Presynaptic inhibition by baclofen of retinohypothalamic excitatory synaptic transmission in rat suprachiasmatic nucleus

Zhi-Gen Jiang, Charles Allen, R. A. North

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Optic nerve stimulation evoked monosynaptic excitatory postsynaptic currents in suprachiasmatic nucleus neurons maintained in vitro. These currents were completely blocked by a combination of glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and 4-aminophosphonovaleric acid. Stimulation of the ipsilateral or contralateral suprachiasmatic nucleus produced a biphasic response consisting of an excitatory postsynaptic current followed by an bicuculline-sensitive inhibitory postsynaptic current. Most suprachiasmatic nucleus neurons had spontaneous inhibitory and excitatory synaptic currents produced by action potential-independent and, less frequently, action potential-dependent release of GABA and glutamate. Baclofen reversibly reduced the amplitude of excitatory postsynaptic currents evoked by optic nerve stimulation and the effect was antagonized by 2-hydroxysaclofen. In addition, baclofen reduced the frequency but not the amplitude of the spontaneous miniature excitatory postsynaptic currents. In a subset of suprachiasmatic nucleus neurons, baclofen induced an outward current, probably by increasing a potassium conductance. Baclofen had no effect on either evoked or spontaneous inhibitory postsynaptic currents or on currents activated by pulse application of glutamate. These data indicate that activation of GABAB receptors can inhibit suprachiasmatic nucleus neurons by two mechanisms. The first is to inhibit the release of glutamate from terminals of the retinohypothalamic tract. The second is the postsynaptic activation of a potassium conductance in a portion of these neurons.

Original languageEnglish (US)
Pages (from-to)813-819
Number of pages7
JournalNeuroscience
Volume64
Issue number3
DOIs
StatePublished - 1995

Fingerprint

Suprachiasmatic Nucleus
Baclofen
Synaptic Transmission
Excitatory Postsynaptic Potentials
Neurons
Glutamic Acid
Inhibitory Postsynaptic Potentials
Optic Nerve
Action Potentials
Potassium
6-Cyano-7-nitroquinoxaline-2,3-dione
Excitatory Amino Acid Antagonists
Bicuculline
gamma-Aminobutyric Acid
Acids

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Presynaptic inhibition by baclofen of retinohypothalamic excitatory synaptic transmission in rat suprachiasmatic nucleus. / Jiang, Zhi-Gen; Allen, Charles; North, R. A.

In: Neuroscience, Vol. 64, No. 3, 1995, p. 813-819.

Research output: Contribution to journalArticle

@article{fbc437b4d2894855b8bc0b9d3518aac1,
title = "Presynaptic inhibition by baclofen of retinohypothalamic excitatory synaptic transmission in rat suprachiasmatic nucleus",
abstract = "Optic nerve stimulation evoked monosynaptic excitatory postsynaptic currents in suprachiasmatic nucleus neurons maintained in vitro. These currents were completely blocked by a combination of glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and 4-aminophosphonovaleric acid. Stimulation of the ipsilateral or contralateral suprachiasmatic nucleus produced a biphasic response consisting of an excitatory postsynaptic current followed by an bicuculline-sensitive inhibitory postsynaptic current. Most suprachiasmatic nucleus neurons had spontaneous inhibitory and excitatory synaptic currents produced by action potential-independent and, less frequently, action potential-dependent release of GABA and glutamate. Baclofen reversibly reduced the amplitude of excitatory postsynaptic currents evoked by optic nerve stimulation and the effect was antagonized by 2-hydroxysaclofen. In addition, baclofen reduced the frequency but not the amplitude of the spontaneous miniature excitatory postsynaptic currents. In a subset of suprachiasmatic nucleus neurons, baclofen induced an outward current, probably by increasing a potassium conductance. Baclofen had no effect on either evoked or spontaneous inhibitory postsynaptic currents or on currents activated by pulse application of glutamate. These data indicate that activation of GABAB receptors can inhibit suprachiasmatic nucleus neurons by two mechanisms. The first is to inhibit the release of glutamate from terminals of the retinohypothalamic tract. The second is the postsynaptic activation of a potassium conductance in a portion of these neurons.",
author = "Zhi-Gen Jiang and Charles Allen and North, {R. A.}",
year = "1995",
doi = "10.1016/0306-4522(94)00429-9",
language = "English (US)",
volume = "64",
pages = "813--819",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "3",

