5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro

Ling-Ling Hwang, N. J. Dun

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5- HT(H)), a slow depolarization (5-HT(D)) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HT(H) were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HT(H); the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K +](o). Barium (Ba 2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HT(H). The 5-HT(1A) receptor agonist (±)-8-hydroxy- dipropylamino-tetralin (8-OH-DPAT; 5-50 μM) hyperpolarized RVLM neurons. The 5-HT(1A) antagonist pindobind-5-HT(1A) (PBD; 1-3 μM) and the 5-HT 2/5-HT 1 receptor antagonist spiperone (1-10 μM) suppressed 5-HT(H) and the hyperpolarizing phase of biphasic responses; the 5-HT 2 receptor antagonist ketanserin (3 μM) was without significant effect 5-HT(D) were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HT(D). 5-HT(D) were reduced in an elevated [K +](o) (7.0 mM) solution and >60% in a low Na + (26 mM) solution and were not significantly changed in a low Cl - (6.7 mM) or Ca 2+-free/high Mg 2+ (10.9 mM) solution. The 5-HT 2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5- HT 2 antagonist ketanserin (1-10 μM) attenuated the 5-HT(D) and the depolarizing phase of biphasic responses, whereas the 5-HT(1A) receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HT(H) as well as the 5-HT(D). The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT(1A) and 5-HT 2 receptors, which are G-proteins coupled. 5-HT(H) may involve an increase of an inwardly rectifying K + conductance, and 5-HT(D) appear to be caused by a decrease of K + conductance and/or increase of nonselective cation conductance.

Original languageEnglish
Pages (from-to)1033-1041
Number of pages9
JournalJournal of Neurophysiology
Volume80
Issue number3
Publication statusPublished - Sep 1998
Externally publishedYes

Fingerprint

Serotonin
Neurons
Receptor, Serotonin, 5-HT1A
Serotonin Receptors
In Vitro Techniques
Ketanserin
Serotonin Antagonists
Spiperone
8-Hydroxy-2-(di-n-propylamino)tetralin
Serotonin Receptor Agonists
Tetraethylammonium
Guanine Nucleotides
Tetrodotoxin
Patch-Clamp Techniques
Barium
GTP-Binding Proteins
Membrane Potentials
Brain Stem
Cations
Hydrolysis

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro. / Hwang, Ling-Ling; Dun, N. J.

In: Journal of Neurophysiology, Vol. 80, No. 3, 09.1998, p. 1033-1041.

Research output: Contribution to journalArticle

@article{47ce1596709b412a986417a8e22ccfbd,
title = "5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro",
abstract = "Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5- HT(H)), a slow depolarization (5-HT(D)) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HT(H) were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HT(H); the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K +](o). Barium (Ba 2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HT(H). The 5-HT(1A) receptor agonist (±)-8-hydroxy- dipropylamino-tetralin (8-OH-DPAT; 5-50 μM) hyperpolarized RVLM neurons. The 5-HT(1A) antagonist pindobind-5-HT(1A) (PBD; 1-3 μM) and the 5-HT 2/5-HT 1 receptor antagonist spiperone (1-10 μM) suppressed 5-HT(H) and the hyperpolarizing phase of biphasic responses; the 5-HT 2 receptor antagonist ketanserin (3 μM) was without significant effect 5-HT(D) were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HT(D). 5-HT(D) were reduced in an elevated [K +](o) (7.0 mM) solution and >60{\%} in a low Na + (26 mM) solution and were not significantly changed in a low Cl - (6.7 mM) or Ca 2+-free/high Mg 2+ (10.9 mM) solution. The 5-HT 2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5- HT 2 antagonist ketanserin (1-10 μM) attenuated the 5-HT(D) and the depolarizing phase of biphasic responses, whereas the 5-HT(1A) receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HT(H) as well as the 5-HT(D). The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT(1A) and 5-HT 2 receptors, which are G-proteins coupled. 5-HT(H) may involve an increase of an inwardly rectifying K + conductance, and 5-HT(D) appear to be caused by a decrease of K + conductance and/or increase of nonselective cation conductance.",
author = "Ling-Ling Hwang and Dun, {N. J.}",
year = "1998",
month = "9",
language = "English",
volume = "80",
pages = "1033--1041",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "3",

}

TY - JOUR

T1 - 5-Hydroxytryptamine responses in immature rat rostral ventrolateral medulla neurons in vitro

AU - Hwang, Ling-Ling

AU - Dun, N. J.

