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Artículo

Glutamatergic mechanisms of comorbidity between acute stress and cocaine self-administration

Garcia Keller, ConstanzaIcon ; Kupchik, Y.M.; Gipson, C.D.; Brown, R. M.; Spencer, S.; Bollati, Flavia AndreaIcon ; Esparza, Maria AlejandraIcon ; Roberts Wolfe, D.J.; Heinsbroek, J. A.; Bobadilla, A. C.; Cancela, Liliana MarinaIcon ; Kalivas, P. W.
Fecha de publicación: 08/2016
Editorial: Nature Publishing Group
Revista: Molecular Psychiatry
ISSN: 1359-4184
e-ISSN: 1476-5578
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Inmunología

Resumen

There is substantial comorbidity between stress disorders and substance use disorders (SUDs), and acute stress augments the locomotor stimulant effect of cocaine in animal models. Here we endeavor to understand the neural underpinnings of comorbid stress disorders and drug use by determining whether the glutamatergic neuroadaptations that characterize cocaine self-administration are induced by acute stress. Rats were exposed to acute (2 h) immobilization stress, and 3 weeks later the nucleus accumbens core was examined for changes in glutamate transport, glutamate-mediated synaptic currents and dendritic spine morphology. We also determined whether acute stress potentiated the acquisition of cocaine self-administration. Acute stress produced an enduring reduction in glutamate transport and potentiated excitatory synapses on medium spiny neurons. Acute stress also augmented the acquisition of cocaine self-administration. Importantly, by restoring glutamate transport in the accumbens core with ceftriaxone the capacity of acute stress to augment the acquisition of cocaine self-administration was abolished. Similarly, ceftriaxone treatment prevented stress-induced potentiation of cocaine-induced locomotor activity. However, ceftriaxone did not reverse stress-induced synaptic potentiation, indicating that this effect of stress exposure did not underpin the increased acquisition of cocaine self-administration. Reversing acute stress-induced vulnerability to self-administer cocaine by normalizing glutamate transport poses a novel treatment possibility for reducing comorbid SUDs in stress disorders.
Palabras clave: Self Administration , Acute Stress , Cocaine , Glutamate
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/50402
DOI: http://dx.doi.org/10.1038/mp.2015.151
URL: https://www.nature.com/articles/mp2015151
URL: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4823171/
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Articulos(IFEC)
Articulos de INST. DE FARMACOLOGIA EXPERIMENTAL DE CORDOBA
Citación
Garcia Keller, Constanza; Kupchik, Y.M.; Gipson, C.D.; Brown, R. M.; Spencer, S.; et al.; Glutamatergic mechanisms of comorbidity between acute stress and cocaine self-administration; Nature Publishing Group; Molecular Psychiatry; 21; 8; 8-2016; 1063-1069
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