TY - JOUR
T1 - Role of medial prefrontal and orbitofrontal monoamine transporters and receptors in performance in an adjusting delay discounting procedure
AU - Yates, Justin R.
AU - Perry, Jennifer L.
AU - Meyer, Andrew C.
AU - Gipson, Cassandra D.
AU - Charnigo, Richard
AU - Bardo, Michael T.
N1 - Publisher Copyright:
© 2014 Elsevier B.V. All rights reserved.
PY - 2014
Y1 - 2014
N2 - Performance in an adjusting delay discounting procedure is predictive of drug abuse vulnerability; however, the shared underlying specific prefrontal neural systems linking delay discounting and increased addiction-like behaviors are unclear. Rats received direct infusions of methylphenidate (MPH; 6.25, 25.0, or 100 μg), amphetamine (AMPH; 0.25, 1.0, or 4.0 μg), or atomoxetine (ATO; 1.0, 4.0, or 16.0 μg) into either medial prefrontal cortex (mPFC) or orbitofrontal cortex (OFC) immediately prior to performance in an adjusting delay task. These drugs were examined because they are efficacious in treating impulse control disorders. Because dopamine (DA) and serotonin (5-HT) receptors are implicated in impulsive behavior, separate groups of rats received microinfusions of the DA receptor-selective drugs SKF 81297 (0.1 or 0.4 mg), SCH 23390 (0.25 or 1.0 mg), quinpirole (1.25 or 5.0 mg), and eticlopride (0.25 or 1.0 mg), or received microinfusions of the 5-HT receptor-selective drugs 8-OH-DPAT (0.025 or 0.1 μg), WAY 100635 (0.01 or 0.04 μg), DOI (2.5 or 10.0 μg), and ketanserin (0.1 or 0.4 μg). Impulsive choice was not altered significantly by MPH, AMPH, or ATO into either mPFC or OFC, indicating that neither of these prefrontal regions alone may mediate the systemic effect of ADHD medications on impulsive choice. However, quinpriole (1.25 μg) and eticlopride infused into mPFC increased impulsive choice, whereas 8-OH-DPAT infused into OFC decreased impulsive choice. These latter results demonstrate that blockade of DA D2 receptors in mPFC or activation of 5-HT1Areceptors in OFC increases impulsive choice in the adjusting delay procedure.
AB - Performance in an adjusting delay discounting procedure is predictive of drug abuse vulnerability; however, the shared underlying specific prefrontal neural systems linking delay discounting and increased addiction-like behaviors are unclear. Rats received direct infusions of methylphenidate (MPH; 6.25, 25.0, or 100 μg), amphetamine (AMPH; 0.25, 1.0, or 4.0 μg), or atomoxetine (ATO; 1.0, 4.0, or 16.0 μg) into either medial prefrontal cortex (mPFC) or orbitofrontal cortex (OFC) immediately prior to performance in an adjusting delay task. These drugs were examined because they are efficacious in treating impulse control disorders. Because dopamine (DA) and serotonin (5-HT) receptors are implicated in impulsive behavior, separate groups of rats received microinfusions of the DA receptor-selective drugs SKF 81297 (0.1 or 0.4 mg), SCH 23390 (0.25 or 1.0 mg), quinpirole (1.25 or 5.0 mg), and eticlopride (0.25 or 1.0 mg), or received microinfusions of the 5-HT receptor-selective drugs 8-OH-DPAT (0.025 or 0.1 μg), WAY 100635 (0.01 or 0.04 μg), DOI (2.5 or 10.0 μg), and ketanserin (0.1 or 0.4 μg). Impulsive choice was not altered significantly by MPH, AMPH, or ATO into either mPFC or OFC, indicating that neither of these prefrontal regions alone may mediate the systemic effect of ADHD medications on impulsive choice. However, quinpriole (1.25 μg) and eticlopride infused into mPFC increased impulsive choice, whereas 8-OH-DPAT infused into OFC decreased impulsive choice. These latter results demonstrate that blockade of DA D2 receptors in mPFC or activation of 5-HT1Areceptors in OFC increases impulsive choice in the adjusting delay procedure.
KW - Adjusting delay discounting
KW - Dopamine receptor
KW - Dopamine transporter
KW - Norepinephrine transporter
KW - Rat
KW - Serotonin receptor
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U2 - 10.1016/j.brainres.2014.06.004
DO - 10.1016/j.brainres.2014.06.004
M3 - Article
C2 - 24928616
AN - SCOPUS:84925359856
SN - 0006-8993
VL - 1574
SP - 26
EP - 36
JO - Brain Research
JF - Brain Research
ER -