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| [[Lateral hypothalamic nucleus|Lateral nucleus]] || See [[Lateral hypothalamus#Function]] – primary source of [[orexin]] neurons throughout the brain and spinal cord
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| [[Tuberomammillary nucleus]]<ref name="Histamine pathways">{{
* [[arousal]] (wakefulness and attention)
* feeding and [[energy balance (biology)|energy balance]]
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===Sexual dimorphism===
Several hypothalamic nuclei are [[sexually dimorphic]]; i.e., there are clear differences in both structure and function between males and females.{{citation needed|date=
Some differences are apparent even in gross neuroanatomy: most notable is the [[sexually dimorphic nucleus]] within the [[preoptic area]]. However most of the differences are subtle changes in the connectivity and chemical sensitivity of particular sets of neurons.{{citation needed|date=
The importance of these changes can be recognised by functional differences between males and females. For instance, males of most species prefer the odor and appearance of females over males, which is instrumental in stimulating male sexual behavior. If the sexually dimorphic nucleus is lesioned, this preference for females by males diminishes. Also, the pattern of secretion of [[growth hormone]] is sexually dimorphic, and this is one reason why in many species, adult males are much larger than females.{{citation needed|date=
;Responsiveness to ovarian steroids
Other striking functional dimorphisms are in the behavioral responses to [[ovarian steroids]] of the adult. Males and females respond to ovarian steroids in different ways, partly because the expression of estrogen-sensitive neurons in the hypothalamus is sexually dimorphic; i.e., estrogen receptors are expressed in different sets of neurons.{{citation needed|date=
[[Estrogen]] and [[progesterone]] can influence gene expression in particular neurons or induce changes in [[cell membrane]] potential and [[kinase]] activation, leading to diverse non-genomic cellular functions. Estrogen and progesterone bind to their cognate [[nuclear hormone receptor]]s, which translocate to the cell nucleus and interact with regions of DNA known as [[hormone response element]]s (HREs) or get tethered to another [[transcription factor]]'s binding site. [[Estrogen receptor]] (ER) has been shown to transactivate other transcription factors in this manner, despite the absence of an [[estrogen response element]] (ERE) in the proximal promoter region of the gene. In general, ERs and [[progesterone receptor]]s (PRs) are gene activators, with increased mRNA and subsequent protein synthesis following hormone exposure.{{citation needed|date=
Male and female brains differ in the distribution of estrogen receptors, and this difference is an irreversible consequence of neonatal steroid exposure. Estrogen receptors (and progesterone receptors) are found mainly in neurons in the anterior and mediobasal hypothalamus, notably:{{citation needed|date=
*the preoptic area (where [[LHRH]] neurons are located)
*the periventricular nucleus (where [[somatostatin]] neurons are located)
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===Development===
[[File:Gray654.png|thumbnail|Median sagittal section of brain of human embryo of three months]]
In neonatal life, gonadal steroids influence the development of the neuroendocrine hypothalamus. For instance, they determine the ability of females to exhibit a normal reproductive cycle, and of males and females to display appropriate reproductive behaviors in adult life.{{citation needed|date=
*If a ''female rat'' is injected once with testosterone in the first few days of postnatal life (during the "critical period" of sex-steroid influence), the hypothalamus is irreversibly masculinized; the adult rat will be incapable of generating an LH surge in response to estrogen (a characteristic of females), but will be capable of exhibiting ''male'' sexual behaviors (mounting a sexually receptive female).{{citation needed|date=
*By contrast, a ''male rat'' castrated just after birth will be ''feminized'', and the adult will show ''female'' sexual behavior in response to estrogen (sexual receptivity, [[lordosis behavior]]).{{citation needed|date=
In primates, the developmental influence of [[androgens]] is less clear, and the consequences are less understood. Within the brain, testosterone is aromatized to ([[estradiol]]), which is the principal active hormone for developmental influences. The human [[testis]] secretes high levels of testosterone from about week 8 of fetal life until 5–6 months after birth (a similar perinatal surge in testosterone is observed in many species), a process that appears to underlie the male phenotype. Estrogen from the maternal circulation is relatively ineffective, partly because of the high circulating levels of steroid-binding proteins in pregnancy.{{citation needed|date=
[[Sex steroid]]s are not the only important influences upon hypothalamic development; in particular, [[Puberty|pre-pubertal]] stress in early life (of rats) determines the capacity of the adult hypothalamus to respond to an acute stressor.<ref>{{cite journal | last = Romeo | first = Russell D |author2=Rudy Bellani |author3=Ilia N. Karatsoreos |author4=Nara Chhua |author5=Mary Vernov |author6=Cheryl D. Conrad |author7=Bruce S. McEwen | title = Stress History and Pubertal Development Interact to Shape Hypothalamic-Pituitary-Adrenal Axis Plasticity | journal = Endocrinology | volume = 147 | issue = 4 | pages = 1664–1674 | publisher = The Endocrine Society | year = 2005 | url = http://endo.endojournals.org/cgi/content/short/147/4/1664 | doi = 10.1210/en.2005-1432 |pmid = 16410296 |deadurl=no |accessdate= 3
==Function==
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===Hormone release===
[[File:Endocrine central nervous en.svg|thumbnail|Endocrine glands in the human head and neck and their hormones]]
