Serotonin-1A receptors in major depression quantified using PET: Controversies, confounds, and recommendations

The serotonin-1A (5-HT1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT1A receptor density, two reported no chan...

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Published inNeuroImage (Orlando, Fla.) Vol. 59; no. 4; pp. 3243 - 3251
Main Authors Shrestha, Saurav, Hirvonen, Jussi, Hines, Christina S., Henter, Ioline D., Svenningsson, Per, Pike, Victor W., Innis, Robert B.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 15.02.2012
Elsevier Limited
Subjects
Anxiety
Blood-brain barrier
Brain research
Depressive Disorder, Major - diagnostic imaging
Depressive Disorder, Major - metabolism
Funding
Humans
Major depressive disorder (MDD)
Medical imaging
Mental depression
Mental health
Neuroimaging
Permeability-glycoprotein (P-gp)
Positron emission tomography (PET)
Positron-Emission Tomography
Radioligand
Receptor, Serotonin, 5-HT1A - metabolism
Serotonin
Serotonin-1A (5-HT1A) receptors
Studies
Systematic review
Neuroimaging
Positron emission tomography (PET)
Radioligand
Serotonin-1A (5-HT1A) receptors
Permeability-glycoprotein (P-gp)
Major depressive disorder (MDD)
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Abstract The serotonin-1A (5-HT1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT1A receptor density, two reported no change, and two reported increased 5-HT1A receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the ‘gold standard’. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter – like P-gp – at the blood–brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT1A receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis. ► PET imaging of 5-HT1A receptor density in MDD patients has yielded mixed results. ► ‘Methodological’ rather than ‘clinical’ factors likely explain these discrepancies. ► One methodological confound is the use of the cerebellum as a reference region. ► Measuring parent radioligand concentrations in arterial plasma is imprecise. ► Other confounds are efflux transporter, radiometabolites, & 5-HT1A affinity states.
AbstractList The serotonin-1A (5-HT1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT1Areceptor density, two reported no change, and two reported increased 5-HT1Areceptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT1Areceptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.
The serotonin-1A (5-HT(1A)) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT(1A) receptor density, two reported no change, and two reported increased 5-HT(1A) receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT(1A) receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.
The serotonin-1A (5-HT1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT1A receptor density, two reported no change, and two reported increased 5-HT1A receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the ‘gold standard’. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter – like P-gp – at the blood–brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT1A receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis. ► PET imaging of 5-HT1A receptor density in MDD patients has yielded mixed results. ► ‘Methodological’ rather than ‘clinical’ factors likely explain these discrepancies. ► One methodological confound is the use of the cerebellum as a reference region. ► Measuring parent radioligand concentrations in arterial plasma is imprecise. ► Other confounds are efflux transporter, radiometabolites, & 5-HT1A affinity states.
The serotonin-1A (5-HT[sub]1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT[sub]1A receptor density, two reported no change, and two reported increased 5-HT[sub]1A receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT[sub]1A receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.
The serotonin-1A (5-HT 1A ) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT 1A receptor density, two reported no change, and two reported increased 5-HT 1A receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the `gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter—like P-gp—at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT 1A receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.
The serotonin-1A (5-HT(1A)) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT(1A) receptor density, two reported no change, and two reported increased 5-HT(1A) receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT(1A) receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.The serotonin-1A (5-HT(1A)) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT(1A) receptor density, two reported no change, and two reported increased 5-HT(1A) receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT(1A) receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis.
Author Hines, Christina S.
Hirvonen, Jussi
Shrestha, Saurav
Henter, Ioline D.
Innis, Robert B.
Svenningsson, Per
Pike, Victor W.
