Hyperpolarization is a change in a cell's membrane potential that makes it more negative. It is the opposite of a depolarization, it inhibits action potentials by increasing the stimulus required to move the membrane potential to the action potential threshold. Hyperpolarization is caused by efflux of K+ through K+ channels, or influx of Cl– through Cl– channels. On the other hand, influx of cations, e.g. Na+ through Na+ channels or Ca2+ through Ca2+ channels, inhibits hyperpolarization. If a cell has Na+ or Ca2+ currents at rest inhibition of those currents will result in a hyperpolarization; this voltage-gated ion channel response is. In neurons, the cell enters a state of hyperpolarization following the generation of an action potential. While hyperpolarized, the neuron is in a refractory period that lasts 2 milliseconds, during which the neuron is unable to generate subsequent action potentials. Sodium-potassium ATPases redistribute K+ and Na+ ions until the membrane potential is back to its resting potential of around –70 millivolts, at which point the neuron is once again ready to transmit another action potential.
Voltage gated ion channels respond to changes in the membrane potential. Voltage gated potassium and sodium channels are key component for generating the action potential as well as hyper-polarization; these channels work by selecting an ion based on electrostatic attraction or repulsion allowing the ion to bind to the channel. This releases the water molecule attached to the channel and the ion is passed through the pore. Voltage gated sodium channels close again; this means the channel either is open or not, there is no part way open. Sometimes the channel closes but is able to be reopened right away, known as channel gating, or it can be closed without being able to be reopened right away, known as channel inactivation. At resting potential, both the voltage gated sodium and potassium channels are closed but as the cell membrane becomes depolarized the voltage gated sodium channels begin to open up and the neuron begins to depolarize, creating a current feedback loop known as the Hodgkin cycle.
However, potassium ions move out of the cell and if the original depolarization event was not significant enough the neuron does not generate an action potential. If all the sodium channels are open, however the neuron becomes ten times more permeable to sodium than potassium depolarizing the cell to a peak of +40 mV. At this level the sodium channels begin to voltage gated potassium channels begin to open; this combination of closed sodium channels and open potassium channels leads to the neuron re-polarizing and becoming negative again. The neuron continues to re-polarize until the cell reaches ~ –75 mV, the equilibrium potential of potassium ions; this is the point at which the neuron is hyperpolarized, between –70 mV and –75 mV. After hyperpolarization the potassium channels close and the natural permeability of the neuron to sodium and potassium allows the neuron to return to its resting potential of –70 mV. During the refractory period, after hyper-polarization but before the neuron has returned to its resting potential the neuron is capable of triggering an action potential due to the sodium channels ability to be opened, because the neuron is more negative it becomes more difficult to reach the action potential threshold.
HCN channels are activated by hyperpolarization. Hyperpolarization is a change in membrane potential, neuroscientists measure it using a technique known as patch clamping. Using this method they are able to record ion currents passing through individual channels; this is done using a glass micropipette called a patch pipette, with a 1 micrometer diameter. There is a small patch that contains a few ion channels and the rest is sealed off, making this the point of entry for the current. Using an amplifier and a voltage clamp, an electronic feedback circuit, allows the experimenter to maintain the membrane potential at a fixed point and the voltage clamp measures tiny changes in current flow; the membrane currents giving rise to hyperpolarization are either an increase in outward current or a decrease in inward current. During the afterhyperpolarization period after an action potential, the membrane potential is more negative than when the cell is at the resting potential. In the figure to the right, this undershoot occurs at 3 to 4 milliseconds on the time scale.
