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

GARCIA KELLER, C.; KUPICHNIK, Y.; GIPSON, C.; BROWN, R.; SPENCER, S.; BOLLATI, F.; ESPARZA, M.A.; ROBERTS-WOLFE, D.J.; HEINSBROEK, J.A.; BOBADILLA, A.C.; CANCELA, L.M.; KALIVAS, P.W.

NATURE PUBLISHING GROUP

Año: 2015 p. 1 - 1

here is substantial comorbidity between stress disorders and substance use disorders (SUDs), and acute stress augments thelocomotor stimulant effect of cocaine in animal models. Here we endeavor to understand the neural underpinnings of comorbidstress disorders and drug use by determining whether the glutamatergic neuroadaptations that characterize cocaine selfadministrationare induced by acute stress. Rats were exposed to acute (2 h) immobilization stress, and 3 weeks later the nucleusaccumbens core was examined for changes in glutamate transport, glutamate-mediated synaptic currents and dendritic spinemorphology. We also determined whether acute stress potentiated the acquisition of cocaine self-administration. Acute stressproduced an enduring reduction in glutamate transport and potentiated excitatory synapses on medium spiny neurons. Acutestress also augmented the acquisition of cocaine self-administration. Importantly, by restoring glutamate transport in theaccumbens core with ce