Dopamine release during cocaine self-administration in rats: effect of SCH23390

Yaprak Egilmez, Marianna E. Jung, John D. Lane, Michael W. Emmett-Oglesby

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

This experiment tested the hypotheses that: (1) self-administration of cocaine would produce an increase in dopamine (DA) oxidation current in the nucleus accumbens (n. acc.); and (2) a faster rate of cocaine intake in the presence of a D1 receptor antagonist would produce a greater increase in DA levels. Rats trained to self-administer cocaine under a fixed-ratio 2 schedule were implanted with stearate-modified graphite paste electrodes bilaterally in the n. acc. The effect of pretreatment with the D1 receptor antagonist, SCH23390, on the DA oxidation current associated with self-administration of cocaine (1 mg/inj.) or saline was investigated using chronoamperometry. Pretreatment with SCH23390 produced a 2-fold increase in the amount of cocaine intake. This in turn resulted in a 2-fold increase in the DA oxidation current recorded in the n. acc. Pretreatment with SCH23390 did not, however, produce any significant change in either the number of saline injections received or the DA oxidation current recorded during saline self-administration. These findings show that cocaine increases DA oxidation currents in the n. acc., and that both the rate of cocaine self-administration and the magnitude of these currents increase even further following SCH23390. The results also imply that the baseline rate of cocaine self-administration does not result in the occupation of all possible DA transporter sites.

Original languageEnglish (US)
Pages (from-to)142-150
Number of pages9
JournalBrain Research
Volume701
Issue number1-2
DOIs
StatePublished - Dec 1 1995

Fingerprint

Self Administration
Cocaine
Dopamine
Stearates
Dopamine Plasma Membrane Transport Proteins
Graphite
SCH 23390
Nucleus Accumbens
Ointments
Occupations
Appointments and Schedules
Electrodes
Injections

Keywords

  • Chronoamoerometry
  • Cocaine
  • Nucleus accumbens
  • Rats
  • SCH23390
  • Self-administration

ASJC Scopus subject areas

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

Cite this

Dopamine release during cocaine self-administration in rats : effect of SCH23390. / Egilmez, Yaprak; Jung, Marianna E.; Lane, John D.; Emmett-Oglesby, Michael W.

In: Brain Research, Vol. 701, No. 1-2, 01.12.1995, p. 142-150.

Research output: Contribution to journalArticle

Egilmez, Yaprak ; Jung, Marianna E. ; Lane, John D. ; Emmett-Oglesby, Michael W. / Dopamine release during cocaine self-administration in rats : effect of SCH23390. In: Brain Research. 1995 ; Vol. 701, No. 1-2. pp. 142-150.
@article{6e8ccbe914eb433d860554879e0b83c9,
title = "Dopamine release during cocaine self-administration in rats: effect of SCH23390",
abstract = "This experiment tested the hypotheses that: (1) self-administration of cocaine would produce an increase in dopamine (DA) oxidation current in the nucleus accumbens (n. acc.); and (2) a faster rate of cocaine intake in the presence of a D1 receptor antagonist would produce a greater increase in DA levels. Rats trained to self-administer cocaine under a fixed-ratio 2 schedule were implanted with stearate-modified graphite paste electrodes bilaterally in the n. acc. The effect of pretreatment with the D1 receptor antagonist, SCH23390, on the DA oxidation current associated with self-administration of cocaine (1 mg/inj.) or saline was investigated using chronoamperometry. Pretreatment with SCH23390 produced a 2-fold increase in the amount of cocaine intake. This in turn resulted in a 2-fold increase in the DA oxidation current recorded in the n. acc. Pretreatment with SCH23390 did not, however, produce any significant change in either the number of saline injections received or the DA oxidation current recorded during saline self-administration. These findings show that cocaine increases DA oxidation currents in the n. acc., and that both the rate of cocaine self-administration and the magnitude of these currents increase even further following SCH23390. The results also imply that the baseline rate of cocaine self-administration does not result in the occupation of all possible DA transporter sites.",
keywords = "Chronoamoerometry, Cocaine, Nucleus accumbens, Rats, SCH23390, Self-administration",
author = "Yaprak Egilmez and Jung, {Marianna E.} and Lane, {John D.} and Emmett-Oglesby, {Michael W.}",
year = "1995",
month = "12",
day = "1",
doi = "10.1016/0006-8993(95)00987-5",
language = "English (US)",
volume = "701",
pages = "142--150",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Dopamine release during cocaine self-administration in rats

T2 - effect of SCH23390

AU - Egilmez, Yaprak

AU - Jung, Marianna E.

AU - Lane, John D.

AU - Emmett-Oglesby, Michael W.

PY - 1995/12/1

Y1 - 1995/12/1

N2 - This experiment tested the hypotheses that: (1) self-administration of cocaine would produce an increase in dopamine (DA) oxidation current in the nucleus accumbens (n. acc.); and (2) a faster rate of cocaine intake in the presence of a D1 receptor antagonist would produce a greater increase in DA levels. Rats trained to self-administer cocaine under a fixed-ratio 2 schedule were implanted with stearate-modified graphite paste electrodes bilaterally in the n. acc. The effect of pretreatment with the D1 receptor antagonist, SCH23390, on the DA oxidation current associated with self-administration of cocaine (1 mg/inj.) or saline was investigated using chronoamperometry. Pretreatment with SCH23390 produced a 2-fold increase in the amount of cocaine intake. This in turn resulted in a 2-fold increase in the DA oxidation current recorded in the n. acc. Pretreatment with SCH23390 did not, however, produce any significant change in either the number of saline injections received or the DA oxidation current recorded during saline self-administration. These findings show that cocaine increases DA oxidation currents in the n. acc., and that both the rate of cocaine self-administration and the magnitude of these currents increase even further following SCH23390. The results also imply that the baseline rate of cocaine self-administration does not result in the occupation of all possible DA transporter sites.

AB - This experiment tested the hypotheses that: (1) self-administration of cocaine would produce an increase in dopamine (DA) oxidation current in the nucleus accumbens (n. acc.); and (2) a faster rate of cocaine intake in the presence of a D1 receptor antagonist would produce a greater increase in DA levels. Rats trained to self-administer cocaine under a fixed-ratio 2 schedule were implanted with stearate-modified graphite paste electrodes bilaterally in the n. acc. The effect of pretreatment with the D1 receptor antagonist, SCH23390, on the DA oxidation current associated with self-administration of cocaine (1 mg/inj.) or saline was investigated using chronoamperometry. Pretreatment with SCH23390 produced a 2-fold increase in the amount of cocaine intake. This in turn resulted in a 2-fold increase in the DA oxidation current recorded in the n. acc. Pretreatment with SCH23390 did not, however, produce any significant change in either the number of saline injections received or the DA oxidation current recorded during saline self-administration. These findings show that cocaine increases DA oxidation currents in the n. acc., and that both the rate of cocaine self-administration and the magnitude of these currents increase even further following SCH23390. The results also imply that the baseline rate of cocaine self-administration does not result in the occupation of all possible DA transporter sites.

KW - Chronoamoerometry

KW - Cocaine

KW - Nucleus accumbens

KW - Rats

KW - SCH23390

KW - Self-administration

UR - http://www.scopus.com/inward/record.url?scp=0028791024&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028791024&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(95)00987-5

DO - 10.1016/0006-8993(95)00987-5

M3 - Article

C2 - 8925277

AN - SCOPUS:0028791024

VL - 701

SP - 142

EP - 150

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -