Excitatory amino acid receptor activation in the raphe pallidus area mediates prostaglandin-evoked thermogenesis

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Abstract

To investigate the role of excitatory amino acid neurotransmission within the rostral raphe pallidus area (RPa) in thermogenic and cardiovascular responses, changes in sympathetic nerve activity to brown adipose tissue (BAT), BAT temperature, expired CO2, arterial pressure, and heart rate were recorded after microinjection of excitatory amino acid (EAA) receptor agonists into the RPa in urethan-chloralose-anesthetized, ventilated rats. To determine whether EAA neurotransmission within the RPa is necessary for the responses evoked by disinhibition of the RPa or by prostaglandin E2 acting within the medial preoptic area, BAT sympathetic nerve activity, BAT temperature, expired CO2, arterial pressure, and heart rate were measured during these treatments both before and after blockade of EAA receptors within the RPa. Microinjection of EAA receptor agonists into the RPa resulted in significant increases in all measured variables; these increases were attenuated by prior microinjection of the respective EAA receptor antagonists into the RPa. Microinjection of prostaglandin E2 into the medial preoptic area or microinjection of bicuculline into the RPa resulted in respective significant increases in BAT sympathetic nerve activity (+approximately 190% and +approximately 235% of resting levels), in BAT temperature (approximately 1.8°C and approximately 2°C), in expired CO2 (approximately 1.1% and approximately 1.1%), and in heart rate (approximately 97 beats per minute (bpm) and approximately 100 bpm). Blockade of ionotropic EAA receptors within the RPa by microinjection of kynurenate completely reversed the prostaglandin E2 or bicuculline-evoked increases in all of the measured variables. Blockade of either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors alone resulted in marked attenuations of the prostaglandin E2-evoked effects on all of the measured variables. These data demonstrate that activation of an EAA input to the RPa is necessary for the BAT thermogenic and the cardiovascular effects resulting from the actions of prostaglandin E2 within the medial preoptic area or from the disinhibition of local neurons in the RPa.

Original languageEnglish (US)
Pages (from-to)5-15
Number of pages11
JournalNeuroscience
Volume122
Issue number1
DOIs
StatePublished - Nov 20 2003

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Brown Adipose Tissue
Thermogenesis
Glutamate Receptors
Microinjections
Prostaglandins
Dinoprostone
Excitatory Amino Acids
Preoptic Area
Excitatory Amino Acid Agonists
Bicuculline
Heart Rate
Synaptic Transmission
Temperature
Arterial Pressure
Kynurenic Acid
Aminoacylation
D-Aspartic Acid
Excitatory Amino Acid Antagonists
Chloralose
Urethane

Keywords

  • Brown adipose tissue
  • Fever
  • Glutamate
  • Medial preoptic area
  • Sympathetic
  • Thermoregulation

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Excitatory amino acid receptor activation in the raphe pallidus area mediates prostaglandin-evoked thermogenesis",
abstract = "To investigate the role of excitatory amino acid neurotransmission within the rostral raphe pallidus area (RPa) in thermogenic and cardiovascular responses, changes in sympathetic nerve activity to brown adipose tissue (BAT), BAT temperature, expired CO2, arterial pressure, and heart rate were recorded after microinjection of excitatory amino acid (EAA) receptor agonists into the RPa in urethan-chloralose-anesthetized, ventilated rats. To determine whether EAA neurotransmission within the RPa is necessary for the responses evoked by disinhibition of the RPa or by prostaglandin E2 acting within the medial preoptic area, BAT sympathetic nerve activity, BAT temperature, expired CO2, arterial pressure, and heart rate were measured during these treatments both before and after blockade of EAA receptors within the RPa. Microinjection of EAA receptor agonists into the RPa resulted in significant increases in all measured variables; these increases were attenuated by prior microinjection of the respective EAA receptor antagonists into the RPa. Microinjection of prostaglandin E2 into the medial preoptic area or microinjection of bicuculline into the RPa resulted in respective significant increases in BAT sympathetic nerve activity (+approximately 190{\%} and +approximately 235{\%} of resting levels), in BAT temperature (approximately 1.8°C and approximately 2°C), in expired CO2 (approximately 1.1{\%} and approximately 1.1{\%}), and in heart rate (approximately 97 beats per minute (bpm) and approximately 100 bpm). Blockade of ionotropic EAA receptors within the RPa by microinjection of kynurenate completely reversed the prostaglandin E2 or bicuculline-evoked increases in all of the measured variables. Blockade of either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors alone resulted in marked attenuations of the prostaglandin E2-evoked effects on all of the measured variables. These data demonstrate that activation of an EAA input to the RPa is necessary for the BAT thermogenic and the cardiovascular effects resulting from the actions of prostaglandin E2 within the medial preoptic area or from the disinhibition of local neurons in the RPa.",
keywords = "Brown adipose tissue, Fever, Glutamate, Medial preoptic area, Sympathetic, Thermoregulation",
author = "Madden, {Christopher (Chris)} and Shaun Morrison",
year = "2003",
month = "11",
day = "20",
doi = "10.1016/S0306-4522(03)00527-X",
language = "English (US)",
volume = "122",
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TY - JOUR

