PM319. δ1, δ2 and μ2, but not μ1 receptors, exert an inhibitory role in regulation of acetylcholine efflux in the nucleus accumbens of freely moving rats

Objective: Cholinergic neurons in the nucleus accumbens (NAc) express δ and μ receptors that are thought to inhibit neural activity (Britt & McGehee, 2008). δ and μ receptors are divided into δ1 and δ2 receptors and μ1 and μ2 receptors, respectively. Therefore, we analysed the roles of δ and μ receptor subtypes in regulating accumbal acetylcholine (ACh) efflux using in vivo microdialysis. Methods: Male Sprague-Dawley rats were used. ACh levels in accumbal perfusates, taken every 15 min, were determined by HPLC-ECD. Apart from the μ1 receptor antagonist naloxonazine, which was given intraperitoneally, δ and μ receptor ligands were administered intracerebrally through the dialysis probe. Doses of these compounds indicate total amount (mol) over a 30-min infusion time. To monitor basal ACh levels, a low concentration of physostigmine (50 nM) was added to the perfusate. Results: The δ1 receptor agonist DPDPE (3 and 300 pmol) and δ2 receptor agonist deltorphin II (3 and 30 pmol) decreased accumbal ACh in a dose-related manner. DPDPE (300 pmol)and deltorphin II (3 pmol)-induced reduction in ACh were each inhibited by co-administration of the δ1 receptor antagonist BNTX (0.3 pmol) and δ2 receptor antagonist NTB (15 pmol), respectively. The μ receptor agonists endomorphin (EM)-1 and EM-2 (6 and 30 nmol) decreased ACh in a dose-related manner. EM-1and EM-2 (30 nmol)-induced reductions in ACh were prevented by co-administration of the μ receptor antagonist CTOP (3 nmol), which failed to alter basal ACh. Naloxonazine (15 mg/kg ip), which inhibits EM-1 (15 nmol)-induced accumbal dopamine efflux (Okutsu et al, 2006), did not alter EM-1 (30 nmol)or EM-2 (30 nmol)-induced reductions in ACh. Conclusion: This study provides in vivo evidence for δ1, δ2 and μ2 receptors, but not μ1 receptors, that are located on accumbal cholinergic neurons and inhibit accumbal ACh efflux. PM320 Different Patterns of ERP components in Internet Gaming Disorder and Alcohol Use Disorder: an auditory event-related potential study Minkyung Park, MAa, Yeon Jin Kim, MD a, Jung-Seok Choi, MD, PhD a,b,* aDepartment of Psychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea bDepartment of Psychiatry and Behavioral Science, Seoul National University College of Medicine, Seoul, Republic of Korea * Correspondence to: Jung-Seok Choi, M.D., Ph.D. Department of Psychiatry, SMG-SNU Boramae Medical center, 20, Boramae-Ro 5-Gil, Dongjak-Gu, Seoul, 07061, Republic of Korea. E-mail: choijs73@gmail. com, Phone: +82-2-870-3461, Fax: +82-2-831-2826 Abstract Background: Internet gaming disorder (IGD), as a behavioral addiction, shares clinical and neuropsychological features with alcohol use disorder (AUD), but few studies exist that identify neurophysiological characteristics in IGD. The aim of this study was to investigate N100 and P300 of auditory event-related potentials (ERPs) in patients with IGD and compare those with patients with AUD and healthy controls. Methods: Twenty-six patients diagnosed with IGD (22.69 ± 4.76 years), 22 patients diagnosed with AUD (28.36 ± 5.40), and 29 healthy controls (24.66 ± 3.80) participated in this study. Electroencephalography (EEG) scans were acquired during an auditory oddball task from all participants who were young adult males. Between-group differences in N100 and P300 were investigated using repeated measures analysis of variance, respectively. Results: Both the IGD and AUD groups showed significantly reduced P300 amplitudes at midline centro-parietal site compared with HCs. The IGD group also exhibited significantly reduced N100 amplitudes at midline fronto-central site compared with HCs. Reduced N100 and P300 amplitudes in the IGD group were not correlated with scores on Internet Addiction severity. Conclusion: These results indicate that IGD has abnormalities of P300 index which are comparable to those in AUD, and N100 amplitudes reduction could be considered as a candidate trait marker of IGD. This study enhances our understanding of neurophysiological characteristics of IGD which differentiate patients with IGD from those with AUD and healthy controls.