The afterhyperpolarization is the time when the membrane potential is hyperpolarized relative to the resting potential. During the rising phase of an action potential, the membrane potential changes from negative to positive, a depolarization. In the figure, the rising phase is from 1 to 2 ms on the graph. During the rising phase, once the membrane potential becomes positive, the membrane potential continues to depolarize until the peak of the action potential is reached at about +40 millivolts. After the peak of the action potential, a hyperpolarization repolarizes the membrane potential to its resting value, first by making it less positive, until 0 mV is reached, by continuing to make it more negative; this repolarization occurs in the figure from 2 to 3 ms on the time scale. Purves D, Augustine GJ, Fitzpatrick D, et al. eds.. Neuroscience. Sunderland, Mass: Sinauer Assoc. ISBN 0-87893-742-0. Basic Neurochemistry Molecular and Medical Aspects by Siegel, et al
Glutamic acid is an α-amino acid, used by all living beings in the biosynthesis of proteins. It is non-essential in humans, it is an excitatory neurotransmitter, in fact the most abundant one, in the vertebrate nervous system. It serves as the precursor for the synthesis of the inhibitory gamma-aminobutyric acid in GABA-ergic neurons, it has a formula C5H9O4N. Its molecular structure could be idealized as HOOC-CH-2-COOH, with two carboxyl groups -COOH and one amino group -NH2. However, in the solid state and mildly acid water solutions, the molecule assumes an electrically neutral zwitterion structure −OOC-CH-2-COOH, it is encoded by the codons GAA or GAG. The acid can lose one proton from its second carboxyl group to form the conjugate base, the singly-negative anion glutamate −OOC-CH-2-COO−; this form of the compound is prevalent in neutral solutions. The glutamate neurotransmitter plays the principal role in neural activation; this anion is responsible for the savory flavor of certain foods, used in glutamate flavorings such as MSG.
In Europe it is classified as food additive E620. In alkaline solutions the doubly negative anion −OOC-CH-2-COO− prevails; the radical corresponding to glutamate is called glutamyl. When glutamic acid is dissolved in water, the amino group may gain a proton, and/or the carboxyl groups may lose protons, depending on the acidity of the medium. In sufficiently acidic environments, the amino group gains a proton and the molecule becomes a cation with a single positive charge, HOOC-CH-2-COOH. At pH values between about 2.5 and 4.1, the carboxylic acid closer to the amine loses a proton, the acid becomes the neutral zwitterion −OOC-CH-2-COOH. This is the form of the compound in the crystalline solid state; the change in protonation state is gradual. At higher pH, the other carboxylic acid group loses its proton and the acid exists entirely as the glutamate anion −OOC-CH-2-COO−, with a single negative charge overall; the change in protonation state occurs at pH 4.07. This form with both carboxylates lacking protons is dominant in the physiological pH range.
At higher pH, the amino group loses the extra proton and the prevalent species is the doubly-negative anion −OOC-CH-2-COO−. The change in protonation state occurs at pH 9.47. The carbon atom adjacent to the amino group is chiral, so glutamic acid can exist in two optical isomers, D and L; the L form is the one most occurring in nature, but the D form occurs in some special contexts, such as the cell walls of the bacteria and the liver of mammals. Although they occur in many foods, the flavor contributions made by glutamic acid and other amino acids were only scientifically identified early in the twentieth century; the substance was discovered and identified in the year 1866, by the German chemist Karl Heinrich Ritthausen who treated wheat gluten with sulfuric acid. In 1908 Japanese researcher Kikunae Ikeda of the Tokyo Imperial University identified brown crystals left behind after the evaporation of a large amount of kombu broth as glutamic acid; these crystals, when tasted, reproduced the ineffable but undeniable flavor he detected in many foods, most in seaweed.
Professor Ikeda termed this flavor umami. He patented a method of mass-producing a crystalline salt of glutamic acid, monosodium glutamate. Glutamic acid is produced on the largest scale of any amino acid, with an estimated annual production of about 1.5 million tons in 2006. Chemical synthesis was supplanted by the aerobic fermentation of sugars and ammonia in the 1950s, with the organism Corynebacterium glutamicum being the most used for production. Isolation and purification can be achieved by crystallization. Glutamate is a key compound in cellular metabolism. In humans, dietary proteins are broken down by digestion into amino acids, which serve as metabolic fuel for other functional roles in the body. A key process in amino acid degradation is transamination, in which the amino group of an amino acid is transferred to an α-ketoacid catalysed by a transaminase; the reaction can be generalised as such: R1-amino acid + R2-α-ketoacid ⇌ R1-α-ketoacid + R2-amino acidA common α-keto acid is α-ketoglutarate, an intermediate in the citric acid cycle.
