Hormone release s 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 hormones (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. ;Anterior pituitary In the hypothalamic–adenohypophyseal axis, releasing hormones, also known as hypophysiotropic or hypothalamic hormones, are released from the median eminence, a prolongation of the hypothalamus, into the
hypophyseal portal system, which carries them to the anterior pituitary where they exert their regulatory functions on the secretion of adenohypophyseal hormones. These hypophysiotropic hormones are stimulated by parvocellular neurosecretory cells located in the periventricular area of the hypothalamus. After their release into the capillaries of the third ventricle, the hypophysiotropic hormones travel through what is known as the hypothalamo-pituitary portal circulation. Once they reach their destination in the anterior pituitary, these hormones bind to specific receptors located on the surface of pituitary cells. Depending on which cells are activated through this binding, the pituitary will either begin secreting or stop secreting hormones into the rest of the bloodstream. Other hormones secreted from the median eminence include
vasopressin,
oxytocin, and
neurotensin. ;Posterior pituitary In the hypothalamic–pituitary–adrenal axis,
neurohypophysial hormones are released from the posterior pituitary, which is actually a prolongation of the hypothalamus, into the circulation. 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.
Stimulation The hypothalamus coordinates many hormonal and behavioural circadian rhythms, complex patterns of
neuroendocrine outputs, complex
homeostatic mechanisms, and important behaviours. The hypothalamus must, therefore, respond to many different signals, some of which are generated externally and some internally.
Delta wave signalling arising either in the thalamus or in the cortex influences the secretion of releasing hormones;
GHRH and
prolactin are stimulated whilst
TRH is inhibited. The hypothalamus is responsive to: • Light: daylength and
photoperiod for regulating
circadian and seasonal rhythms •
Olfactory stimuli, including
pheromones •
Steroids, including
gonadal steroids and
corticosteroids • Neurally transmitted information arising in particular from the heart,
enteric nervous system (of the
gastrointestinal tract), and the reproductive tract. •
Autonomic inputs • Blood-borne stimuli, including
leptin,
ghrelin,
angiotensin,
insulin,
pituitary hormones,
cytokines, plasma concentrations of glucose and osmolarity etc. •
Stress • Invading microorganisms by increasing body temperature, resetting the body's thermostat upward.
Olfactory stimuli Olfactory stimuli are important for
sexual reproduction and
neuroendocrine function in many species. For instance, if a pregnant mouse is exposed to the urine of a 'strange' male during a critical period after coitus then the pregnancy fails (the
Bruce effect). Thus, during coitus, a female mouse forms a precise 'olfactory memory' of her partner that persists for several days. Pheromonal cues aid synchronization of
oestrus in many species; in women, synchronized
menstruation may also arise from pheromonal cues, although the role of pheromones in humans is disputed.
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 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
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. 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. 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
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 receptors have been found in these
neurons, indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed
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. The hypothalamus functions as a type of
thermostat for the body. It sets a desired body temperature, and stimulates either heat production and retention to raise the blood temperature to a higher setting or sweating and
vasodilation to cool the blood to a lower temperature. All
fevers result from a raised setting in the hypothalamus; elevated body temperatures due to any other cause are classified as
hyperthermia. • Lipostatic hypothesis: This hypothesis holds that
adipose tissue produces a
humoral signal that is proportionate to the amount of fat and acts on the hypothalamus to decrease food intake and increase energy output. It has been evident that a
hormone leptin acts on the hypothalamus to decrease food intake and increase energy output. • Gutpeptide hypothesis:
gastrointestinal hormones like Grp,
glucagons,
CCK and others claimed to inhibit food intake. The food entering the gastrointestinal tract triggers the release of these hormones, which act on the brain to produce satiety. The brain contains both CCK-A and CCK-B receptors. • Glucostatic hypothesis: The activity of the satiety center in the ventromedial nuclei is probably governed by the
glucose utilization in the neurons. It has been postulated that when their glucose utilization is low and consequently when the arteriovenous blood glucose difference across them is low, the activity across the neurons decrease. Under these conditions, the activity of the feeding center is unchecked and the individual feels hungry. Food intake is rapidly increased by intraventricular administration of
2-deoxyglucose therefore decreasing glucose utilization in cells. • Thermostatic hypothesis: According to this hypothesis, a decrease in body temperature below a given set-point stimulates appetite, whereas an increase above the set-point inhibits appetite.
Fear processing The medial zone of hypothalamus is part of a circuitry that controls motivated behaviors, like defensive behaviors. Analyses of
Fos-labeling showed that a series of nuclei in the "behavioral control column" is important in regulating the expression of innate and conditioned defensive behaviors. ;Antipredatory defensive behavior Exposure to a predator (such as a cat) elicits defensive behaviors in laboratory rodents, even when the animal has never been exposed to a cat. In the hypothalamus, this exposure causes an increase in
Fos-labeled cells in the anterior hypothalamic nucleus, the dorsomedial part of the ventromedial nucleus, and in the ventrolateral part of the premammillary nucleus (PMDvl). The premammillary nucleus has an important role in expression of defensive behaviors towards a predator, since lesions in this nucleus abolish defensive behaviors, like freezing and flight. The PMD has important connections to the dorsal
periaqueductal gray, an important structure in fear expression. In addition, animals display risk assessment behaviors to the environment previously associated with the cat. Fos-labeled cell analysis showed that the PMDvl is the most activated structure in the hypothalamus, and inactivation with
muscimol prior to exposure to the context abolishes the defensive behavior. Such structures are important in other social behaviors, such as sexual and aggressive behaviors. Moreover, the premammillary nucleus also is mobilized, the dorsomedial part but not the ventrolateral part. ==Additional images==