The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat

Mona Boules, Iver Iversen, Alfredo Oliveros, Amanda Shaw, Katrina Williams, Jessica Robinson, Paul Fredrickson, Elliott Richelson

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

NT69L is a neurotensin analog that can be administered peripherally. It blocks amphetamine- and cocaine-induced hyperactivity in rats. It also blocks nicotine-induced locomotor activity and has shown sustained efficacy in a rat model of nicotine-induced sensitization. The present study tested the effect of NT69L on responding for sucrose reinforcement on a continuous reinforcement schedule (CRF) and incrementing (FR1-FR5) discrimination schedule. Male Sprague-Dawley rats, on restricted food intake, were trained to press a lever for sucrose pellets on a CRF and incrementing discrimination schedule of reinforcement. On the following day, the testing session was followed by an extinction session, where lever pressing was not reinforced. Immediately after extinction, a reversal to CRF was implemented to test for relapse. Trained rats were injected with NT69L (1 mg/kg) or saline 30 min before each testing session. Dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels were determined. NT69L significantly suppressed the lever pressing behavior for sucrose reinforcement on CRF which measures the "hedonic" value of the reward. NT69L also suppressed sucrose self-administration on the incrementing discrimination schedule of reinforcement (FR3-FR5) that is analogous to the motivational incentive. Reversal to CRF was significantly reduced by pretreatment with NT69L. The suppression of sucrose self-administration behavior by pretreatment with NT69L had a pattern similar to that for extinction. The effect of NT69L on dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels is discussed relative to changes occurring during extinction.

Original languageEnglish (US)
Pages (from-to)90-98
Number of pages9
JournalBrain Research
Volume1127
Issue number1
DOIs
StatePublished - Jan 5 2007

Fingerprint

Neurotensin Receptors
Reinforcement Schedule
Sucrose
Self Administration
Dopamine Receptors
Tyrosine 3-Monooxygenase
Nicotine
Dopamine
Neurotensin
Messenger RNA
Pleasure
neurotensin 69L
Amphetamine
Locomotion
Reward
Cocaine
Sprague Dawley Rats
Motivation
Appointments and Schedules
Eating

Keywords

  • Dopamine
  • Extinction
  • Glucocorticoid
  • Neurotensin
  • Reinforcement

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Developmental Biology
  • Molecular Biology

Cite this

Boules, M., Iversen, I., Oliveros, A., Shaw, A., Williams, K., Robinson, J., ... Richelson, E. (2007). The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat. Brain Research, 1127(1), 90-98. https://doi.org/10.1016/j.brainres.2006.10.025

The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat. / Boules, Mona; Iversen, Iver; Oliveros, Alfredo; Shaw, Amanda; Williams, Katrina; Robinson, Jessica; Fredrickson, Paul; Richelson, Elliott.

In: Brain Research, Vol. 1127, No. 1, 05.01.2007, p. 90-98.

Research output: Contribution to journalArticle

Boules, M, Iversen, I, Oliveros, A, Shaw, A, Williams, K, Robinson, J, Fredrickson, P & Richelson, E 2007, 'The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat', Brain Research, vol. 1127, no. 1, pp. 90-98. https://doi.org/10.1016/j.brainres.2006.10.025
Boules, Mona ; Iversen, Iver ; Oliveros, Alfredo ; Shaw, Amanda ; Williams, Katrina ; Robinson, Jessica ; Fredrickson, Paul ; Richelson, Elliott. / The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat. In: Brain Research. 2007 ; Vol. 1127, No. 1. pp. 90-98.
@article{9cf29f7e3fb14e5dac83dd79743eb505,
title = "The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat",
abstract = "NT69L is a neurotensin analog that can be administered peripherally. It blocks amphetamine- and cocaine-induced hyperactivity in rats. It also blocks nicotine-induced locomotor activity and has shown sustained efficacy in a rat model of nicotine-induced sensitization. The present study tested the effect of NT69L on responding for sucrose reinforcement on a continuous reinforcement schedule (CRF) and incrementing (FR1-FR5) discrimination schedule. Male Sprague-Dawley rats, on restricted food intake, were trained to press a lever for sucrose pellets on a CRF and incrementing discrimination schedule of reinforcement. On the following day, the testing session was followed by an extinction session, where lever pressing was not reinforced. Immediately after extinction, a reversal to CRF was implemented to test for relapse. Trained rats were injected with NT69L (1 mg/kg) or saline 30 min before each testing session. Dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels were determined. NT69L significantly suppressed the lever pressing behavior for sucrose reinforcement on CRF which measures the {"}hedonic{"} value of the reward. NT69L also suppressed sucrose self-administration on the incrementing discrimination schedule of reinforcement (FR3-FR5) that is analogous to the motivational incentive. Reversal to CRF was significantly reduced by pretreatment with NT69L. The suppression of sucrose self-administration behavior by pretreatment with NT69L had a pattern similar to that for extinction. The effect of NT69L on dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels is discussed relative to changes occurring during extinction.",
keywords = "Dopamine, Extinction, Glucocorticoid, Neurotensin, Reinforcement",
author = "Mona Boules and Iver Iversen and Alfredo Oliveros and Amanda Shaw and Katrina Williams and Jessica Robinson and Paul Fredrickson and Elliott Richelson",
year = "2007",
month = "1",
day = "5",
doi = "10.1016/j.brainres.2006.10.025",
language = "English (US)",
volume = "1127",
pages = "90--98",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - The neurotensin receptor agonist NT69L suppresses sucrose-reinforced operant behavior in the rat