Transamination of α-ketoglutarate gives glutamate. The resulting α-ketoacid product is a useful one as well, which can contribute as fuel or as a substrate for further metabolism processes. Examples are as follows: Alanine + α-ketoglutarate ⇌ pyruvate + glutamateAspartate + α-ketoglutarate ⇌ oxaloacetate + glutamateBoth pyruvate and oxaloacetate are key components of cellular metabolism, contributing as substrates or intermediates in fundamental processes such as glycolysis and the citric acid cycle. Glutamate plays an important role in the body's disposal of excess or waste nitrogen. Glutamate undergoes deamination, an oxidative reaction catalysed by glutamate dehydrogenase, as follows: glutamate + H2O + NADP+ → α-ketoglutarate + NADPH + NH3 + H+Ammonia is excreted predominantly as urea, synthesised in the liver. Transamination can thus be linked to deamination allowing nitrogen from the amine groups of amino acids to be removed, via glutamate as an intermediate, excreted from the body in the form of urea.
Glutamate is a
Midshipman fish belong to the genus Porichthys of toadfishes. They are distinguished by having four lateral lines. Typical midshipman fishes, such as the plainfin midshipman, are nocturnal and bury themselves in sand or mud in the intertidal zone during the day. At night they float just above the seabed; some species are capable of inflicting serious injuries if handled. Male midshipman fish have two morphs: type I and type II. Type I and type II males have different reproductive strategies, can be distinguished from each other based on physical characteristics. Type I males are eight times larger in body mass, have much larger vocal organs. Type II males’ reproductive organs are seven times larger in size than those of type I males. Female and type II male midshipman fish can be distinguished from each other by the female’s larger size, the type II male midshipman’s large reproductive organs. There are 14 recognized extant species in this genus: Porichthys analis C. L. Hubbs & L. P. Schultz, 1939 Porichthys bathoiketes C. R. Gilbert, 1968 Porichthys ephippiatus H. J. Walker & Rosenblatt, 1988 Porichthys greenei C. H. Gilbert & Starks, 1904 Porichthys kymosemeum C. R. Gilbert, 1968 Porichthys margaritatus Porichthys mimeticus H. J. Walker & Rosenblatt, 1988 Porichthys myriaster C. L. Hubbs & L. P. Schultz, 1939 Porichthys notatus Girard, 1854 Porichthys oculellus H. J. Walker & Rosenblatt, 1988 Porichthys oculofrenum C. R. Gilbert, 1968 Porichthys pauciradiatus D. K.
Caldwell & M. C. Caldwell, 1963 Porichthys plectrodon D. S. Jordan & C. H. Gilbert, 1882 Porichthys porosissimus †Porichthys analis - Early Pliocene Onzole Formation, Ecuador †Porichthys margaritatus - idem †Porichthys pedemontanus Robba 1970 - Tortonian Italy Mating in midshipman fishes depends on auditory communication. Male midshipman fish produce several different vocalizations while females only make grunts in non-breeding situations. Media related to Porichthys at Wikimedia Commons
The goldfish is a freshwater fish in the family Cyprinidae of order Cypriniformes. It is one of the most kept aquarium fish. A small member of the carp family, the goldfish is native to East Asia, it was first selectively bred in Ancient China more than a thousand years ago, several distinct breeds have since been developed. Goldfish breeds vary in size, body shape, fin configuration and colouration. Starting in ancient China, various species of carp have been bred and reared as food fish for thousands of years; some of these gray or silver species have a tendency to produce red, orange or yellow colour mutations. During the Tang dynasty, it was popular to raise carp in ornamental watergardens. A natural genetic mutation produced gold rather than silver colouration. People began to breed the gold variety instead of the silver variety, keeping them in ponds or other bodies of water. On special occasions at which guests were expected, they would be moved to a much smaller container for display. By the Song dynasty, the selective domestic breeding of goldfish was established.
In 1162, the empress of the Song Dynasty ordered the construction of a pond to collect the red and gold variety. By this time, people outside the imperial family were forbidden to keep goldfish of the gold variety, yellow being the imperial colour; this is the reason why there are more orange goldfish than yellow goldfish though the latter are genetically easier to breed. The occurrence of other colours was first recorded in 1276. During the Ming dynasty, goldfish began to be raised indoors, which permitted selection for mutations that would not be able to survive in ponds; the first occurrence of fancy-tailed goldfish was recorded in the Ming Dynasty. In 1603, goldfish were introduced to Japan. In 1611, goldfish were introduced from there to other parts of Europe. During the 1620s, goldfish were regarded in southern Europe because of their metallic scales, symbolised good luck and fortune, it became tradition for married men to give their wives a goldfish on their first anniversary, as a symbol for the prosperous years to come.
This tradition died, as goldfish became more available, losing their status. Goldfish were first introduced to North America around 1850 and became popular in the United States; as of April 2008, the largest goldfish in the world was believed by the BBC to measure 19 inches, be living in the Netherlands. At the time, a goldfish named "Goldie", kept as a pet in a tank in Folkestone, was measured as 15 inches and over 2 pounds, named as the second largest in the world behind the Netherlands fish; the secretary of the Federation of British Aquatic Societies stated of Goldie's size that "I would think there are a few bigger goldfish that people don't think of as record holders in ornamental lakes". In July 2010, a goldfish measuring 16 inches and 5 pounds was caught in a pond in Poole, thought to have been abandoned there after outgrowing a tank. Goldfish have one of the most studied senses of vision in fish. Goldfish have four kinds of cone cells, which are sensitive to different colours: red, green and ultraviolet.
The ability to distinguish between four different primary colours classifies them as tetrachromats. Goldfish have one of the most studied senses of hearing in fish, they have two otoliths, permitting the detection of sound particle motion, Weberian ossicles connecting the swimbladder to the otoliths, facilitating the detection of sound pressure. Goldfish have strong associative learning abilities, as well as social learning skills. In addition, their visual acuity allows them to distinguish between individual humans. Owners may notice that fish react favorably to them while hiding when other people approach the tank. Over time, goldfish learn to associate their owners and other humans with food "begging" for food whenever their owners approach. Goldfish that have constant visual contact with humans stop considering them to be a threat. After being kept in a tank for several weeks, sometimes months, it becomes possible to feed a goldfish by hand without it shying away. Goldfish have a memory-span of at least three months and can distinguish between different shapes and sounds.
By using positive reinforcement, goldfish can be trained to recognize and to react to light signals of different colours or to perform tricks. Fish respond to certain colours most evidently in relation to feeding. Fish learn to anticipate feedings provided. Goldfish are gregarious, displaying schooling behaviour, as well as displaying the same types of feeding behaviours. Goldfish may display similar behaviours. Goldfish have learned behaviours, both as groups and as individuals, that stem from native carp behaviour, they are a generalist species with varied feeding and predator avoidance behaviours that contribute to their success. As fish they can be described as "friendly" towards each other. Does a goldfish harm another goldfish, nor do the males harm the females during breeding; the only real threat that goldfish present to each other is competing for food. Commons and other f
Signal transduction is the process by which a chemical or physical signal is transmitted through a cell as a series of molecular events, most protein phosphorylation catalyzed by protein kinases, which results in a cellular response. Proteins responsible for detecting stimuli are termed receptors, although in some cases the term sensor is used; the changes elicited by ligand binding in a receptor give rise to a biochemical cascade, a chain of biochemical events as a signaling pathway. When signaling pathways interact with one another they form networks, which allow cellular responses to be coordinated by combinatorial signaling events. At the molecular level, such responses include changes in the transcription or translation of genes, post-translational and conformational changes in proteins, as well as changes in their location; these molecular events are the basic mechanisms controlling cell growth, proliferation and many other processes. In multicellular organisms, signal transduction pathways have evolved to regulate cell communication in a wide variety of ways.
