Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (588 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Almond-shaped group of basal nuclei anterior to the inferior horn OF the lateral ventricle of the temporal lobe. The amygdala is part of the limbic system.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Amygdaloid Body; Amygdaloid Bodies; Amygdaloid Nuclear Complex; Amygdaloid Nuclear Complices; Complex, Amygdaloid Nuclear; Complices, Amygdaloid Nuclear; Nuclear Complex, Amygdaloid; Nuclear Complices, Amygdaloid.
Where it fits in the MeSH classification
- Broader topics
- Limbic System; Basal Ganglia
- Narrower topics
- Basolateral Nuclear Complex; Central Amygdaloid Nucleus; Corticomedial Nuclear Complex
Related concepts
- Inferior Horn
- The Lateral Ventricle
- Temporal Lobe
Research landscape
PubMed indexes 26,491 records tagged with the MeSH heading “Amygdala” (counts retrieved 2026-10-29). 4,626 of them (17.5%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 8,436 records.
Reviews account for 1,925 records (7.3%) and meta-analyses for 139. Randomized controlled trials number 360 (1.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 7,423 |
| 2000-2009 | 6,006 |
| 2010-2019 | 8,436 |
| 2020 onward | 4,626 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,925 | 7.3% |
| Meta-analyses | 139 | 0.5% |
| Randomized controlled trials | 360 | 1.4% |
Method: PubMed query "Amygdala"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The basolateral amygdala-anterior cingulate cortex circuit contributes to postherpetic neuralgia-anxiety comorbidity | 2025 | Research article Design not recorded in structured metadata | 21 | cc by PMID 40225572 · DOI · PMC11984391 |
| Transcription of GABAA receptor subunits in circulating monocytes and association to emotional brain function in premenstrual dysphoric disorder | 2025 | Research article Design not recorded in structured metadata | 13 | cc by PMID 40701967 · DOI · PMC12287299 |
| Astrocytes enable amygdala neural representations supporting memory | 2026 | Research article Design not recorded in structured metadata | 12 | cc by PMID 41673152 · DOI · PMC13061616 |
The basolateral amygdala-anterior cingulate cortex circuit contributes to postherpetic neuralgia-anxiety comorbidity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background: Postherpetic neuralgia (PHN) causes chronic pain and emotional dysfunction, but its underlying mechanisms are unknown.
- Closing excerpt
- Conclusion: Findings in this study will provide new insight for understanding the central pathomechanism underlying PHN-anxiety comorbidity, as well as serve as solid theoretical underpinnings for the management of PHN.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (260 words)
Background: Postherpetic neuralgia (PHN) causes chronic pain and emotional dysfunction, but its underlying mechanisms are unknown. Methods: We first compared the structural and functional magnetic resonance imaging (MRI) of PHN-anxiety patients with healthy controls (HCs). Then, we created a PHN comorbid anxiety-like model by injecting resiniferatoxin (RTX) intraperitoneally and used Fos-CreER::Ai9 mice to validate brain regions with volume differences in MRI. Furthermore, we combined behavioral experiments with electrophysiology, viral tracing, in vivo fiber-photometry, optogenetics, and chemogenetics, to analyze the role of the basolateral amygdala (BLA)-anterior cingulate cortex (ACC) circuit in PHN comorbid anxiety-like mice multi-dimensionally. Results: According to neuroimages, patients with PHN-anxiety comorbidity have decreased amygdala volume and decreased functional connection (FC) of the BLA and ACC. Furthermore, we created a PHN comorbid anxiety-like model by injection of RTX intraperitoneally, and these mice showed dysesthesia and anxiety-like behaviors 3 weeks after RTX injection. Then, we discovered that BLA and ACC were related to PHN comorbid anxiety-like behaviors using Fos-CreER::Ai9 mice. Immunohistochemistry and electrophysiology revealed enhanced activation of BLA glutamatergic (BLAGlu) neurons in PHN comorbid anxiety-like mice. Opto/chemogenetic activating BLAGlu neurons aggravated pain threshold in PHN comorbid anxiety-like mice. Inhibiting BLAGlu alleviates mechanical nociception, thermal hyperalgesia, and anxiety-like behavior. Moreover, the elevated excitability of BLAGlu neurons resulted in increased excitatory inputs to the ACC. Selective activation or inhibition of the BLAGlu-ACC pathway exacerbated or alleviated the pain and anxiety behavior, respectively. Conclusion: Findings in this study will provide new insight for understanding the central pathomechanism underlying PHN-anxiety comorbidity, as well as serve as solid theoretical underpinnings for the management of PHN.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40225572 · DOI · PMC11984391
Transcription of GABAA receptor subunits in circulating monocytes and association to emotional brain function in premenstrual dysphoric disorder [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Premenstrual dysphoric disorder (PMDD) has been hypothesized to be related to an altered sensitivity of the γ-aminobutyric acid type A (GABAA) receptor to progesterone-derived neurosteroids.
