Control of extracellular dopamine at dendrite and axon terminals

Christopher P. Ford, Stephanie C. Gantz, Paul E M Phillips, John Williams

Research output: Contribution to journalArticle

77 Citations (Scopus)

Abstract

Midbrain dopamine neurons release dopamine from both axons and dendrites. The mechanism underlying release at these different sites has been proposed to differ. This study used electrochemical and electrophysiological methods to compare the time course and calcium dependence of somatodendritic dopamine release in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) to that of axonal dopamine release in the dorsal striatum. The amount of dopamine released in the striatum was ∼20-fold greater than in cell body regions of the VTA or SNc. However, the calcium dependence and time to peak of the dopamine transients were similar. These results illustrate an unexpected overall similarity in the mechanisms of dopamine release in the striatum and cell body regions. To examine how diffusion regulates the time course of dopamine following release, dextran was added to the extracellular solution to slow diffusion. In the VTA, dextran slowed the rate of rise and fall of the extracellular dopamine transient as measured by fast-scan cyclic voltammetry yet did not alter the kinetics of the dopamine-dependent IPSC. Dextran failed to significantly alter the time course of the rise and fall of the dopamine transient in the striatum, suggesting a more influential role for reuptake in the striatum. The conclusion is that the time course of dopamine within the extracellular space of the VTA is dependent on both diffusion and reuptake, whereas the activation of D2 receptors on dopamine neurons is primarily limited by reuptake.

Original languageEnglish (US)
Pages (from-to)6975-6983
Number of pages9
JournalJournal of Neuroscience
Volume30
Issue number20
DOIs
StatePublished - May 19 2010

Fingerprint

Presynaptic Terminals
Dendrites
Dopamine
Ventral Tegmental Area
Dextrans
Body Regions
Dopaminergic Neurons
Calcium
Extracellular Space
Mesencephalon
Axons

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Control of extracellular dopamine at dendrite and axon terminals. / Ford, Christopher P.; Gantz, Stephanie C.; Phillips, Paul E M; Williams, John.

In: Journal of Neuroscience, Vol. 30, No. 20, 19.05.2010, p. 6975-6983.

Research output: Contribution to journalArticle

Ford, Christopher P. ; Gantz, Stephanie C. ; Phillips, Paul E M ; Williams, John. / Control of extracellular dopamine at dendrite and axon terminals. In: Journal of Neuroscience. 2010 ; Vol. 30, No. 20. pp. 6975-6983.
@article{dcb6a3a2bd664a1a9117a3448678b809,
title = "Control of extracellular dopamine at dendrite and axon terminals",
abstract = "Midbrain dopamine neurons release dopamine from both axons and dendrites. The mechanism underlying release at these different sites has been proposed to differ. This study used electrochemical and electrophysiological methods to compare the time course and calcium dependence of somatodendritic dopamine release in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) to that of axonal dopamine release in the dorsal striatum. The amount of dopamine released in the striatum was ∼20-fold greater than in cell body regions of the VTA or SNc. However, the calcium dependence and time to peak of the dopamine transients were similar. These results illustrate an unexpected overall similarity in the mechanisms of dopamine release in the striatum and cell body regions. To examine how diffusion regulates the time course of dopamine following release, dextran was added to the extracellular solution to slow diffusion. In the VTA, dextran slowed the rate of rise and fall of the extracellular dopamine transient as measured by fast-scan cyclic voltammetry yet did not alter the kinetics of the dopamine-dependent IPSC. Dextran failed to significantly alter the time course of the rise and fall of the dopamine transient in the striatum, suggesting a more influential role for reuptake in the striatum. The conclusion is that the time course of dopamine within the extracellular space of the VTA is dependent on both diffusion and reuptake, whereas the activation of D2 receptors on dopamine neurons is primarily limited by reuptake.",
author = "Ford, {Christopher P.} and Gantz, {Stephanie C.} and Phillips, {Paul E M} and John Williams",
year = "2010",
month = "5",
day = "19",
doi = "10.1523/JNEUROSCI.1020-10.2010",
language = "English (US)",
volume = "30",
pages = "6975--6983",
journal = "Journal of Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "20",

}

TY - JOUR

T1 - Control of extracellular dopamine at dendrite and axon terminals

AU - Ford, Christopher P.

AU - Gantz, Stephanie C.

AU - Phillips, Paul E M

AU - Williams, John

PY - 2010/5/19

Y1 - 2010/5/19

N2 - Midbrain dopamine neurons release dopamine from both axons and dendrites. The mechanism underlying release at these different sites has been proposed to differ. This study used electrochemical and electrophysiological methods to compare the time course and calcium dependence of somatodendritic dopamine release in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) to that of axonal dopamine release in the dorsal striatum. The amount of dopamine released in the striatum was ∼20-fold greater than in cell body regions of the VTA or SNc. However, the calcium dependence and time to peak of the dopamine transients were similar. These results illustrate an unexpected overall similarity in the mechanisms of dopamine release in the striatum and cell body regions. To examine how diffusion regulates the time course of dopamine following release, dextran was added to the extracellular solution to slow diffusion. In the VTA, dextran slowed the rate of rise and fall of the extracellular dopamine transient as measured by fast-scan cyclic voltammetry yet did not alter the kinetics of the dopamine-dependent IPSC. Dextran failed to significantly alter the time course of the rise and fall of the dopamine transient in the striatum, suggesting a more influential role for reuptake in the striatum. The conclusion is that the time course of dopamine within the extracellular space of the VTA is dependent on both diffusion and reuptake, whereas the activation of D2 receptors on dopamine neurons is primarily limited by reuptake.

AB - Midbrain dopamine neurons release dopamine from both axons and dendrites. The mechanism underlying release at these different sites has been proposed to differ. This study used electrochemical and electrophysiological methods to compare the time course and calcium dependence of somatodendritic dopamine release in the ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) to that of axonal dopamine release in the dorsal striatum. The amount of dopamine released in the striatum was ∼20-fold greater than in cell body regions of the VTA or SNc. However, the calcium dependence and time to peak of the dopamine transients were similar. These results illustrate an unexpected overall similarity in the mechanisms of dopamine release in the striatum and cell body regions. To examine how diffusion regulates the time course of dopamine following release, dextran was added to the extracellular solution to slow diffusion. In the VTA, dextran slowed the rate of rise and fall of the extracellular dopamine transient as measured by fast-scan cyclic voltammetry yet did not alter the kinetics of the dopamine-dependent IPSC. Dextran failed to significantly alter the time course of the rise and fall of the dopamine transient in the striatum, suggesting a more influential role for reuptake in the striatum. The conclusion is that the time course of dopamine within the extracellular space of the VTA is dependent on both diffusion and reuptake, whereas the activation of D2 receptors on dopamine neurons is primarily limited by reuptake.

UR - http://www.scopus.com/inward/record.url?scp=77952663432&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77952663432&partnerID=8YFLogxK

U2 - 10.1523/JNEUROSCI.1020-10.2010

DO - 10.1523/JNEUROSCI.1020-10.2010

M3 - Article

VL - 30

SP - 6975

EP - 6983

JO - Journal of Neuroscience

JF - Journal of Neuroscience

SN - 0270-6474

IS - 20

ER -