Inhibition by 5-hydroxytryptamine and noradrenaline in substantia gelatinosa of guinea-pig spinal trigeminal nucleus

T. J. Grudt, John Williams, R. A. Travagli

Research output: Contribution to journalArticle

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Abstract

1. Whole-cell and intracellular recordings were made from neurons in slices of guinea-pig spinal trigeminal nucleus pars caudalis. 2. 5-Hydroxytryptamine (5-HT) hyperpolarized 70% of neurons by activating 5-HT(1A) receptors. The effect was mimicked by 5-carboxamidotryptamine (5-CT) and (±)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronapthalene hydrobromide (8-OH-DPAT) and antagonized by 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)-butyl]-piperazine hydrobromide (NAN 190) and pindobind-5-HT(1A). Nine per cent of the neurons were depolarized by 5-HT. 3. In about 20% of recordings, 5-HT also evoked repetitive inhibitory postsynaptic potentials that were mediated by glycine. 4. Noradrenaline (NA) hyperpolarized 71% of neurons. This effect was mediated by activation of α2-adrenoceptors, since 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6- quinoxalinamine (UR14304) also caused a hyperpolarization and idazoxan (1 μM) blocked the hyperpolarization to both NA and UK14304. Phenylephrine depolarized a subset of neurons and this depolarization was blocked by prazosin, suggesting an action mediated by activation of α1-adrenoceptors. 5. NA also evoked repetitive GABA(A)-mediated inhibitory postsynaptic potentials in about 20% of recordings. The increase in synaptic activity was mimicked by phenylephrine and blocked by prazosin. These results indicate that there are at least two mechanisms through which 5-HT and NA inhibit neurons: (i) in many cells both 5-HT and NA mediate a hyperpolarization through an increase of a potassium conductance; (ii) 5-HT and NA also activated GABA- and glycine-containing interneurons to cause IPSPs in separate groups of cells.

Original languageEnglish (US)
Pages (from-to)113-120
Number of pages8
JournalJournal of Physiology
Volume485
Issue number1
StatePublished - 1995

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Substantia Gelatinosa
Spinal Trigeminal Nucleus
Serotonin
Norepinephrine
Guinea Pigs
Neurons
Inhibitory Postsynaptic Potentials
Prazosin
Phenylephrine
Glycine
gamma-Aminobutyric Acid
Adrenergic Receptors
Idazoxan
8-Hydroxy-2-(di-n-propylamino)tetralin
Receptor, Serotonin, 5-HT1A
Patch-Clamp Techniques
Interneurons
Potassium

ASJC Scopus subject areas

  • Physiology

Cite this

Inhibition by 5-hydroxytryptamine and noradrenaline in substantia gelatinosa of guinea-pig spinal trigeminal nucleus. / Grudt, T. J.; Williams, John; Travagli, R. A.

In: Journal of Physiology, Vol. 485, No. 1, 1995, p. 113-120.

Research output: Contribution to journalArticle

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abstract = "1. Whole-cell and intracellular recordings were made from neurons in slices of guinea-pig spinal trigeminal nucleus pars caudalis. 2. 5-Hydroxytryptamine (5-HT) hyperpolarized 70{\%} of neurons by activating 5-HT(1A) receptors. The effect was mimicked by 5-carboxamidotryptamine (5-CT) and (±)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronapthalene hydrobromide (8-OH-DPAT) and antagonized by 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)-butyl]-piperazine hydrobromide (NAN 190) and pindobind-5-HT(1A). Nine per cent of the neurons were depolarized by 5-HT. 3. In about 20{\%} of recordings, 5-HT also evoked repetitive inhibitory postsynaptic potentials that were mediated by glycine. 4. Noradrenaline (NA) hyperpolarized 71{\%} of neurons. This effect was mediated by activation of α2-adrenoceptors, since 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6- quinoxalinamine (UR14304) also caused a hyperpolarization and idazoxan (1 μM) blocked the hyperpolarization to both NA and UK14304. Phenylephrine depolarized a subset of neurons and this depolarization was blocked by prazosin, suggesting an action mediated by activation of α1-adrenoceptors. 5. NA also evoked repetitive GABA(A)-mediated inhibitory postsynaptic potentials in about 20{\%} of recordings. The increase in synaptic activity was mimicked by phenylephrine and blocked by prazosin. These results indicate that there are at least two mechanisms through which 5-HT and NA inhibit neurons: (i) in many cells both 5-HT and NA mediate a hyperpolarization through an increase of a potassium conductance; (ii) 5-HT and NA also activated GABA- and glycine-containing interneurons to cause IPSPs in separate groups of cells.",
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AB - 1. Whole-cell and intracellular recordings were made from neurons in slices of guinea-pig spinal trigeminal nucleus pars caudalis. 2. 5-Hydroxytryptamine (5-HT) hyperpolarized 70% of neurons by activating 5-HT(1A) receptors. The effect was mimicked by 5-carboxamidotryptamine (5-CT) and (±)-2-dipropylamino-8-hydroxy-1,2,3,4-tetrahydronapthalene hydrobromide (8-OH-DPAT) and antagonized by 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)-butyl]-piperazine hydrobromide (NAN 190) and pindobind-5-HT(1A). Nine per cent of the neurons were depolarized by 5-HT. 3. In about 20% of recordings, 5-HT also evoked repetitive inhibitory postsynaptic potentials that were mediated by glycine. 4. Noradrenaline (NA) hyperpolarized 71% of neurons. This effect was mediated by activation of α2-adrenoceptors, since 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6- quinoxalinamine (UR14304) also caused a hyperpolarization and idazoxan (1 μM) blocked the hyperpolarization to both NA and UK14304. Phenylephrine depolarized a subset of neurons and this depolarization was blocked by prazosin, suggesting an action mediated by activation of α1-adrenoceptors. 5. NA also evoked repetitive GABA(A)-mediated inhibitory postsynaptic potentials in about 20% of recordings. The increase in synaptic activity was mimicked by phenylephrine and blocked by prazosin. These results indicate that there are at least two mechanisms through which 5-HT and NA inhibit neurons: (i) in many cells both 5-HT and NA mediate a hyperpolarization through an increase of a potassium conductance; (ii) 5-HT and NA also activated GABA- and glycine-containing interneurons to cause IPSPs in separate groups of cells.

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