Each component of a signaling pathway is classified according to the role it plays with respect to the initial stimulus. Ligands are termed first messengers, while receptors are the signal transducers, which activate primary effectors; such effectors are linked to second messengers, which can activate secondary effectors, so on. Depending on the efficiency of the nodes, a signal can be amplified, so that one signaling molecule can generate a response involving hundreds to millions of molecules; as with other signals, the transduction of biological signals is characterised by delay, signal feedback and feedforward and interference, which can range from negligible to pathological. With the advent of computational biology, the analysis of signaling pathways and networks has become an essential tool to understand cellular functions and disease, including signaling rewiring mechanisms underlying responses to acquired drug resistance; the basis for signal transduction is the transformation of a certain stimulus into a biochemical signal.
The nature of such stimuli can vary ranging from extracellular cues, such as the presence of EGF, to intracellular events, such as the DNA damage resulting from replicative telomere attrition. Traditionally, signals that reach the central nervous system are classified as senses; these are transmitted from neuron to neuron in a process called synaptic transmission. Many other intercellular signal relay mechanisms exist in multicellular organisms, such as those that govern embryonic development; the majority of signal transduction pathways involve the binding of signaling molecules, known as ligands, to receptors that trigger events inside the cell. The binding of a signaling molecule with a receptor causes a change in the conformation of the receptor, known as receptor activation. Most ligands are soluble molecules from the extracellular medium which bind to cell surface receptors; these include growth factors and neurotransmitters. Components of the extracellular matrix such as fibronectin and hyaluronan can bind to such receptors.
In addition, some molecules such as steroid hormones are lipid-soluble and thus cross the plasma membrane to reach nuclear receptors. In the case of steroid hormone receptors, their stimulation leads to binding to the promoter region of steroid-responsive genes. Not all classifications of signaling molecules take into account the molecular nature of each class member. For example, odorants belong to a wide range of molecular classes, as do neurotransmitters, which range in size from small molecules such as dopamine to neuropeptides such as endorphins. Moreover, some molecules may fit into more than one class, e.g. epinephrine is a neurotransmitter when secreted by the central nervous system and a hormone when secreted by the adrenal medulla. Some receptors such as HER2 are capable of ligand-independent activation when overexpressed or mutated; this leads to constituitive activation of the pathway, which may or may not be overturned by compensation mechanisms. In the case of HER2, which acts as a dimerization partner of other EGFRs, constituitive activation leads to hyperproliferation and cancer.
The prevalence of basement membranes in the tissues of Eumetazoans means that most cell types require attachment to survive. This requirement has led to the development of complex mechanotransduction pathways, allowing cells to sense the stiffness of the substratum; such signaling is orchestrated in focal adhesions, regions where the integrin-bound actin cytoskeleton detects changes and transmits them downstream through YAP1. Calcium-dependent cell adhesion molecules such as cadherins and selectins can mediate mechanotransduction. Specialised forms of mechanotransduction within the nervous system are responsible for mechanosensation: hearing, touch and balance. Cellular and systemic control of osmotic pressure is critical for homeostasis. There are three ways in which cells can detect osmotic stimuli: as changes in macromolecular crowding, ionic strength, changes in the properties of the plasma membrane or cytoskeleton; these changes are detected by proteins known as osmoreceptors. In humans, the best characterised osmosensors are transient receptor potential channels present in the primary cilium of human cells.
In yeast, the HOG pathway has been extensively characterised. The sensing of temperature in cells is known as thermoception and is mediated by transient receptor potential channels. Addi
Acetylcholine is an organic chemical that functions in the brain and body of many types of animals, including humans, as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells. Its name is derived from its chemical structure: it is an ester of acetic acid and choline. Parts in the body that use or are affected by acetylcholine are referred to as cholinergic. Substances that interfere with acetylcholine activity are called anticholinergics. Acetylcholine is the neurotransmitter used at the neuromuscular junction—in other words, it is the chemical that motor neurons of the nervous system release in order to activate muscles; this property means that drugs that affect cholinergic systems can have dangerous effects ranging from paralysis to convulsions. Acetylcholine is a neurotransmitter in the autonomic nervous system, both as an internal transmitter for the sympathetic nervous system and as the final product released by the parasympathetic nervous system.
Acetylcholine, has been traced in cells of non-neural origins and microbes. Enzymes related to its synthesis and cellular uptake have been traced back to early origins of unicellular eukaryotes; the protist pathogen Acanthamoeba spp. has shown the presence of ACh, which provides growth and proliferative signals via a membrane located M1-muscarinic receptor homolog. In the brain, acetylcholine functions as a neurotransmitter and as a neuromodulator; the brain contains a number of cholinergic areas, each with distinct functions. Because of its muscle-activating function, but because of its functions in the autonomic nervous system and brain, a large number of important drugs exert their effects by altering cholinergic transmission. Numerous venoms and toxins produced by plants and bacteria, as well as chemical nerve agents such as Sarin, cause harm by inactivating or hyperactivating muscles via their influences on the neuromuscular junction. Drugs that act on muscarinic acetylcholine receptors, such as atropine, can be poisonous in large quantities, but in smaller doses they are used to treat certain heart conditions and eye problems.
Scopolamine, which acts on muscarinic receptors in the brain, can cause delirium and amnesia. The addictive qualities of nicotine are derived from its effects on nicotinic acetylcholine receptors in the brain. Acetylcholine is a choline molecule, acetylated at the oxygen atom; because of the presence of a polar, charged ammonium group, acetylcholine does not penetrate lipid membranes. Because of this, when the drug is introduced externally, it remains in the extracellular space and does not pass through the blood–brain barrier. A synonym of this drug is miochol. Acetylcholine is synthesized in certain neurons by the enzyme choline acetyltransferase from the compounds choline and acetyl-CoA. Cholinergic neurons are capable of producing ACh. An example of a central cholinergic area is the nucleus basalis of Meynert in the basal forebrain; the enzyme acetylcholinesterase converts acetylcholine into the inactive metabolites choline and acetate. This enzyme is abundant in the synaptic cleft, its role in clearing free acetylcholine from the synapse is essential for proper muscle function.
Certain neurotoxins work by inhibiting acetylcholinesterase, thus leading to excess acetylcholine at the neuromuscular junction, causing paralysis of the muscles needed for breathing and stopping the beating of the heart. Acetylcholine functions in both the central nervous system and the peripheral nervous system. In the CNS, cholinergic projections from the basal forebrain to the cerebral cortex and hippocampus support the cognitive functions of those target areas. In the PNS, acetylcholine activates muscles and is a major neurotransmitter in the autonomic nervous system. Like many other biologically active substances, acetylcholine exerts its effects by binding to and activating receptors located on the surface of cells. There are two main classes of acetylcholine receptor and muscarinic, they are named for chemicals that can selectively activate each type of receptor without activating the other: muscarine is a compound found in the mushroom Amanita muscaria. Nicotinic acetylcholine receptors are ligand-gated ion channels permeable to sodium and calcium ions.