T1 - Excitatory amino acid receptor activation in the raphe pallidus area mediates prostaglandin-evoked thermogenesis

AU - Madden, Christopher (Chris)

AU - Morrison, Shaun

PY - 2003/11/20

Y1 - 2003/11/20

N2 - To investigate the role of excitatory amino acid neurotransmission within the rostral raphe pallidus area (RPa) in thermogenic and cardiovascular responses, changes in sympathetic nerve activity to brown adipose tissue (BAT), BAT temperature, expired CO2, arterial pressure, and heart rate were recorded after microinjection of excitatory amino acid (EAA) receptor agonists into the RPa in urethan-chloralose-anesthetized, ventilated rats. To determine whether EAA neurotransmission within the RPa is necessary for the responses evoked by disinhibition of the RPa or by prostaglandin E2 acting within the medial preoptic area, BAT sympathetic nerve activity, BAT temperature, expired CO2, arterial pressure, and heart rate were measured during these treatments both before and after blockade of EAA receptors within the RPa. Microinjection of EAA receptor agonists into the RPa resulted in significant increases in all measured variables; these increases were attenuated by prior microinjection of the respective EAA receptor antagonists into the RPa. Microinjection of prostaglandin E2 into the medial preoptic area or microinjection of bicuculline into the RPa resulted in respective significant increases in BAT sympathetic nerve activity (+approximately 190% and +approximately 235% of resting levels), in BAT temperature (approximately 1.8°C and approximately 2°C), in expired CO2 (approximately 1.1% and approximately 1.1%), and in heart rate (approximately 97 beats per minute (bpm) and approximately 100 bpm). Blockade of ionotropic EAA receptors within the RPa by microinjection of kynurenate completely reversed the prostaglandin E2 or bicuculline-evoked increases in all of the measured variables. Blockade of either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors alone resulted in marked attenuations of the prostaglandin E2-evoked effects on all of the measured variables. These data demonstrate that activation of an EAA input to the RPa is necessary for the BAT thermogenic and the cardiovascular effects resulting from the actions of prostaglandin E2 within the medial preoptic area or from the disinhibition of local neurons in the RPa.

AB - To investigate the role of excitatory amino acid neurotransmission within the rostral raphe pallidus area (RPa) in thermogenic and cardiovascular responses, changes in sympathetic nerve activity to brown adipose tissue (BAT), BAT temperature, expired CO2, arterial pressure, and heart rate were recorded after microinjection of excitatory amino acid (EAA) receptor agonists into the RPa in urethan-chloralose-anesthetized, ventilated rats. To determine whether EAA neurotransmission within the RPa is necessary for the responses evoked by disinhibition of the RPa or by prostaglandin E2 acting within the medial preoptic area, BAT sympathetic nerve activity, BAT temperature, expired CO2, arterial pressure, and heart rate were measured during these treatments both before and after blockade of EAA receptors within the RPa. Microinjection of EAA receptor agonists into the RPa resulted in significant increases in all measured variables; these increases were attenuated by prior microinjection of the respective EAA receptor antagonists into the RPa. Microinjection of prostaglandin E2 into the medial preoptic area or microinjection of bicuculline into the RPa resulted in respective significant increases in BAT sympathetic nerve activity (+approximately 190% and +approximately 235% of resting levels), in BAT temperature (approximately 1.8°C and approximately 2°C), in expired CO2 (approximately 1.1% and approximately 1.1%), and in heart rate (approximately 97 beats per minute (bpm) and approximately 100 bpm). Blockade of ionotropic EAA receptors within the RPa by microinjection of kynurenate completely reversed the prostaglandin E2 or bicuculline-evoked increases in all of the measured variables. Blockade of either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors alone resulted in marked attenuations of the prostaglandin E2-evoked effects on all of the measured variables. These data demonstrate that activation of an EAA input to the RPa is necessary for the BAT thermogenic and the cardiovascular effects resulting from the actions of prostaglandin E2 within the medial preoptic area or from the disinhibition of local neurons in the RPa.

KW - Brown adipose tissue

KW - Fever

KW - Glutamate

KW - Medial preoptic area

KW - Sympathetic

KW - Thermoregulation

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DO - 10.1016/S0306-4522(03)00527-X

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JF - Neuroscience

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