Neonatal handling impairs intradimensional shift and alters plasticity markers in the medial prefrontal cortex of adult rats

2018 ◽  
Vol 197 ◽  
pp. 29-36
Author(s):  
Camilla Lazzaretti ◽  
Grasielle Clotildes Kincheski ◽  
Pablo Pandolfo ◽  
Rachel Krolow ◽  
Ana Paula Toniazzo ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Adult Rats ◽  
Neonatal Handling

scholarly journals ALTERATIONS IN THE MRNA EXPRESSION OF D2 DOPAMINE RECEPTOR SPLICE VARIANTS AS POSSIBLE MECHANISM OF PREFRONTAL DYSFUNCTION AFTER EARLY-LIFE IMMUNE CHALLENGE

2019 ◽  
Vol 19 (1S) ◽  
pp. 109-111
Author(s):  
A P Schwarz ◽  
A N Trofimov ◽  
A M Ischenko ◽  
O E Zubareva ◽  
V M Klimenko
Keyword(s):  
Prefrontal Cortex ◽  
Dopamine Receptor ◽  
Medial Prefrontal Cortex ◽  
Early Life ◽  
Splice Variants ◽  
Neuropsychiatric Symptoms ◽  
Developmental Expression ◽  
Immune Challenge ◽  
D2 Dopamine Receptor ◽  
Adult Rats

Various detrimental factors during early life may affect CNS development and increase risk of neuropsychiatric symptoms in later life. Disruption in brain dopaminergic system maturation is believed to be one of the mechanism of different neurodevelopmental disordrers. In this article we review behavioral peculiarities and changes of prefrontal D2 dopamine receptor splice variants (D2S and D2L) expression in rats after chronic experimental increase of proinflammatory cytokine interleukin(IL)-1β during 3rd week of life. Early life IL-1β treatment produce long lasting working memory deficit originating in juvenile adult animals. Elevation of IL-1β during 3rd week of life also affect developmental expression of D2 dopamine receptor mRNAs leading to increased D2S/D2L ratio in the medial prefrontal cortex of adolescent but not adult rats. Early life IL-1β treatment cancelled the learning-induced D2L mRNA downregulation during active avoidance conditioning in adult rats. Thus, dysregulation of expression of distinct D2 dopamine receptor splice variants within medial prefrontal cortex is supposed to be implicated in cognitive decline caused by early life immune challenge.

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