AU - Boules, Mona

AU - Iversen, Iver

AU - Oliveros, Alfredo

AU - Shaw, Amanda

AU - Williams, Katrina

AU - Robinson, Jessica

AU - Fredrickson, Paul

AU - Richelson, Elliott

PY - 2007/1/5

Y1 - 2007/1/5

N2 - NT69L is a neurotensin analog that can be administered peripherally. It blocks amphetamine- and cocaine-induced hyperactivity in rats. It also blocks nicotine-induced locomotor activity and has shown sustained efficacy in a rat model of nicotine-induced sensitization. The present study tested the effect of NT69L on responding for sucrose reinforcement on a continuous reinforcement schedule (CRF) and incrementing (FR1-FR5) discrimination schedule. Male Sprague-Dawley rats, on restricted food intake, were trained to press a lever for sucrose pellets on a CRF and incrementing discrimination schedule of reinforcement. On the following day, the testing session was followed by an extinction session, where lever pressing was not reinforced. Immediately after extinction, a reversal to CRF was implemented to test for relapse. Trained rats were injected with NT69L (1 mg/kg) or saline 30 min before each testing session. Dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels were determined. NT69L significantly suppressed the lever pressing behavior for sucrose reinforcement on CRF which measures the "hedonic" value of the reward. NT69L also suppressed sucrose self-administration on the incrementing discrimination schedule of reinforcement (FR3-FR5) that is analogous to the motivational incentive. Reversal to CRF was significantly reduced by pretreatment with NT69L. The suppression of sucrose self-administration behavior by pretreatment with NT69L had a pattern similar to that for extinction. The effect of NT69L on dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels is discussed relative to changes occurring during extinction.

AB - NT69L is a neurotensin analog that can be administered peripherally. It blocks amphetamine- and cocaine-induced hyperactivity in rats. It also blocks nicotine-induced locomotor activity and has shown sustained efficacy in a rat model of nicotine-induced sensitization. The present study tested the effect of NT69L on responding for sucrose reinforcement on a continuous reinforcement schedule (CRF) and incrementing (FR1-FR5) discrimination schedule. Male Sprague-Dawley rats, on restricted food intake, were trained to press a lever for sucrose pellets on a CRF and incrementing discrimination schedule of reinforcement. On the following day, the testing session was followed by an extinction session, where lever pressing was not reinforced. Immediately after extinction, a reversal to CRF was implemented to test for relapse. Trained rats were injected with NT69L (1 mg/kg) or saline 30 min before each testing session. Dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels were determined. NT69L significantly suppressed the lever pressing behavior for sucrose reinforcement on CRF which measures the "hedonic" value of the reward. NT69L also suppressed sucrose self-administration on the incrementing discrimination schedule of reinforcement (FR3-FR5) that is analogous to the motivational incentive. Reversal to CRF was significantly reduced by pretreatment with NT69L. The suppression of sucrose self-administration behavior by pretreatment with NT69L had a pattern similar to that for extinction. The effect of NT69L on dopamine, tyrosine 3-hydroxylase, and dopamine receptor mRNA levels is discussed relative to changes occurring during extinction.

KW - Dopamine

KW - Extinction

KW - Glucocorticoid

KW - Neurotensin

KW - Reinforcement

UR - http://www.scopus.com/inward/record.url?scp=33845211168&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845211168&partnerID=8YFLogxK

U2 - 10.1016/j.brainres.2006.10.025

DO - 10.1016/j.brainres.2006.10.025

M3 - Article

VL - 1127

SP - 90

EP - 98

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -