Desensitization of 5-HT1A Receptors by 5-HT2A Receptors in Neuroendocrine Neurons in Vivo

An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was...

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Published inThe Journal of pharmacology and experimental therapeutics Vol. 310; no. 1; pp. 59 - 66
Main Authors Zhang, Yahong, Gray, Thackery S., D’Souza, Deborah N., Carrasco, Gonzalo A., Damjanoska, Katerina J., Dudas, Bertalan, Garcia, Francisca, Zainelli, Gina M., Sullivan Hanley, Nicole R., Battaglia, George, Muma, Nancy A., Van de Kar, Louis D.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.07.2004
American Society for Pharmacology and Experimental Therapeutics
Subjects
8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology
Adrenocorticotropic Hormone - metabolism
Amphetamines - pharmacology
Animals
Antibody Specificity
Corticotropin-Releasing Hormone - metabolism
Fluorobenzenes - pharmacology
Microinjections
Neurons - drug effects
Neurons - metabolism
Neurosecretory Systems - cytology
Oxytocin - metabolism
Paraventricular Hypothalamic Nucleus - cytology
Piperidines - pharmacology
Rats
Rats, Sprague-Dawley
Receptor, Serotonin, 5-HT1A - immunology
Receptor, Serotonin, 5-HT1A - metabolism
Receptor, Serotonin, 5-HT2A - immunology
Receptor, Serotonin, 5-HT2A - metabolism
Serotonin Antagonists - pharmacology
Serotonin Receptor Agonists - pharmacology
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Abstract An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 μg/kg s.c.). The 5-HT2A/2C receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.
AbstractList An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 μg/kg s.c.). The 5-HT2A/2C receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.
An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 microg/kg s.c.). The 5-HT(2A/2C) receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.
An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 microg/kg s.c.). The 5-HT(2A/2C) receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors interact with 5-HT1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 microg/kg s.c.). The 5-HT(2A/2C) receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT1A receptors. Microinjection of the 5-HT2A receptor antagonist MDL100,907 [(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT1A receptors induced by the 5-HT2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT1A and 5-HT2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT1A receptor signaling after changes in function of 5-HT2A receptors; for example, during pharmacotherapy of mood disorders.
An imbalance between serotonin-2A (5-HT 2A ) and 5-HT 1A receptors may underlie several mood disorders. The present studies determined whether 5-HT 2A receptors interact with 5-HT 1A receptors in the rat hypothalamic paraventricular nucleus (PVN). The sensitivity of the hypothalamic 5-HT 1A receptors was measured as oxytocin and adrenocorticotropic hormone (ACTH) responses to the 5-HT 1A receptor agonist (+)-8-hydroxy-2-(di-n-propylamino) tetralin hydrobromide [(+)8-OH-DPAT] (40 μg/kg s.c.). The 5-HT 2A/2C receptor agonist (-)DOI [(-)-1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCl] (1 mg/kg s.c.) injected 2 h prior to (+)8-OH-DPAT significantly reduced the oxytocin and ACTH responses to (+)8-OH-DPAT, producing a heterologous desensitization of the 5-HT 1A receptors. Microinjection of the 5-HT 2A receptor antagonist MDL100,907 [(+)-α-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenylethyl)]-4-piperidinemethanol; 0, 10, or 20 nmol, 15 min prior to (-)DOI] into the PVN dose-dependently prevented the desensitization of 5-HT 1A receptors induced by the 5-HT 2A receptor agonist (-)DOI. Double-label immunocytochemistry revealed a high degree of colocalization of 5-HT 1A and 5-HT 2A receptors in the oxytocin and corticotropin-releasing factor neurons of the PVN. Thus, activation of 5-HT 2A receptors in the PVN may directly induce a heterologous desensitization of 5-HT 1A receptors within individual neuroendocrine cells. These findings may provide insight into the long-term adaptation of 5-HT 1A receptor signaling after changes in function of 5-HT 2A receptors; for example, during pharmacotherapy of mood disorders.
