Morphological reorganization after repeated corticosterone administration in the hippocampus, nucleus accumbens and amygdala in the rat.
Elevated levels of corticosteroids and stress play key roles in the pathophysiology of affective disorders. Corticosterone (CORT)-treated rats have emerged as a pharmacological model of depression-like behaviors. Previous studies have shown that CORT administration induces neuronal atrophy in the CA3 subfield of the hippocampus and laminae II/III of the prefrontal cortex. However, little attention has been given to other limbic structures such as the amygdala and the nucleus accumbens (NAcc). We investigated here whether 3 weeks of CORT administration in rats causes dendritic remodeling and spine density reorganization in the basolateral amygdala and pyramidal neurons of the CA1 subfield of the hippocampus as well as in spiny medium neurons of NAcc. Quantitative morphological analysis revealed retracted neuronal arborizations and modified configuration of length depending on branch order in medium spiny neurons of the NAcc of CORT-treated animals. Moreover, distal dendritic sections of the NAcc showed massive reductions in the number of spines caused by the CORT treatment. This treatment also induced a reduction in total dendritic length specific to fourth and sixth branch orders of pyramidal CA1 hippocampal neurons. These neurons also showed decreased branching and diminished number of spines. Finally, pyramidal neurons of the basolateral amygdala were apparently not significantly affected by the CORT treatment. Taken together, these data show for the first time neuronal morphological alterations in the NAcc in the CORT model of depression-like behaviors. Our results also add further information about the morphological reorganization occurring in CORT-sensitive regions of the limbic system.
Morales-Medina
Julio César
JC
Dept of Neurology & Neurosurgery, McGill University, Montréal, QC, Canada.
Sanchez
Fremioht
F
Flores
Gonzalo
G
Dumont
Yvan
Y
Quirion
Rémi
R
D000679:Amygdala / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000378:metabolism / Q000633:toxicity; D048430:Cell Shape / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000378:metabolism / Q000633:toxicity*; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D049229:Dendritic Spines / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008032:Limbic System / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D009714:Nucleus Accumbens / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D017966:Pyramidal Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining; D013315:Stress, Psychological / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology
D000893:Anti-Inflammatory Agents; D003345:Corticosterone