- Closing excerpt
- It is possible that the mood symptoms of PMDD are mediated by an inability to effectively adjust the expression of this receptor type in response to neurosteroid fluctuations, leading to dysregulation GABAergic tone and increased activity in emotion-generating brain circuits.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (202 words)
Premenstrual dysphoric disorder (PMDD) has been hypothesized to be related to an altered sensitivity of the γ-aminobutyric acid type A (GABAA) receptor to progesterone-derived neurosteroids. GABAA receptor sensitivity to neurosteroid-modulation is dependent on its subunit composition. In the present study, we used quantitative reverse transcription polymerase chain reactions (RT-qPCR) to compare messenger ribonucleic acid (mRNA) expression of GABAA receptor subunits in peripheral mononuclear cells (PBMCs) across the menstrual cycle in 29 women with PMDD and 27 controls. We related mRNA subunit expression to serum levels of neurosteroids and to functional activation of the amygdala, a key brain region involved in emotion generation, measured using functional magnetic resonance imaging (fMRI). Women with PMDD had lower mRNA expression of the delta GABAA receptor subunit during the symptomatic, luteal phase (compared to the asymptomatic, follicular phase) of the menstrual cycle. Lower delta mRNA expression was related to higher amygdala activation in PMDD women. GABAA receptors incorporating the delta subunit are especially sensitive to neurosteroid modulation. It is possible that the mood symptoms of PMDD are mediated by an inability to effectively adjust the expression of this receptor type in response to neurosteroid fluctuations, leading to dysregulation GABAergic tone and increased activity in emotion-generating brain circuits.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40701967 · DOI · PMC12287299
Astrocytes enable amygdala neural representations supporting memory [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Brain systems mediating responses to previously encountered threats provide critical survival functions.
- Closing excerpt
- Our findings reveal a key role for astrocytes in the generation and adaptation of fear-state-related neural representations, revising neurocentric models of critical amygdala-mediated adaptive functions.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (126 words)
Brain systems mediating responses to previously encountered threats provide critical survival functions. Fear memory and extinction are underpinned by neural representations in the basolateral amygdala (BLA)1-7, but the contribution of non-neuronal cells, including astrocytes, to these processes remains unresolved. Here, using in vivo calcium (Ca2+) imaging and causal astrocyte manipulations, we find that BLA astrocytes dynamically track fear state and support fear memory retrieval and extinction. By combining astrocyte manipulations with in vivo BLA neuronal Ca2+ imaging and electrophysiological recordings, we show that astrocyte Ca2+ signalling enables neuronal encoding of fear memory retrieval and extinction, and readout through a BLA-prefrontal circuit. Our findings reveal a key role for astrocytes in the generation and adaptation of fear-state-related neural representations, revising neurocentric models of critical amygdala-mediated adaptive functions.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41673152 · DOI · PMC13061616
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article From circuits to behaviour in the amygdala [4]
- Research article Emotion processing and the amygdala: from a 'low road' to 'many roads' of evaluating biological significance [5]
- Research article Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex [6]
- Research article The Interaction of Person-Affect-Cognition-Execution (I-PACE) model for addictive behaviors: Update, generalization to addictive behaviors beyond internet-use disorders, and specification of the process character of addictive behaviors [7]
- Research article Amygdala microcircuits controlling learned fear [8]
- Research article Emotion modulation in PTSD: Clinical and neurobiological evidence for a dissociative subtype [9]
References
- Jiang X, Yan Y, Chen Z, Xiong J, Zhang X, Gu L, et al.. The basolateral amygdala-anterior cingulate cortex circuit contributes to postherpetic neuralgia-anxiety comorbidity. . 2025. PMID 40225572 · DOI · PMC11984391
- Stiernman L, Comasco E, Johansson M, Bixo M. Transcription of GABAA receptor subunits in circulating monocytes and association to emotional brain function in premenstrual dysphoric disorder. . 2025. PMID 40701967 · DOI · PMC12287299
- Bukalo O, O'Sullivan R, Tanisumi Y, Mendez A, Weinholtz C, Zimmerman S, et al.. Astrocytes enable amygdala neural representations supporting memory. . 2026. PMID 41673152 · DOI · PMC13061616
- Janak PH, Tye KM. From circuits to behaviour in the amygdala. Nature. 2015. PMID 25592533 · DOI · PMC4565157
- Pessoa L, Adolphs R. Emotion processing and the amygdala: from a 'low road' to 'many roads' of evaluating biological significance. Nat Rev Neurosci. 2010. PMID 20959860 · DOI · PMC3025529
- McEwen BS, Nasca C, Gray JD. Stress Effects on Neuronal Structure: Hippocampus, Amygdala, and Prefrontal Cortex. Neuropsychopharmacology. 2016. PMID 26076834 · DOI · PMC4677120
- Brand M, Wegmann E, Stark R, Müller A, Wölfling K, Robbins TW, et al.. The Interaction of Person-Affect-Cognition-Execution (I-PACE) model for addictive behaviors: Update, generalization to addictive behaviors beyond internet-use disorders, and specification of the process character of addictive behaviors. Neurosci Biobehav Rev. 2019. PMID 31247240 · DOI
- Duvarci S, Pare D. Amygdala microcircuits controlling learned fear. Neuron. 2014. PMID 24908482 · DOI · PMC4103014
- Lanius RA, Vermetten E, Loewenstein RJ, Brand B, Schmahl C, Bremner JD, et al.. Emotion modulation in PTSD: Clinical and neurobiological evidence for a dissociative subtype. Am J Psychiatry. 2010. PMID 20360318 · DOI · PMC3226703
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.