophrenia / Q000503:physiopathology*; D013315:Stress, Psychological; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D005680:gamma-Aminobutyric Acid; D004298:Dopamine