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Hypothalamus

Neuroscience · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 3 min read

Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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 (594 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

Ventral part of the diencephalon extending from the region of the optic chiasm to the caudal border of the mammillary bodies and forming the inferior and lateral walls of the third ventricle.

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: Preoptico-Hypothalamic Area; Area, Preoptico-Hypothalamic; Areas, Preoptico-Hypothalamic; Preoptico Hypothalamic Area; Preoptico-Hypothalamic Areas; Lamina Terminalis.

Where it fits in the MeSH classification

Broader topics
Limbic System; Diencephalon
Narrower topics
Hypothalamic Area, Lateral; Hypothalamus, Anterior; Hypothalamus, Middle; Hypothalamus, Posterior

Related concepts

  • Diencephalon
  • Optic Chiasm
  • Mammillary Bodies
  • Third Ventricle

Research landscape

PubMed indexes 158,040 records tagged with the MeSH heading “Hypothalamus” (counts retrieved 2026-10-29). 12,129 of them (7.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 98,658 records.

Reviews account for 16,727 records (10.6%) and meta-analyses for 191. Randomized controlled trials number 1,001 (0.6%) 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.

PubMed records by publication periodthrough 1999: 98,658 records; 2000-2009: 24,664 records; 2010-2019: 22,589 records; 2020 onward: 12,129 records98,658through 199924,6642000-200922,5892010-201912,1292020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 199998,658
2000-200924,664
2010-201922,589
2020 onward12,129
Share of records by publication typeReviews: 10.6 percent; Meta-analyses: 0.1 percent; Randomized controlled trials: 0.6 percentReviews10.6% (16,727)Meta-analyses0.1% (191)Randomized controlled trials0.6% (1,001)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 158,040 PubMed records
TypeRecordsShare
Reviews16,72710.6%
Meta-analyses1910.1%
Randomized controlled trials1,0010.6%

Method: PubMed query "Hypothalamus"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
A hypothalamic circuit for circadian regulation of corticosterone secretion
Ramirez-Plascencia OD, De Luca R, Machado NLS, Eghlidi D, Khanday MA, Bandaru SS, et al.
2026Research article
Design not recorded in structured metadata
9cc by
PMID 41946720 · DOI · PMC13233844
A prefrontal cortex-lateral hypothalamus circuit controls stress-driven increased food intake
Supiot LF, Kooij KL, Du W, Benschop AAC, Nicolson ASJ, Haak R, et al.
2026Research article
Design not recorded in structured metadata
5cc by
PMID 41912543 · DOI · PMC13199376
Hypothalamic and sex-related hormones in migraine
Warfvinge K, Edvinsson JCA, Maddahi A, Edvinsson L
2026Review article
Design not recorded in structured metadata
5cc by
PMID 41680623 · DOI · PMC12927229

A hypothalamic circuit for circadian regulation of corticosterone secretion [1]

Research article Ramirez-Plascencia OD, De Luca R, Machado NLS, Eghlidi D, Khanday MA, Bandaru SS, et al. · · 2026 · cited 9 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
There is a strong circadian rhythm of corticosteroid secretion in animals and humans, but the circuit for translating the suprachiasmatic (SCN) clock light-dark cycle rhythm into an increase in corticosteroid secretion beginning several hours before the active period is not known.
Closing excerpt
This circuit underlies the daily surge in corticosteroid secretion that is temporally linked but phase advanced compared to the SCN activity cycle.
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 (142 words)

There is a strong circadian rhythm of corticosteroid secretion in animals and humans, but the circuit for translating the suprachiasmatic (SCN) clock light-dark cycle rhythm into an increase in corticosteroid secretion beginning several hours before the active period is not known. We show here that in male mice, this rhythm depends upon input from the SCN to the subparaventricular zone (SPZ), and then to the dorsomedial nucleus of the hypothalamus (DMH). Both glutamatergic and GABAergic DMH neurons are required for the daily surge of corticosteroid secretion in anticipation of the active period. Glutamatergic DMH neurons directly excite paraventricular nucleus corticotrophin-releasing hormone (PVH-CRH) neurons, whereas DMH GABA neurons disinhibit PVH-CRH neurons via a relay in GABAergic neurons in the caudoventral PVH. This circuit underlies the daily surge in corticosteroid secretion that is temporally linked but phase advanced compared to the SCN activity cycle.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41946720 · DOI · PMC13233844

