Abstract

Mood disorders affect the lives and functioning of millions each year. Epidemiological studies indicate that childhood trauma is predominantly associated with higher rates of both mood and anxiety disorders. Exposure of rats to stress during juvenility (JS) (27–29 days of age) has comparable effects and was suggested as a model of induced predisposition for these disorders. The importance of the environment in the regulation of brain, behavior and physiology has long been recognized in biological, social and medical sciences. Here, we studied the effects of JS on emotional and cognitive aspects of depressive-like behavior in adulthood, on Hypothalamic-Pituitary-Adrenal (HPA) axis reactivity and on the expression of cell adhesion molecule L1 (L1-CAM). Furthermore, we combined it with the examination of potential reversibility by enriched environment (EE) of JS – induced disturbances of emotional and cognitive aspects of behavior in adulthood. Three groups were tested: Juvenile Stress –subjected to Juvenile stress; Enriched Environment – subjected to Juvenile stress and then, from day 30 on to EE; and Naïves. In adulthood, coping and stress responses were examined using the elevated plus-maze, open field, novel setting exploration and two way shuttle avoidance learning. We found that, JS rats showed anxiety- and depressive-like behaviors in adulthood, altered HPA axis activity and altered L1-CAM expression. Increased expression of L1-CAM was evident among JS rats in the basolateral amygdala (BLA) and Thalamus (TL). Furthermore, we found that EE could reverse most of the effects of Juvenile stress, both at the behavioral, endocrine and at the biochemical levels. The interaction between JS and EE resulted in an increased expression of L1-CAM in dorsal cornu ammonis (CA) area 1 (dCA1).

Highlights

  • Mood disorders affect the lives and functioning of millions each year

  • Cognitive deficits progressively emerging with development are the results of complex interactions between genetic and environmental factors [55,56,57], and evidence suggests that EE experience can attenuate or reverse a variety of cognitive deficits [58]

  • JS rats showed anxiety- and depressive-like behaviors in adulthood, altered HPA axis activity and L1-cell adhesion molecules (CAMs) expression pattern through limbic system areas and the thalamus

Read more

Summary

Introduction

Mood disorders affect the lives and functioning of millions each year. A greater understanding of the neural circuits underlying mood in both normal and abnormal affective states has been identified as one of the critical needs in the field of mood disorders research [1]. We studied the effects of stress during juvenility (JS) (27–29 days of age) on emotional and cognitive aspects of depressive-like behavior in adulthood, on HPA axis reactivity and on the expression of L1-CAM. Alterations in expression level of L1-CAM was checked in the prefrontal cortex (PFC), basolateral amygdala (BLA), dorsal cornu ammonis (CA) area 1 (dCA1) and thalamus (TL) This areas were chosen because they share extensive anatomic connections [51] and found to be affected by early life stress [52,53,54]. EE could reverse most of the effects of JS, at the behavioral, endocrine and at the biochemical levels

Results
Discussion
Methods
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.