Pharmacological NOS-1 Inhibition Within the Hippocampus Prevented Expression of Cocaine Sensitization: Correlation with Reduced Synaptic Transmission

ARTUR DE LA VILLARMOIS, EMILCE; GABACH, LAURA A.; BIANCONI, SANTIAGO; PORETTI, MARIA BELEN; OCCHIEPPO, VICTORIA; SCHIÖTH, HELGI B.; CARLINI, VALERIA P.; PÉREZ, MARIELA FERNANDA

MOLECULAR NEUROBIOLOGY

HUMANA PRESS INC

Año: 2019

0893-7648

ehavioral sensitization to psychostimulants hyperlocomotor effect is a useful model of addiction and craving. Particularly, cocaine sensitization in rats enhanced synaptic plasticity within the hippocampus, an important brain region for the associative learning processes underlying drug addiction. Nitric oxide (NO) is a neurotransmitter involved in both, hippocampal synaptic plasticity and cocaine sensitization. It has been previously demonstrated a key role of NOS-1/NO/sGC/cGMP signaling pathway in the development of cocaine sensitization and in the associated enhancement of hippocampal synaptic plasticity. The aim of the present investigation was to determine whether NOS-1 inhibition after development of cocaine sensitization was able to reverse it, and to characterize the involvement of the hippocampus in this phenomenon. Male Wistar rats were administered only with cocaine (15 mg/kg/day i.p.) for 5 days. Then, animals received 7-nitroindazole (NOS-1 inhibitor) either systemically