A prefrontal cortex-lateral hypothalamus circuit controls stress-driven increased food intake [2]

Research article Supiot LF, Kooij KL, Du W, Benschop AAC, Nicolson ASJ, Haak R, et al. · · 2026 · cited 5 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Stress can drive overconsumption of high-fat foods.
Closing excerpt
Overall, we identify the mPFC-LHA as a multi-branched network, indispensable for stress-eating.
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 (150 words)

Stress can drive overconsumption of high-fat foods. The medial prefrontal cortex (mPFC) is implicated in such stress-eating, but the underlying circuit mechanisms remain unclear. Here, we show that mPFC projections to the lateral hypothalamus (LHA) are required for stress-induced fat intake in male mice. We find that mPFC-LHA stimulation in sated states increases fat intake. Social stress acutely engages mPFC-LHA neurons, and inhibiting this pathway selectively prevents stress-driven excess fat intake. Circuit mapping shows that mPFC neurons innervate GABAergic and glutamatergic LHA (LHAVGLUT2) neurons, but that social stress preferentially engages mPFC-LHAVGLUT2 neurons and causes plasticity at mPFC-LHAVGLUT2 synapses. Specifically, stress weakens mPFC synapses onto LHAVGLUT2 neurons that curtail food intake, while strengthening mPFC synapses onto midbrain-projecting LHAVGLUT2 neurons linked to stress-eating. We show that LHAVGLUT2 neurons are required downstream mPFC targets for transforming stress into heightened fat intake. Overall, we identify the mPFC-LHA as a multi-branched network, indispensable for stress-eating.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41912543 · DOI · PMC13199376

Hypothalamic and sex-related hormones in migraine [3]

Review article Warfvinge K, Edvinsson JCA, Maddahi A, Edvinsson L · · 2026 · cited 5 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The hypothalamus and sex hormones are closely linked to primary headache disorders.
Closing excerpt
Recent data have demonstrated a close transcriptional relationship between oestrogen and calcitonin gene-related peptide (CGRP), as well as the receptor component “receptor activity-modifying protein 1” (RAMP1), in migraine pathology and current successful treatments.
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 (302 words)

The hypothalamus and sex hormones are closely linked to primary headache disorders. Migraine is the most prevalent disabling neurological disorder, affecting up to 15% of the global population, with enormous socioeconomic and personal impacts. It ranks second among years lived with disability (YLD), with women being the most affected, experiencing a threefold higher prevalence than men. Women report more severe migraine symptoms during periods of sex hormone fluctuations, particularly at puberty, during pregnancy, and around perimenopause. The reason for this sex-based difference remains unclear. However, it is apparent that dynamic fluctuations in female sex hormone levels (oestrogen, progesterone) have a key influence on the susceptibility to attacks in women. A fall in plasma levels of oestrogen, progesterone, and hypothalamic oxytocin may trigger migraine attacks, whereas higher levels appear to be protective. Circulating hormones show dynamic alterations, and, more importantly, their receptors are expressed in the trigeminovascular system (TGVS). Notably, other hormones, such as testosterone and vasopressin (AVP), are less extensively studied but are also highlighted in this review. The underlying mechanisms of their effects on migraine targets have yet to be explained. This review highlights the interplay between sex/reproductive hormones and hypothalamic hormones and their receptors in migraine-related neural structures, both in the central nervous system and in the TGVS. We have included the hypothalamic hormones oxytocin and the molecularly related AVP due to the significant drop in oxytocin levels at the onset of menstruation, as well as its role in parturition and lactation. Recent data have revealed expression of oxytocin receptors in the TGVS. Oestrogen, acting through multiple receptor subtypes, influences expression levels of oxytocin and its receptor. Recent data have demonstrated a close transcriptional relationship between oestrogen and calcitonin gene-related peptide (CGRP), as well as the receptor component “receptor activity-modifying protein 1” (RAMP1), in migraine pathology and current successful treatments.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41680623 · DOI · PMC12927229

