User:Jrouhana18/sandbox

Wiki Assignment #2: A delta fiber
Edit #1: re-naming "Structure" Section to "Anatomy", reorganizing useful information, and adding sources

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Structure[edit | edit source]
They are thin (2 to 5 μm in diameter), myelinated axons with a moderate conduction velocity, or speed of travel of a nerve signal (2 to 30 m/s). These nerve fibers are associated with acute (sharp) pain and therefore constitute the afferent portion of the reflex arc that results in "pulling away" from noxious stimuli (e.g. retracting your hand away from a hot stove). A certain proportion of Aδ fibers are also associated with sensations of temperature (also known as 'cold receptors' in mammals) and pressure. Slowly conducting, unmyelinated C fibers, by contrast, carry slow, burning pain.

Like other sensory fibers, the Aδ fiber is an extension of a pseudounipolar neuron with its cell body located in a dorsal root ganglion or trigeminal ganglion. Within the spinal cord, afferent nociceptor fibers synapse at or near the spinal cord level where they enter.

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Structure
Aδ fibers are thin (2 to 5 μm in diameter), myelinated axons with moderate conduction velocities, defined as the speed at which a nerve signal travels (2 to 30 m/s). Like other sensory neurons, the Aδ fiber is an extension of a pseudounipolar neuron in that its axons diverge into two main branches after leaving the cell body with two distinct synapse targets: the periphery and the spinal cord.

Location
The cell bodies of Aδ fibers are located in dorsal root ganglia ''and send axons to the periphery to innervate their target organs as well as through the dorsal roots to enter the spinal cord. Within the spinal cord, the axons reach the dorsal horn and terminate at Rexed laminae I and V - cross-sectional, systematic layers within the grey matter of the spinal cord''.

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Edit #2: adding a "Function" section

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Function
Aδ fibers serve to receive and transmit information primarily relating to acute pain - described as sharp, immediate, and relatively short lasting. This type of pain can result from several classifications of stimulants: temperature-induced, mechanical, and chemical.

Temperature
Aδ fibers respond to temperature on both the noxiously cold and hot ends of the spectrum. For both extremes, there exists a temperature threshold at which receptors begin to respond. Two main classes divide Aδ fibers: Type I and Type II. Type I receptors have higher heat thresholds then Type II. Thus, Type II Aδ fibers likely act as a first response to dangerously high temperatures. Mechanistically, temperatures above 43°C activate a receptor associated with Aδ fibers called transient receptor potential vanilloid subfamily, member 1 (TRPV1) which subsequently depolarizes the neuron. This depolarization is transmitted to the spinal cord where axons of Aδ fibers terminate on second-order neurons in the dorsal horn. These neurons relay the nociceptive signal to the brain (specifically the thalamus and the brainstem) for further processing. At the cold end of the spectrum, it is clear that a significant proportion of Aδ fibers plays a role in perceiving cold temperatures, but the mechanism and related receptors are currently up for debate. Temperatures at or below ~ 15°C are cited as the cold threshold for painful stimuli. However, the threshold for Aδ fibers specifically seems to be lower (less than 0°C).

Mechanical
Aδ fibers are responsible for relaying information regarding harmful mechanical stimulation which often results in pinching, cutting, or stinging sensations. Both Type I and Type II Aδ fibers respond to intense mechanical stimuli and communicate this information through the spinal cord to the brain for perception processing through similar pathway as seen in temperature nociception. Mechanisms for cellular transduction of painful mechanical stimuli are currently largely unknown, but could involve a family of mechanoreceptors associated with harmless touch perception called ENaC/DEG-channels.

Chemical
Conclusions in the literature remain largely mixed pertaining to the interaction between chemical stimuli and Aδ fibers. However, there is evidence that chemically noxious stimuli, such as capsaicin or certain acids, activate Aδ fibers to elicit pain associated with the potential for tissue damage. It has been suggested that acid-sensing ion channels (ASICS) play a role in acid-stimulated nociception involving Aδ fibers. Capsaicin, the primary component of hot peppers which yields the experience of spice, may stimulate a common transducer, vanilloid receptor (VR1), in Aδ fibers.

Nociceptive Flexion Reflex
Aδ fibers also play an integral role in rapid musculatory reactions to acute pain known commonly as reflexes. Reflexes that specifically respond to painful stimuli by driving appropriate withdrawal responses are known as nociceptive flexion reflexes (NFR) and are often used as a measure of nociception in research experiments. In the case of Aδ fibers, the pathway of a reflex arc begins with an external, acutely painful stimulus (e.g. a pin pricking a finger). The stimulus activates Aδ fibers, which act as afferent neurons, through one of the stimulant pathways described above (in the case of a pin prick, through mechanical stimulation). A signal is subsequently transduced to the spinal cord, passed along to a short interneuron, and finally affects a motor neuron which carries out the musculoskelatal response, withdrawing the appropriate part of the body from the harmful stimulus. These reflex arcs function much faster than normal neuromuscular processes because they are able to bypass processing in the brain.