The hypothalamus has a central [[neuroendocrine]] function, most notably by its control of the [[anterior pituitary]], which in turn regulates various endocrine glands and organs. [[Releasing hormone]]s (also called releasing factors) are produced in hypothalamic nuclei then transported along [[axons]] to either the [[median eminence]] or the [[posterior pituitary]], where they are stored and released as needed.<ref>{{cite web|last1=Bowen|first1=R.|title=Overview of Hypothalamic and Pituitary Hormones|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/overview.html|accessdate= 5
;Anterior pituitary
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| GnRH or LHRH || [[Neuroendocrine]] cells of the [[Preoptic area]] || Stimulate [[Follicle-stimulating hormone|follicle-stimulating hormone (FSH)]] release from [[anterior pituitary]] <br>Stimulate [[Luteinizing hormone|luteinizing hormone (LH)]] release from [[anterior pituitary]]
|-
! [[Somatostatin]]<ref>{{cite journal|last=Ben-Shlomo|first=Anat|author2=Melmed, Shlomo|title=Pituitary somatostatin receptor signaling|journal=Trends in Endocrinology & Metabolism|date= 28
| SS, GHIH, or SRIF || [[Neuroendocrine]] cells of the [[Periventricular nucleus]] || Inhibit [[Growth hormone|growth-hormone (GH)]] release from [[anterior pituitary]] <br>Inhibit (moderately) [[Thyroid-stimulating hormone|thyroid-stimulating hormone (TSH)]] release from [[anterior pituitary]]
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Other hormones secreted from the median eminence include [[vasopressin]], [[oxytocin]], and [[neurotensin]].<ref name=horn>{{cite journal|last=Horn|first=A. M.|author2=Robinson, I. C. A. F. |author3=Fink, G. |title=Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats|journal=Journal of Endocrinology|date= 1
;Posterior pituitary
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|}
It is also known that [[hypothalamic-pituitary-adrenal axis]] (HPA) hormones are related to certain skin diseases and skin homeostasis. There is evidence linking hyperactivity of HPA hormones to stress-related skin diseases and skin tumors.<ref>{{cite web|title=Expression of Hypothalamic-Pituitary-Adrenal Axis in Common Skin Diseases: Evidence of its Association with Stress-related Disease Activity|url=http://web.b.ebscohost.com/ehost/pdfviewer/pdfviewer?sid=8239d5d4-8cd4-48b0-b25c-e1218229f462%40sessionmgr115&vid=11&hid=122|publisher=National Research Foundation of Korea|accessdate= 4
===Stimulation===
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====Blood-borne stimuli====
[[Peptide]] hormones have important influences upon the hypothalamus, and to do so they must pass through the [[blood–brain barrier]]. The hypothalamus is bounded in part by specialized brain regions that lack an effective blood–brain barrier; the [[Capillary#Types|capillary]] [[endothelium]] at these sites is fenestrated to allow free passage of even large proteins and other molecules. Some of these sites are the sites of neurosecretion - the [[neurohypophysis]] and the [[median eminence]]. However, others are sites at which the brain samples the composition of the blood. Two of these sites, the SFO ([[subfornical organ]]) and the OVLT ([[organum vasculosum of the lamina terminalis]]) are so-called [[circumventricular organs]], where neurons are in intimate contact with both blood and [[Cerebrospinal fluid|CSF]]. These structures are densely vascularized, and contain osmoreceptive and sodium-receptive neurons that control [[drinking]], [[vasopressin]] release, sodium excretion, and sodium appetite. They also contain neurons with receptors for [[angiotensin]], [[atrial natriuretic factor]], [[endothelin]] and [[relaxin]], each of which important in the regulation of fluid and electrolyte balance. Neurons in the OVLT and SFO project to the [[supraoptic nucleus]] and [[paraventricular nucleus]], and also to preoptic hypothalamic areas. The circumventricular organs may also be the site of action of [[interleukins]] to elicit both fever and ACTH secretion, via effects on paraventricular neurons.{{citation needed|date=
It is not clear how all peptides that influence hypothalamic activity gain the necessary access. In the case of [[prolactin]] and [[leptin]], there is evidence of active uptake at the [[choroid plexus]] from the blood into the [[cerebrospinal fluid]] (CSF). Some pituitary hormones have a negative feedback influence upon hypothalamic secretion; for example, [[growth hormone]] feeds back on the hypothalamus, but how it enters the brain is not clear. There is also evidence for central actions of [[prolactin]].{{citation needed|date=
Findings have suggested that [[thyroid hormone]] (T4) is taken up by the hypothalamic [[glial cells]] in the [[infundibular nucleus]]/ [[median eminence]], and that it is here converted into [[Triiodothyronine|T3]] by the type 2 deiodinase (D2). Subsequent to this, T3 is transported into the [[thyrotropin-releasing hormone]] ([[TRH]])-producing [[neurons]] in the [[paraventricular nucleus]]. [[Thyroid hormone receptor]]s have been found in these [[neurons]], indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed [[SLC16A2|MCT8]], a [[thyroid hormone]] transporter, supporting the theory that T3 is transported into them. T3 could then bind to the thyroid hormone receptor in these neurons and affect the production of thyrotropin-releasing hormone, thereby regulating thyroid hormone production.<ref>{{cite journal|last=Fliers|first=Eric|author2=Unmehopa, Alkemade|title=Functional neuroanatomy of thyroid hormone feedback in the human hypothalamus and pituitary gland|journal=Molecular and Cellular Endocrinology|date= 7
The hypothalamus functions as a type of [[thermostat]] for the body.<ref name=Harrisons>{{cite book
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{{Diencephalon}}
{{Endocrine system}}
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[[Category:Endocrine system]]
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