Dopamine and baclofen inhibit the hyperpolarization-activated cation current in rat ventral tegmental neurones

Zhi-Gen Jiang, M. Pessia, R. A. North

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Whole-cell patch-clamp recordings were made from dopamine-containing ventral tegmental area neurones in slices of rat midbrain. An inward current (1(h)) was activated by hyperpolarization from -60 mV. Dopamine (30 μM) reduced the amplitude of I(h) by 10-30% at potentials from -70 to -120 mV. The effect was concentration dependent, mimicked by the D2 agonist quinpirole, and prevented by the D2 antagonist (-)-sulpiride. Baclofen (0.3-3 μM) also inhibited I(h); this action was antagonized by 2-hydroxysaclofen but not by (-)-sulpiride. The decrease in I(h) resulted from a reduction in the maximal current with no change in the voltage dependence. The action of dopamine was unaffected by cadmium (200 μM), forskolin (10 μM), the adenylyl cyclase inhibitor 2',3'-dideoxyadenosine (100 μM), or by intracellular solution containing cyclic AMP (2 mM). I(h) was progressively reduced during the first 5-10 min of recording with electrodes containing guanosine 5'-O-(3-thiotriphosphate); after this time, dopamine had no further effect. It is concluded that agonists acting at D2 receptors and GABA(B) receptors reduce I(h) in ventral tegmental neurones.

Original languageEnglish (US)
Pages (from-to)753-764
Number of pages12
JournalJournal of Physiology
Volume462
StatePublished - 1993

Fingerprint

Baclofen
Cations
Dopamine
Neurons
Sulpiride
Dideoxyadenosine
GABA-B Receptors
Quinpirole
Guanosine 5'-O-(3-Thiotriphosphate)
Ventral Tegmental Area
Colforsin
Mesencephalon
Cadmium
Cyclic AMP
Electrodes

ASJC Scopus subject areas

  • Physiology

Cite this

Dopamine and baclofen inhibit the hyperpolarization-activated cation current in rat ventral tegmental neurones. / Jiang, Zhi-Gen; Pessia, M.; North, R. A.

In: Journal of Physiology, Vol. 462, 1993, p. 753-764.

Research output: Contribution to journalArticle

@article{50f4c698db004a49a1a17c99c48f11b3,
title = "Dopamine and baclofen inhibit the hyperpolarization-activated cation current in rat ventral tegmental neurones",
abstract = "Whole-cell patch-clamp recordings were made from dopamine-containing ventral tegmental area neurones in slices of rat midbrain. An inward current (1(h)) was activated by hyperpolarization from -60 mV. Dopamine (30 μM) reduced the amplitude of I(h) by 10-30{\%} at potentials from -70 to -120 mV. The effect was concentration dependent, mimicked by the D2 agonist quinpirole, and prevented by the D2 antagonist (-)-sulpiride. Baclofen (0.3-3 μM) also inhibited I(h); this action was antagonized by 2-hydroxysaclofen but not by (-)-sulpiride. The decrease in I(h) resulted from a reduction in the maximal current with no change in the voltage dependence. The action of dopamine was unaffected by cadmium (200 μM), forskolin (10 μM), the adenylyl cyclase inhibitor 2',3'-dideoxyadenosine (100 μM), or by intracellular solution containing cyclic AMP (2 mM). I(h) was progressively reduced during the first 5-10 min of recording with electrodes containing guanosine 5'-O-(3-thiotriphosphate); after this time, dopamine had no further effect. It is concluded that agonists acting at D2 receptors and GABA(B) receptors reduce I(h) in ventral tegmental neurones.",
author = "Zhi-Gen Jiang and M. Pessia and North, {R. A.}",
year = "1993",
language = "English (US)",
volume = "462",
pages = "753--764",
journal = "Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Dopamine and baclofen inhibit the hyperpolarization-activated cation current in rat ventral tegmental neurones

AU - Jiang, Zhi-Gen

AU - Pessia, M.

AU - North, R. A.

PY - 1993

Y1 - 1993

N2 - Whole-cell patch-clamp recordings were made from dopamine-containing ventral tegmental area neurones in slices of rat midbrain. An inward current (1(h)) was activated by hyperpolarization from -60 mV. Dopamine (30 μM) reduced the amplitude of I(h) by 10-30% at potentials from -70 to -120 mV. The effect was concentration dependent, mimicked by the D2 agonist quinpirole, and prevented by the D2 antagonist (-)-sulpiride. Baclofen (0.3-3 μM) also inhibited I(h); this action was antagonized by 2-hydroxysaclofen but not by (-)-sulpiride. The decrease in I(h) resulted from a reduction in the maximal current with no change in the voltage dependence. The action of dopamine was unaffected by cadmium (200 μM), forskolin (10 μM), the adenylyl cyclase inhibitor 2',3'-dideoxyadenosine (100 μM), or by intracellular solution containing cyclic AMP (2 mM). I(h) was progressively reduced during the first 5-10 min of recording with electrodes containing guanosine 5'-O-(3-thiotriphosphate); after this time, dopamine had no further effect. It is concluded that agonists acting at D2 receptors and GABA(B) receptors reduce I(h) in ventral tegmental neurones.

AB - Whole-cell patch-clamp recordings were made from dopamine-containing ventral tegmental area neurones in slices of rat midbrain. An inward current (1(h)) was activated by hyperpolarization from -60 mV. Dopamine (30 μM) reduced the amplitude of I(h) by 10-30% at potentials from -70 to -120 mV. The effect was concentration dependent, mimicked by the D2 agonist quinpirole, and prevented by the D2 antagonist (-)-sulpiride. Baclofen (0.3-3 μM) also inhibited I(h); this action was antagonized by 2-hydroxysaclofen but not by (-)-sulpiride. The decrease in I(h) resulted from a reduction in the maximal current with no change in the voltage dependence. The action of dopamine was unaffected by cadmium (200 μM), forskolin (10 μM), the adenylyl cyclase inhibitor 2',3'-dideoxyadenosine (100 μM), or by intracellular solution containing cyclic AMP (2 mM). I(h) was progressively reduced during the first 5-10 min of recording with electrodes containing guanosine 5'-O-(3-thiotriphosphate); after this time, dopamine had no further effect. It is concluded that agonists acting at D2 receptors and GABA(B) receptors reduce I(h) in ventral tegmental neurones.

UR - http://www.scopus.com/inward/record.url?scp=0027406974&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027406974&partnerID=8YFLogxK

M3 - Article

C2 - 8392580

AN - SCOPUS:0027406974

VL - 462

SP - 753

EP - 764

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

ER -