BOLLATI FLAVIA ANDREA
Congresos y reuniones científicas
Título:
Stress and vulnerability to develop cocaine addiction: role of glutamatergic transmission
Autor/es:
AVALOS MARIA PAULA; GARCIA-KELLER CONSTANZA; BOLLATI FLAVIA; KALIVAS PETER W; CANCELA LILIANA M
Lugar:
Huerta Grande
Reunión:
Congreso; Sociedad Argentina de Investigación en Neurociencias. XXIX Annual Meeting; 2014
Institución organizadora:
Sociedad Argentina de Investigación en Neurociencias.
Resumen:
Clinical evidence supports the idea that individuals suffering posttraumatic stress disorder (PTSD) are vulnerable to developing substance use disorders (SUDs). We previously investigated the role of excitatory synapses and glutamate (Glu) transmission in nucleus accumbens (NA) in mediating the cross-sensitization between acute and chronic stress and cocaine and found evidence supporting stress-induced plasticity in glutamatergic synapses.
Here, we attempted to mimic how exposure to a single acute stressful life event can create an enduring vulnerability to developing SUDs. Thus, rats were exposed to acute restraint stress (2 hours) and 3 weeks later the NA core was examined for changes in glutamate transport and Glu receptor-mediated synaptic currents. We also determined if acute stress potentiated the acquisition of cocaine self-administration (SA).
Our results showed that acute stress produced a reduction in Glu transport, as the level of GLT-1 transporter was reduced and the electrically released synaptic Glu induces an NMDA current that has a longer decay time. Acute restraint stress also augmented the acquisition of cocaine SA. Thereby, acute stress produced enduring changes in glutamatergic transmission in the NA similarly to those observed after cocaine which supports the idea that a shared neuropathology may contribute to comorbidity between PTSD and SUDs.
Here, we attempted to mimic how exposure to a single acute stressful life event can create an enduring vulnerability to developing SUDs. Thus, rats were exposed to acute restraint stress (2 hours) and 3 weeks later the NA core was examined for changes in glutamate transport and Glu receptor-mediated synaptic currents. We also determined if acute stress potentiated the acquisition of cocaine self-administration (SA).
Our results showed that acute stress produced a reduction in Glu transport, as the level of GLT-1 transporter was reduced and the electrically released synaptic Glu induces an NMDA current that has a longer decay time. Acute restraint stress also augmented the acquisition of cocaine SA. Thereby, acute stress produced enduring changes in glutamatergic transmission in the NA similarly to those observed after cocaine which supports the idea that a shared neuropathology may contribute to comorbidity between PTSD and SUDs.