}

TY - JOUR

T1 - Presynaptic inhibition by baclofen of retinohypothalamic excitatory synaptic transmission in rat suprachiasmatic nucleus

AU - Jiang, Zhi-Gen

AU - Allen, Charles

AU - North, R. A.

PY - 1995

Y1 - 1995

N2 - Optic nerve stimulation evoked monosynaptic excitatory postsynaptic currents in suprachiasmatic nucleus neurons maintained in vitro. These currents were completely blocked by a combination of glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and 4-aminophosphonovaleric acid. Stimulation of the ipsilateral or contralateral suprachiasmatic nucleus produced a biphasic response consisting of an excitatory postsynaptic current followed by an bicuculline-sensitive inhibitory postsynaptic current. Most suprachiasmatic nucleus neurons had spontaneous inhibitory and excitatory synaptic currents produced by action potential-independent and, less frequently, action potential-dependent release of GABA and glutamate. Baclofen reversibly reduced the amplitude of excitatory postsynaptic currents evoked by optic nerve stimulation and the effect was antagonized by 2-hydroxysaclofen. In addition, baclofen reduced the frequency but not the amplitude of the spontaneous miniature excitatory postsynaptic currents. In a subset of suprachiasmatic nucleus neurons, baclofen induced an outward current, probably by increasing a potassium conductance. Baclofen had no effect on either evoked or spontaneous inhibitory postsynaptic currents or on currents activated by pulse application of glutamate. These data indicate that activation of GABAB receptors can inhibit suprachiasmatic nucleus neurons by two mechanisms. The first is to inhibit the release of glutamate from terminals of the retinohypothalamic tract. The second is the postsynaptic activation of a potassium conductance in a portion of these neurons.

AB - Optic nerve stimulation evoked monosynaptic excitatory postsynaptic currents in suprachiasmatic nucleus neurons maintained in vitro. These currents were completely blocked by a combination of glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione and 4-aminophosphonovaleric acid. Stimulation of the ipsilateral or contralateral suprachiasmatic nucleus produced a biphasic response consisting of an excitatory postsynaptic current followed by an bicuculline-sensitive inhibitory postsynaptic current. Most suprachiasmatic nucleus neurons had spontaneous inhibitory and excitatory synaptic currents produced by action potential-independent and, less frequently, action potential-dependent release of GABA and glutamate. Baclofen reversibly reduced the amplitude of excitatory postsynaptic currents evoked by optic nerve stimulation and the effect was antagonized by 2-hydroxysaclofen. In addition, baclofen reduced the frequency but not the amplitude of the spontaneous miniature excitatory postsynaptic currents. In a subset of suprachiasmatic nucleus neurons, baclofen induced an outward current, probably by increasing a potassium conductance. Baclofen had no effect on either evoked or spontaneous inhibitory postsynaptic currents or on currents activated by pulse application of glutamate. These data indicate that activation of GABAB receptors can inhibit suprachiasmatic nucleus neurons by two mechanisms. The first is to inhibit the release of glutamate from terminals of the retinohypothalamic tract. The second is the postsynaptic activation of a potassium conductance in a portion of these neurons.

UR - http://www.scopus.com/inward/record.url?scp=0028816564&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028816564&partnerID=8YFLogxK

U2 - 10.1016/0306-4522(94)00429-9

DO - 10.1016/0306-4522(94)00429-9

M3 - Article

C2 - 7715789

AN - SCOPUS:0028816564

VL - 64

SP - 813

EP - 819

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 3

ER -