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Wiki Assignment #1: Hypophyseal portal system
Edit #1: re-writing the "Development" Subsection (there are no valid sources cited for this section and the structure/ content can be improved significantly)

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Development [edit | edit source]
Proper hormone secretion in the developing fetus is crucial for its growth in the womb of the mother. In order to allow a controlled hormone secretion in the developing organs of the fetus, stimulating hormones must be exchanged in the regulating structures in the brain in early stages of the development. Hormone-exchanging blood vessels between the hypothalamus and the pituitary gland, similar to those of the hypophyseal portal system, can be observed in early developmental stages of the fetus. A study performed on ovine fetuses, about 48-67 days of gestation, showed extensive and very well-developed capillary connections between the median eminence, the pituitary stalk, and the pituitary gland. In some of the fetuses, portal capillary loops had penetrated into the median eminence. These findings suggest that, in the ovine fetus, hypothalamic releasing hormones can be transported directly via a portal vascular way to the pituitary gland that develops as early as 45 days of gestation. These experimental results give evidence for an early development of what is later the fully developed hypophysial portal system. 4,5,6

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Proper hormone secretion in the developing fetus is crucial for its growth in the womb of the mother. In order to allow a controlled hormone secretion in the developing organs of the fetus, stimulating hormones must be exchanged in the regulating structures in the brain in early stages of the development. Hormone-exchanging blood vessels between the hypothalamus and the pituitary gland, similar to those of the hypophyseal portal system, can be detected in early growth stages of the fetus. ''In the current literature, most research is conducted using mice as model species. In such studies, development of the hypophyseal portal system begins as early as 14.5 dpc (days post coitum). Two populations of pericytes arise from the mesoderm and the neuroectoderm and form at the approximate location of the portal system in what will eventually become the mature brain. Additionally, in research involving human fetuses it has been observed that the hypophyseal portal system fully develops by week 11.5 of the human fetal gestation period. This was determined by injecting a silicone rubber compound into specimens of various stages of gestation. In a specimen at week 11.5, the median eminence and infundibular stem contained the compound, suggesting the existence of the fully developed portal system. However, further research in this area would help determine whether or not development could be complete at an even earlier stage.''

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Edit #2: add on to "Clinical significance" section

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Clinical significance [edit | edit source]
Over- or under-function as well as insufficiencies of the hypothalamus or the pituitary gland can cause a negative effect on the ability of the hypophyseal portal system to exchange hormones between both structures rapidly. This can have major effects on the respective target glands, making it impossible for them to carry out their functions properly. Occlusions and other issues in the blood vessels of the hypophyseal portal system can also cause complications in the exchange of hormones between the hypothalamus and the pituitary gland.

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The hypophyseal portal system also plays an important role in several diseases involving the pituitary and central nervous system. In several cases of hypophyseal and pituitary metastatic tumors, the portal system acts as the pathway for metastasis from the hypothalamus to the pituitary. That is, cancerous cells from the hypothalamus multiply and spread to the pituitary using the hypophyseal portal system as a means of transportation. However, because the portal system receives an indirect supply of arterial blood, tumor formation in the anterior pituitary is less likely than in the posterior pituitary. This is because the posterior pituitary is vascularized by direct arterial blood flow. Pituitary apoplexy is described as hemorrhaging or reduction of blood supply to the pituitary gland. The physiological mechanisms of this condition have not been clearly defined in current research. It has been suggested, nonetheless, that damage to the pituitary stalk leads to an obstruction of blood flow in the hypophyseal portal system and contributes to this defective state. In Erdheim-Chester Disease, cells of the immune system called histiocytes proliferate at an abnormal rate causing a plethora of symptoms and, in more severe cases, death. The disruption of the hypophyseal portal system has been implicated as the mechanism for several symptoms involving the central nervous symptom, most notably diabetes insipidus.

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Edit #3: Adding a section: "Relevant Hormones"

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Relevant Hormones
The following is a list of hormones that rely on the hypophyseal portal system to indirectly mediate their function by acting as a means of transportation from various nuclei of the hypothalamus to the anterior pituitary. - end original text-
 * Gonadotropin-releasing hormone (GnRH): regulates the release of follicle stimulating hormone and luteinizing hormone from the anterior pituitary; this pathway plays a critical role in reproductive activity and development
 * Corticotropin-releasing hormone (CRH): regulates the release of adrenocorticotropic hormone from the anterior pituitary; this cascade is primarily responsible for stress response
 * Growth hormone-releasing hormone (GHRH): regulates the release of growth hormone from the anterior pituitary; as the name suggests, its main function is to help control cell growth, metabolism, and reproduction
 * Thyrotropin-releasing hormone (TRH): regulates the release of thyroid-stimulating hormone from the anterior pituitary; functions to mediate various responses in the thyroid gland, including additional hormone synthesis

N.B. be mindful of which sources are for which Wiki assignment

- also: Basbam, et al. is already cited in the article --> coordinate