Effects of Intra-Accumbal Administration of Dopamine and Ionotropic Glutamate Receptor Drugs on Delay Discounting Performance in Rats

• Published in: Behavioral neuroscience 2017-10, Vol.131 (5), p.392-405
• Main Authors: Yates, Justin R, Bardo, Michael T
• Format: Article
• Language: English
• Subjects: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; Animal; Animal behavior; Animal Ethology; Animals; Benzazepines; Brain; Choice Behavior; Choice Behavior - drug effects; Delay Discounting; Delay Discounting - drug effects; Delayed reinforcement; Dizocilpine; Dopamine; Dopamine - administration & dosage; Dopamine - pharmacology; Dopamine D1 receptors; Dopamine D2 receptors; Dopamine receptors; Drug Administration Methods; Glutamic Acid - metabolism; Glutamic Acid - pharmacology; Glutamic acid receptors (ionotropic); Implantation; Impulsive Behavior - drug effects; Impulsiveness; Ligands; Male; N-Methyl-D-aspartic acid receptors; Nucleus Accumbens; Nucleus Accumbens - drug effects; Nucleus Accumbens - physiology; Quinpirole; Rats; Rats, Sprague-Dawley; Receptors, Dopamine D1 - antagonists & inhibitors; Receptors, Dopamine D1 - metabolism; Receptors, Dopamine D2 - metabolism; Receptors, Ionotropic Glutamate - drug effects; Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors; Receptors, N-Methyl-D-Aspartate - metabolism; Reinforcement; Reinforcement, Psychology; Rodents; Salicylamides; Sensitivity; α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid
• ISSN: 0735-7044; 1939-0084
• DOI: 10.1037/bne0000214

Nucleus accumbens core (NAcc) has been implicated in impulsive choice, as measured in delay discounting. The role of dopamine (DA) in impulsive choice has received considerable attention, whereas glutamate (Glu) has recently been shown to be an important mediator of discounting. However, research has not examined how DA or Glu receptors in NAcc mediate different aspects of delay discounting performance, that is, (a) sensitivity to reinforcer magnitude and (b) sensitivity to delayed reinforcement. Adult male Sprague-Dawley rats were first trained in a delay discounting task, in which the delay to a large magnitude food reinforcer increased across blocks of trials. Following behavioral training, rats received bilateral implantation of guide cannulas into NAcc. Half of the rats (n = 12) received infusions of the DA-selective ligands SKF 38393 (D1-like agonist: 0.03 or 0.1 μg), SCH 23390 (D1-like antagonist: 0.3 or 1.0 μg), quinpirole (D2-like agonist: 0.3 or 1.0 μg), and eticlopride (D2-like antagonist: 0.3 or 1.0 μg). The other half received infusions of the ionotropic Glu ligands MK-801 (NMDA uncompetitive antagonist: 0.3 or 1.0 μg), AP-5 (NMDA competitive antagonist: 0.3 or 1.0 μg), ifenprodil (noncompetitive antagonist at NR2B-containing NMDA receptors: 0.3 or 1.0 μg), and CNQX (AMPA competitive antagonist: 0.2 or 0.5 μg). Results showed that SCH 23390 (0.3 μg) decreased sensitivity to reinforcer magnitude without altering impulsive choice, whereas ifenprodil (1.0 μg) decreased sensitivity to delayed reinforcement (i.e., impulsive choice). The current results show that DA and NMDA receptors in NAcc mediate distinct aspects of discounting performance.