Opioid inhibition of spontaneously active neurons of the rat arcuate nucleus in vitro

Michael D. Loose; Martin J. Kelly

doi:10.1016/0361-9230(89)90024-5

Opioid inhibition of spontaneously active neurons of the rat arcuate nucleus in vitro

Michael D. Loose
, Martin J. Kelly

Chemical Physiology and Biochemistry

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

The effects of opioid agonists were determined on single-unit activity recorded from the arcuate nucleus (ARC) in perfused, coronal slices of hypothalamus taken from proestrous rats., The selective, μ-receptor agonist Tyr-D-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) produced a concentration-dependent decrease in the firing rate of 70-78% of the units tested. The concentration of DAGO that induced maximal inhibition of firing was approximately 0.5 μM. This inhibition of firing frequency occurred irrespective of cell location, firing pattern or baseline firing frequency. The effect of DAGO was antagonized by the opioid antagonist naloxone (0.1 μM). The selective κ-receptor agonist trans-(+)-34 dichloro-N-methyl-[2-(1-pyrrolidinyl) cyclohexyl] benzeneacetamide methane sulfonate (U50,488H) did not decrease the firing rate in cells which did respond to DAGO. Blockade of synaptic activity decreased the level of spontaneous activity but did not prevent the inhibitory action of DAGO. These data support the hypothesis that opioids through activation of μ-receptors, inhibit neuronal activity in the arcuate nucleus. Furthermore, the opioid inhibition occurs in part via a direct postsynaptic action.

Original language	English (US)
Pages (from-to)	819-823
Number of pages	5
Journal	Brain Research Bulletin
Volume	22
Issue number	5
DOIs	https://doi.org/10.1016/0361-9230(89)90024-5
State	Published - May 1989

Funding

ACKNOWLEDGEMENTS The authors wish to thank Martha Bosch for technical assistancea nd Joan Vaughan for typing the manuscript.T his work was supportedb y PHS grants DA 05158, HD 19905 and a grant from the Eli Lilly Foundation. Dr. Michael Loose was supported by an NRSA (HD 07133). and Dr. Martin Kelly by an RCDA (HD 00718).

Funders	Funder number
Eli Lilly Foundation
RCDA	HD 00718
Presbyterian Historical Society	DA 05158, HD 19905
Israel National Road Safety Authority	HD 07133
Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health	T32HD007133

Keywords

Opioids μ-Receptor Arcuate Hypothalamus DAGO

ASJC Scopus subject areas

General Neuroscience

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10.1016/0361-9230(89)90024-5

Cite this

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title = "Opioid inhibition of spontaneously active neurons of the rat arcuate nucleus in vitro",

abstract = "The effects of opioid agonists were determined on single-unit activity recorded from the arcuate nucleus (ARC) in perfused, coronal slices of hypothalamus taken from proestrous rats., The selective, μ-receptor agonist Tyr-D-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) produced a concentration-dependent decrease in the firing rate of 70-78\% of the units tested. The concentration of DAGO that induced maximal inhibition of firing was approximately 0.5 μM. This inhibition of firing frequency occurred irrespective of cell location, firing pattern or baseline firing frequency. The effect of DAGO was antagonized by the opioid antagonist naloxone (0.1 μM). The selective κ-receptor agonist trans-(+)-34 dichloro-N-methyl-[2-(1-pyrrolidinyl) cyclohexyl] benzeneacetamide methane sulfonate (U50,488H) did not decrease the firing rate in cells which did respond to DAGO. Blockade of synaptic activity decreased the level of spontaneous activity but did not prevent the inhibitory action of DAGO. These data support the hypothesis that opioids through activation of μ-receptors, inhibit neuronal activity in the arcuate nucleus. Furthermore, the opioid inhibition occurs in part via a direct postsynaptic action.",

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author = "Loose, \{Michael D.\} and Kelly, \{Martin J.\}",

note = "Funding Information: ACKNOWLEDGEMENTS The authors wish to thank Martha Bosch for technical assistancea nd Joan Vaughan for typing the manuscript.T his work was supportedb y PHS grants DA 05158, HD 19905 and a grant from the Eli Lilly Foundation. Dr. Michael Loose was supported by an NRSA (HD 07133). and Dr. Martin Kelly by an RCDA (HD 00718).",

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N2 - The effects of opioid agonists were determined on single-unit activity recorded from the arcuate nucleus (ARC) in perfused, coronal slices of hypothalamus taken from proestrous rats., The selective, μ-receptor agonist Tyr-D-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) produced a concentration-dependent decrease in the firing rate of 70-78% of the units tested. The concentration of DAGO that induced maximal inhibition of firing was approximately 0.5 μM. This inhibition of firing frequency occurred irrespective of cell location, firing pattern or baseline firing frequency. The effect of DAGO was antagonized by the opioid antagonist naloxone (0.1 μM). The selective κ-receptor agonist trans-(+)-34 dichloro-N-methyl-[2-(1-pyrrolidinyl) cyclohexyl] benzeneacetamide methane sulfonate (U50,488H) did not decrease the firing rate in cells which did respond to DAGO. Blockade of synaptic activity decreased the level of spontaneous activity but did not prevent the inhibitory action of DAGO. These data support the hypothesis that opioids through activation of μ-receptors, inhibit neuronal activity in the arcuate nucleus. Furthermore, the opioid inhibition occurs in part via a direct postsynaptic action.

AB - The effects of opioid agonists were determined on single-unit activity recorded from the arcuate nucleus (ARC) in perfused, coronal slices of hypothalamus taken from proestrous rats., The selective, μ-receptor agonist Tyr-D-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) produced a concentration-dependent decrease in the firing rate of 70-78% of the units tested. The concentration of DAGO that induced maximal inhibition of firing was approximately 0.5 μM. This inhibition of firing frequency occurred irrespective of cell location, firing pattern or baseline firing frequency. The effect of DAGO was antagonized by the opioid antagonist naloxone (0.1 μM). The selective κ-receptor agonist trans-(+)-34 dichloro-N-methyl-[2-(1-pyrrolidinyl) cyclohexyl] benzeneacetamide methane sulfonate (U50,488H) did not decrease the firing rate in cells which did respond to DAGO. Blockade of synaptic activity decreased the level of spontaneous activity but did not prevent the inhibitory action of DAGO. These data support the hypothesis that opioids through activation of μ-receptors, inhibit neuronal activity in the arcuate nucleus. Furthermore, the opioid inhibition occurs in part via a direct postsynaptic action.

KW - Opioids μ-Receptor Arcuate Hypothalamus DAGO

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Opioid inhibition of spontaneously active neurons of the rat arcuate nucleus in vitro

Abstract

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Keywords

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