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 If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans [4]
    Miller GE, Chen E, Zhou ES · Psychol Bull · 2007 · cited 1,619 times (Europe PMC)
  • Research article Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis [5]
    Zorn JV, Schür RR, Boks MP, Kahn RS, Joëls M, Vinkers CH · Psychoneuroendocrinology · 2017 · cited 539 times (Europe PMC)
  • Research article HPA axis and aging in depression: systematic review and meta-analysis [6]
    Belvederi Murri M, Pariante C, Mondelli V, Masotti M, Atti AR, Mellacqua Z, et al. · Psychoneuroendocrinology · 2014 · cited 277 times (Europe PMC)
  • Research article The HPA axis in bipolar disorder: Systematic review and meta-analysis [7]
    Belvederi Murri M, Prestia D, Mondelli V, Pariante C, Patti S, Olivieri B, et al. · Psychoneuroendocrinology · 2016 · cited 271 times (Europe PMC)
  • Research article Chronic Stress-Associated Depressive Disorders: The Impact of HPA Axis Dysregulation and Neuroinflammation on the Hippocampus-A Mini Review [8]
    Lei AA, Phang VWX, Lee YZ, Kow ASF, Tham CL, Ho YC, et al. · Int J Mol Sci · 2025 · cited 146 times (Europe PMC)
  • Research article Stress, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, and aggression [9]
    Mbiydzenyuy NE, Qulu LA · Metab Brain Dis · 2024 · cited 139 times (Europe PMC)

References

  1. Ramirez-Plascencia OD, De Luca R, Machado NLS, Eghlidi D, Khanday MA, Bandaru SS, et al.. A hypothalamic circuit for circadian regulation of corticosterone secretion. . 2026. PMID 41946720 · DOI · PMC13233844
  2. Supiot LF, Kooij KL, Du W, Benschop AAC, Nicolson ASJ, Haak R, et al.. A prefrontal cortex-lateral hypothalamus circuit controls stress-driven increased food intake. . 2026. PMID 41912543 · DOI · PMC13199376
  3. Warfvinge K, Edvinsson JCA, Maddahi A, Edvinsson L. Hypothalamic and sex-related hormones in migraine. . 2026. PMID 41680623 · DOI · PMC12927229
  4. Miller GE, Chen E, Zhou ES. If it goes up, must it come down? Chronic stress and the hypothalamic-pituitary-adrenocortical axis in humans. Psychol Bull. 2007. PMID 17201569 · DOI
  5. Zorn JV, Schür RR, Boks MP, Kahn RS, Joëls M, Vinkers CH. Cortisol stress reactivity across psychiatric disorders: A systematic review and meta-analysis. Psychoneuroendocrinology. 2017. PMID 28012291 · DOI
  6. Belvederi Murri M, Pariante C, Mondelli V, Masotti M, Atti AR, Mellacqua Z, et al.. HPA axis and aging in depression: systematic review and meta-analysis. Psychoneuroendocrinology. 2014. PMID 24495607 · DOI
  7. Belvederi Murri M, Prestia D, Mondelli V, Pariante C, Patti S, Olivieri B, et al.. The HPA axis in bipolar disorder: Systematic review and meta-analysis. Psychoneuroendocrinology. 2016. PMID 26547798 · DOI
  8. Lei AA, Phang VWX, Lee YZ, Kow ASF, Tham CL, Ho YC, et al.. Chronic Stress-Associated Depressive Disorders: The Impact of HPA Axis Dysregulation and Neuroinflammation on the Hippocampus-A Mini Review. Int J Mol Sci. 2025. PMID 40243556 · DOI · PMC11988747
  9. Mbiydzenyuy NE, Qulu LA. Stress, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, and aggression. Metab Brain Dis. 2024. PMID 39083184 · DOI · PMC11535056

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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At a glance

158,040
PubMed records on this heading
8%
published since 2020
16,727
review articles
1,001
randomized trials
9
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

Related topics See all →

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  • PubMed search used ↗

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