title: Behavioral changes after maternal separation are reversed by chronic constant light treatment.
abstract: BACKGROUND
  Rats subjected to maternal separation display behavioral alterations (e.g. increased immobility in the forced swim test) and molecular changes (e.g. in growth factors and related signal transduction proteins). Light treatment has previously been shown to have antidepressant effects in rat models of depression, but has not been studied in a rodent model of maternal separation.
  
  
  METHODS
  This study focused on maternally separated rat pups. The aim of this study was to compare the effects of chronic constant light exposure during adolescence with the selective serotonin reuptake inhibitor (SSRI), escitalopram. Behavioral changes (exploratory activity in the open field and elevated plus maze, 22 kHz ultrasonic vocalizations, immobility in the forced swim test) and molecular changes (brain-derived neurotrophic factor (BDNF), mitogen-activated protein kinase phosphatase-1 (MKP-1) in the ventral hippocampus, and mu-opioid receptors in the nucleus accumbens) were measured.
  
  
  RESULTS
  Animals that had been subjected to maternal separation displayed an increased number and duration of 22 kHz vocalizations, increased immobility in the forced swim test, increased hippocampal BDNF, and decreased mu-opioid receptor levels in the nucleus accumbens in adulthood compared to controls. MKP-1 levels in the ventral hippocampus were not affected. After chronic light treatment, there was normalization of ultrasonic vocalizations, immobility on the forced swim test, and mu-opioid receptor levels in the nucleus accumbens. Chronic saline treatment reduced anxiety-like behavior and immobility in the forced swim test. Escitalopram did not have any significant effect in this rat model of depression.
  
  
  CONCLUSIONS
  Chronic constant light treatment reversed a number of the behavioral and molecular effects of maternal separation. Light-induced up-regulation of mu-opioid receptors in the nucleus accumbens may play a key role in mediating such effects.
authors.affiliation: Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Observatory, Cape Town 7925, South Africa. jacqueline.dimatelis@uct.ac.za
authors.forename: J J
authors.initials: JJ
authors.lastname: Dimatelis
authors.forename: D J
authors.initials: DJ
authors.lastname: Stein
authors.forename: V A
authors.initials: VA
authors.lastname: Russell
mesh_terms: D000818:Animals; D000928:Antidepressive Agents / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D015283:Citalopram / Q000494:pharmacology; D003866:Depressive Disorder / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D054638:Dual Specificity Phosphatase 1 / Q000378:metabolism; D005260:Female; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism*; D008029:Lighting; D008297:Male; D008426:Maternal Deprivation; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009714:Nucleus Accumbens / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000378:metabolism; D013550:Swimming
chemical_list: D000928:Antidepressive Agents; D019208:Brain-Derived Neurotrophic Factor; D017450:Receptors, Opioid, mu; D015283:Citalopram; D054638:Dual Specificity Phosphatase 1