Author Carrasco, Gonzalo A.
Garcia, Francisca
Zhang, Yahong
Damjanoska, Katerina J.
Sullivan Hanley, Nicole R.
D’Souza, Deborah N.
Battaglia, George
Van de Kar, Louis D.
Zainelli, Gina M.
Gray, Thackery S.
Muma, Nancy A.
Dudas, Bertalan
Author_xml – sequence: 1
  givenname: Yahong
  surname: Zhang
  fullname: Zhang, Yahong
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  givenname: Thackery S.
  surname: Gray
  fullname: Gray, Thackery S.
– sequence: 3
  givenname: Deborah N.
  surname: D’Souza
  fullname: D’Souza, Deborah N.
– sequence: 4
  givenname: Gonzalo A.
  surname: Carrasco
  fullname: Carrasco, Gonzalo A.
– sequence: 5
  givenname: Katerina J.
  surname: Damjanoska
  fullname: Damjanoska, Katerina J.
– sequence: 6
  givenname: Bertalan
  surname: Dudas
  fullname: Dudas, Bertalan
– sequence: 7
  givenname: Francisca
  surname: Garcia
  fullname: Garcia, Francisca
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  givenname: Gina M.
  surname: Zainelli
  fullname: Zainelli, Gina M.
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  givenname: Nicole R.
  surname: Sullivan Hanley
  fullname: Sullivan Hanley, Nicole R.
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  givenname: George
  surname: Battaglia
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  givenname: Nancy A.
  surname: Muma
  fullname: Muma, Nancy A.
– sequence: 12
  givenname: Louis D.
  surname: Van de Kar
  fullname: Van de Kar, Louis D.
  email: lvandek@lumc.edu
BackLink https://www.ncbi.nlm.nih.gov/pubmed/15064330$$D View this record in MEDLINE/PubMed
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PublicationCentury 2000
PublicationDate July 2004
20040701
2004-07-00
2004-Jul
PublicationDateYYYYMMDD 2004-07-01
PublicationDate_xml – month: 07
  year: 2004
  text: July 2004
PublicationDecade 2000
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle The Journal of pharmacology and experimental therapeutics
PublicationTitleAlternate J Pharmacol Exp Ther
PublicationYear 2004
Publisher Elsevier Inc
American Society for Pharmacology and Experimental Therapeutics
Publisher_xml – name: Elsevier Inc
– name: American Society for Pharmacology and Experimental Therapeutics
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SSID ssj0014463
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Snippet An imbalance between serotonin-2A (5-HT2A) and 5-HT1A receptors may underlie several mood disorders. The present studies determined whether 5-HT2A receptors...
An imbalance between serotonin-2A (5-HT 2A ) and 5-HT 1A receptors may underlie several mood disorders. The present studies determined whether 5-HT 2A...
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StartPage 59
SubjectTerms 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology
Adrenocorticotropic Hormone - metabolism
Amphetamines - pharmacology
Animals
Antibody Specificity
Corticotropin-Releasing Hormone - metabolism
Fluorobenzenes - pharmacology
Microinjections
Neurons - drug effects
Neurons - metabolism
Neurosecretory Systems - cytology
Oxytocin - metabolism
Paraventricular Hypothalamic Nucleus - cytology
Piperidines - pharmacology
Rats
Rats, Sprague-Dawley
Receptor, Serotonin, 5-HT1A - immunology
Receptor, Serotonin, 5-HT1A - metabolism
Receptor, Serotonin, 5-HT2A - immunology
Receptor, Serotonin, 5-HT2A - metabolism
Serotonin Antagonists - pharmacology
Serotonin Receptor Agonists - pharmacology
Title Desensitization of 5-HT1A Receptors by 5-HT2A Receptors in Neuroendocrine Neurons in Vivo
URI https://dx.doi.org/10.1124/jpet.103.062224
http://jpet.aspetjournals.org/content/310/1/59.abstract
https://www.ncbi.nlm.nih.gov/pubmed/15064330
https://www.proquest.com/docview/66654476
Volume 310
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