AuthorAffiliation b Translational Neuropharmacology, Center for Molecular Medicine, Karolinska University Hospital L8:01, 171 76 Stockholm, Sweden
a Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, Maryland 20892, USA
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– name: a Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, Maryland 20892, USA
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  surname: Shrestha
  fullname: Shrestha, Saurav
  email: saurav.shrestha@nih.gov
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
– sequence: 2
  givenname: Jussi
  surname: Hirvonen
  fullname: Hirvonen, Jussi
  email: jussi.hirvonen@utu.fi
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
– sequence: 3
  givenname: Christina S.
  surname: Hines
  fullname: Hines, Christina S.
  email: christina.hines@nih.gov
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
– sequence: 4
  givenname: Ioline D.
  surname: Henter
  fullname: Henter, Ioline D.
  email: ioline.henter@nih.gov
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
– sequence: 5
  givenname: Per
  surname: Svenningsson
  fullname: Svenningsson, Per
  email: per.svenningsson@ki.se
  organization: Translational Neuropharmacology, Center for Molecular Medicine, Karolinska University Hospital L8:01, 171 76 Stockholm, Sweden
– sequence: 6
  givenname: Victor W.
  surname: Pike
  fullname: Pike, Victor W.
  email: pikev@mail.nih.gov
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
– sequence: 7
  givenname: Robert B.
  surname: Innis
  fullname: Innis, Robert B.
  email: robert.innis@nih.gov
  organization: Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/22155042$$D View this record in MEDLINE/PubMed
http://kipublications.ki.se/Default.aspx?queryparsed=id:124248577$$DView record from Swedish Publication Index
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ContentType Journal Article
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IngestDate Mon Aug 25 03:23:42 EDT 2025
Thu Aug 21 18:27:37 EDT 2025
Tue Aug 05 10:04:20 EDT 2025
Tue Aug 05 09:38:41 EDT 2025
Wed Aug 13 03:32:42 EDT 2025
Mon Jul 21 06:07:35 EDT 2025
Thu Apr 24 23:10:54 EDT 2025
Tue Jul 01 02:14:44 EDT 2025
Fri Feb 23 02:20:29 EST 2024
Tue Aug 26 16:36:50 EDT 2025
IsPeerReviewed true
IsScholarly true
Issue 4
Keywords Neuroimaging
Positron emission tomography (PET)
Radioligand
Serotonin-1A (5-HT1A) receptors
Permeability-glycoprotein (P-gp)
Major depressive disorder (MDD)
Language English
License https://www.elsevier.com/tdm/userlicense/1.0
Published by Elsevier Inc.
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content type line 23
ObjectType-Review-3
CH: christina.hines@nih.gov
RI: robert.innis@nih.gov
JH: jussi.hirvonen@utu.fi
Author e-mail addresses
IH: ioline.henter@nih.gov
PS: per.svenningsson@ki.se
VP: pikev@mail.nih.gov
SS: saurav.shrestha@nih.gov
PMID 22155042
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PublicationTitle NeuroImage (Orlando, Fla.)
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Snippet The serotonin-1A (5-HT1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the...
The serotonin-1A (5-HT(1A)) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the...
The serotonin-1A (5-HT[sub]1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of...
The serotonin-1A (5-HT 1A ) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the...
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pubmedcentral
proquest
pubmed
crossref
elsevier
SourceType Open Access Repository
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StartPage 3243
SubjectTerms Anxiety
Blood-brain barrier
Brain research
Depressive Disorder, Major - diagnostic imaging
Depressive Disorder, Major - metabolism
Funding
Humans
Major depressive disorder (MDD)
Medical imaging
Mental depression
Mental health
Neuroimaging
Permeability-glycoprotein (P-gp)
Positron emission tomography (PET)
Positron-Emission Tomography
Radioligand
Receptor, Serotonin, 5-HT1A - metabolism
Serotonin
Serotonin-1A (5-HT1A) receptors
Studies
Systematic review
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Title Serotonin-1A receptors in major depression quantified using PET: Controversies, confounds, and recommendations
URI https://www.clinicalkey.com/#!/content/1-s2.0-S1053811911013103
https://dx.doi.org/10.1016/j.neuroimage.2011.11.029
https://www.ncbi.nlm.nih.gov/pubmed/22155042
https://www.proquest.com/docview/1834302250
https://www.proquest.com/docview/920799534
https://www.proquest.com/docview/922501063
https://pubmed.ncbi.nlm.nih.gov/PMC3288718
http://kipublications.ki.se/Default.aspx?queryparsed=id:124248577
Volume 59
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