Evidence map›Paper›PMID 28087766›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

Control of Amygdala Circuits by 5-HT Neurons via 5-HT and Glutamate Cotransmission.

Ayesha Sengupta, Marco Bocchio, David M Bannerman, Trevor Sharp, Marco Capogna

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
6.7field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 135 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Role of the Amygdala in the Complex Relationship Between Sleep and Anxiety.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Serotonergic Input into the Cerebellar Cortex Modulates Anxiety-Like Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Ayesha SenguptaDepartment of Pharmacology, University of Oxford, Oxford, OX1 3QT United Kingdom.ORCID 0000-0002-8348-1799
Marco BocchioMedical Research Council Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Oxford, OX1 3TH United Kingdom.ORCID 0000-0002-7005-3453
David M BannermanDepartment of Experimental Psychology, University of Oxford, Oxford, OX1 3UD United Kingdom.
Trevor SharpDepartment of Pharmacology, University of Oxford, Oxford, OX1 3QT United Kingdom, trevor.sharp@pharm.ox.ac.uk marco.capogna@biomed.au.dk.ORCID 0000-0001-7434-9713
Marco CapognaMedical Research Council Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Oxford, OX1 3TH United Kingdom, trevor.sharp@pharm.ox.ac.uk marco.capogna@biomed.au.dk.ORCID 0000-0002-2742-5485
University of Oxford · GBAarhus University · DK

Funding

Medical Research Council U138197106Wellcome Trust
6 · The paper itself

Abstract

The serotonin (5-HT) system and the amygdala are key regulators of emotional behavior. Several lines of evidence suggest that 5-HT transmission in the amygdala is implicated in the susceptibility and drug treatment of mood disorders. Therefore, elucidating the physiological mechanisms through which midbrain 5-HT neurons modulate amygdala circuits could be pivotal in understanding emotional regulation in health and disease. To shed light on these mechanisms, we performed patch-clamp recordings from basal amygdala (BA) neurons in brain slices from mice with channelrhodopsin genetically targeted to 5-HT neurons. Optical stimulation of 5-HT terminals at low frequencies (≤1 Hz) evoked a short-latency excitation of BA interneurons (INs) that was depressed at higher frequencies. Pharmacological analysis revealed that this effect was mediated by glutamate and not 5-HT because it was abolished by ionotropic glutamate receptor antagonists. Optical stimulation of 5-HT terminals at higher frequencies (10-20 Hz) evoked both slow excitation and slow inhibition of INs. These effects were mediated by 5-HT because they were blocked by antagonists of 5-HT

Indexed as

AmygdalaAnimalsAnimals, NewbornChannelrhodopsinsExcitatory Amino Acid AgentsFemaleGABA AntagonistsGlutamic AcidLuminescent ProteinsMaleMiceMice, Inbred C57BLMice, TransgenicNerve NetNeuronsPiperazinesChannelrhodopsinsExcitatory Amino Acid AgentsGABA AntagonistsGlutamic AcidLuminescent ProteinsN-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-N-(2-pyridinyl)cyclohexanecarboxamidePiperazinesPyridinesReceptors, SerotoninSerotoninSerotonin AntagonistsSerotonin Plasma Membrane Transport ProteinsSlc6a4 protein, mouseamygdalaelectrophysiologyinterneuronoptogeneticsserotoninsynaptic transmission

Identifiers

PMID28087766
PMCPMC5320609
OpenAlexW2573649328

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.