PY - 1998/9

Y1 - 1998/9

N2 - Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5- HT(H)), a slow depolarization (5-HT(D)) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HT(H) were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HT(H); the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K +](o). Barium (Ba 2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HT(H). The 5-HT(1A) receptor agonist (±)-8-hydroxy- dipropylamino-tetralin (8-OH-DPAT; 5-50 μM) hyperpolarized RVLM neurons. The 5-HT(1A) antagonist pindobind-5-HT(1A) (PBD; 1-3 μM) and the 5-HT 2/5-HT 1 receptor antagonist spiperone (1-10 μM) suppressed 5-HT(H) and the hyperpolarizing phase of biphasic responses; the 5-HT 2 receptor antagonist ketanserin (3 μM) was without significant effect 5-HT(D) were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HT(D). 5-HT(D) were reduced in an elevated [K +](o) (7.0 mM) solution and >60% in a low Na + (26 mM) solution and were not significantly changed in a low Cl - (6.7 mM) or Ca 2+-free/high Mg 2+ (10.9 mM) solution. The 5-HT 2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5- HT 2 antagonist ketanserin (1-10 μM) attenuated the 5-HT(D) and the depolarizing phase of biphasic responses, whereas the 5-HT(1A) receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HT(H) as well as the 5-HT(D). The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT(1A) and 5-HT 2 receptors, which are G-proteins coupled. 5-HT(H) may involve an increase of an inwardly rectifying K + conductance, and 5-HT(D) appear to be caused by a decrease of K + conductance and/or increase of nonselective cation conductance.

AB - Whole cell patch recordings were made from rostral ventrolateral medulla (RVLM) neurons of brainstem slices from 8- to 12-day-old rats. By superfusion or pressure ejection to RVLM neurons, 5-hydroxytryptamine (5-HT) elicited three types of membrane potential changes: a slow hyperpolarization (5- HT(H)), a slow depolarization (5-HT(D)) and a biphasic response, which persisted in a tetrodotoxin (TTX, 0.3 μM)-containing solution. 5-HT(H) were accompanied by a decrease of input resistance in the majority of responsive neurons. Hyperpolarization reduced and depolarization increased the 5-HT(H); the mean reversal potential was -92.3 mV in 3.1 mM and shifted to -69.3 mV in 7 mM [K +](o). Barium (Ba 2+, 0.1 mM) but not tetraethylammonium (TEA, 10 mM) suppressed 5-HT(H). The 5-HT(1A) receptor agonist (±)-8-hydroxy- dipropylamino-tetralin (8-OH-DPAT; 5-50 μM) hyperpolarized RVLM neurons. The 5-HT(1A) antagonist pindobind-5-HT(1A) (PBD; 1-3 μM) and the 5-HT 2/5-HT 1 receptor antagonist spiperone (1-10 μM) suppressed 5-HT(H) and the hyperpolarizing phase of biphasic responses; the 5-HT 2 receptor antagonist ketanserin (3 μM) was without significant effect 5-HT(D) were associated with an increase or no apparent change of input resistance in RVLM neurons. Hyperpolarization of the membrane decreased or caused no apparent change in 5-HT(D). 5-HT(D) were reduced in an elevated [K +](o) (7.0 mM) solution and >60% in a low Na + (26 mM) solution and were not significantly changed in a low Cl - (6.7 mM) or Ca 2+-free/high Mg 2+ (10.9 mM) solution. The 5-HT 2 receptor agonist α-methyl-5-HT (50 μM) depolarized RVLM neurons, and the 5- HT 2 antagonist ketanserin (1-10 μM) attenuated the 5-HT(D) and the depolarizing phase of biphasic responses, whereas the 5-HT(1A) receptor antagonist PBD (2 μM) was without effect. Inclusion of the hydrolysis resistant guanine nucleotide GDP-β-S in patch solution significantly reduced the 5-HT(H) as well as the 5-HT(D). The present study shows that, in the immature rat RVLM neurons, 5-HT causes a slow hyperpolarization and depolarization probably by interacting with 5-HT(1A) and 5-HT 2 receptors, which are G-proteins coupled. 5-HT(H) may involve an increase of an inwardly rectifying K + conductance, and 5-HT(D) appear to be caused by a decrease of K + conductance and/or increase of nonselective cation conductance.

UR - http://www.scopus.com/inward/record.url?scp=0031761033&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031761033&partnerID=8YFLogxK

M3 - Article

VL - 80

SP - 1033

EP - 1041

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 3

ER -