Repeated restraint stress-induced atrophy of glutamatergic pyramidal neurons and decreases in glutamatergic efflux in the rat amygdala are prevented by the antidepressant agomelatine
Autor: | Lawrence P. Reagan, A.L. Bumgardner, C. Gabriel, M. Risher, E. Mocaër, Jim R. Fadel, A. Hang, Victoria A. Macht, Claudia A. Grillo, Gerardo G. Piroli |
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Rok vydání: | 2015 |
Předmět: |
Male
Restraint Physical Glutamic Acid Amygdala Rats Sprague-Dawley Glutamatergic Neurochemical Acetamides Neuroplasticity medicine Animals Agomelatine Depressive Disorder Neuronal Plasticity Basolateral Nuclear Complex Pyramidal Cells General Neuroscience Central nucleus of the amygdala Glutamate receptor food and beverages Dendrites Antidepressive Agents Disease Models Animal medicine.anatomical_structure Atrophy Corticosterone Psychology Neuroscience Stress Psychological medicine.drug Basolateral amygdala |
Zdroj: | Neuroscience. 284:430-443 |
ISSN: | 0306-4522 |
DOI: | 10.1016/j.neuroscience.2014.09.047 |
Popis: | Major depressive illness is among the most prevalent neuropsychiatric disorders and is associated with neuroplasticity deficits in limbic structures such as the amygdala. Since exposure to stressful life events is proposed to contribute to depressive illness, our recent studies examined the effects of stress on amygdalar neuroplasticity. These studies determined that repeated stress elicits deficits in glutamatergic activity in the amygdala, neuroplasticity deficits that can be prevented by some but not all antidepressants. In view of these observations, the goal of the current study was to determine the effects of repeated restraint stress (RRS) on the dendritic architecture of pyramidal neurons in the rat basolateral nucleus of the amygdala (CBL), as well as glutamate efflux in the CBL and central nucleus of the amygdala (CMX) via in vivo microdialysis. We also examined the ability of the antidepressant agomelatine to prevent RRS-induced neuroplasticity deficits. Compared with control rats, rats subjected to RRS exhibited atrophy of CBL pyramidal neurons, including decreases in total dendritic length, branch points, and dendritic complexity index. In addition, glutamate efflux was significantly reduced in the CMX of rats subjected to RRS, thereby identifying a potential neurochemical consequence of stress-induced dendritic atrophy of CBL pyramidal neurons. Lastly, an acute stress challenge increased corticosterone (CORT) levels in the CBL, suggesting that stress-induced increases in CORT levels may contribute to the neuroanatomical and neurochemical effects of RRS in the CBL. Importantly, these RRS-induced changes were prevented by daily agomelatine administration. These results demonstrate that the neuroanatomical and neurochemical properties of glutamatergic neurons in the rat amygdala are adversely affected by repeated stress and suggest that the therapeutic effects of agomelatine may include protection of structural and neurochemical plasticity in limbic structures like the amygdala. |
Databáze: | OpenAIRE |
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