In other words, they are ion channels embedded in cell membranes, capable of switching from a closed to an open state when acetylcholine binds to them. Nicotinic receptors come in two main types, known as neuronal-type; the muscle-type can be selectively blocked by the neuronal-type by hexamethonium. The main location of muscle-type receptors is on muscle cells. Neuronal-type receptors are located in autonomic ganglia, in the central nervous system. Muscarinic acetylcholine receptors have a more complex mechanism, affect target cells over a longer time frame. In mammals, five subtypes of muscarinic receptors have been identified, labeled M1 through M5. All of them function as G protein-coupled receptors, meaning that they exert their effects via a second messenger system; the M1, M3, M5 subtypes are Gq-coupled. Their effect on target cells is excitatory; the M2 and M4 subtypes are Gi/Go-coupled. Their effect on target cells is inhibitory. Muscarinic acetylcholine receptors are found in both
A mechanoreceptor is a sensory receptor that responds to mechanical pressure or distortion. There are four main types in glabrous, or hairless, mammalian skin: lamellar corpuscles, tactile corpuscles, Merkel nerve endings, bulbous corpuscles. There are mechanoreceptors in hairy skin, the hair cells in thoreceptors of primates like rhesus monkeys and other mammals are similar to those of humans and studied in early 20th century anatomically and neurophysiologically. Invertebrate mechanoreceptors include campaniform slit sensilla, among others. In somatosensory transduction, the afferent neurons transmit messages through synapses in the dorsal column nuclei, where second-order neurons send the signal to the thalamus and synapse with third-order neurons in the ventrobasal complex; the third-order neurons send the signal to the somatosensory cortex. More recent work has expanded the role of the cutaneous mechanoreceptors for feedback in fine motor control. Single action potentials from Meissner's corpuscle, Pacinian corpuscle and Ruffini ending afferents are directly linked to muscle activation, whereas Merkel cell-neurite complex activation does not trigger muscle activity.
In glabrous skin, there are four principal types of mechanoreceptors, each shaped according to its function. The tactile corpuscles respond to light touch, adapt to changes in texture; the bulbous corpuscles detect tension deep in the fascia. The Merkel nerve endings detect sustained pressure; the lamellar corpuscles in the skin and fascia detect rapid vibrations. Receptors in hair follicles sense. Indeed, the most sensitive mechanoreceptors in humans are the hair cells in the cochlea of the inner ear. Mechanosensory free nerve endings detect touch and stretching. Baroreceptors are a type of mechanoreceptor sensory neuron, excited by stretch of the blood vessel. Cutaneous mechanoreceptors respond to mechanical stimuli that result from physical interaction, including pressure and vibration, they are located like other cutaneous receptors. They are all innervated by Aβ fibers, except the mechanorecepting free nerve endings, which are innervated by Aδ fibers. Cutaneous mechanoreceptors can be categorized by morphology, by what kind of sensation they perceive, by the rate of adaptation.
Furthermore, each has a different receptive field. The Slowly Adapting type 1 mechanoreceptor, with the Merkel corpuscle end-organ, underlies the perception of form and roughness on the skin, they produce sustained responses to static stimulation. The Slowly Adapting type 2 mechanoreceptors, with the Ruffini corpuscle end-organ, respond to skin stretch, but have not been linked to either proprioceptive or mechanoreceptive roles in perception, they produce sustained responses to static stimulation, but have large receptive fields. The Rapidly Adapting or Meissner corpuscle end-organ mechanoreceptor underlies the perception of flutter and slip on the skin, they have small receptive fields and produce transient responses to the onset and offset of stimulation. The Pacinian corpuscle or Vater-Pacinian corpuscles or Lamellar corpuscles underlie the perception of high frequency vibration, they produce transient responses, but have large receptive fields. Cutaneous mechanoreceptors can be separated into categories based on their rates of adaptation.
When a mechanoreceptor receives a stimulus, it begins to fire impulses or action potentials at an elevated frequency. The cell, will soon "adapt" to a constant or static stimulus, the pulses will subside to a normal rate. Receptors that adapt are referred to as "phasic"; those receptors that are slow to return to their normal firing rate are called tonic. Phasic mechanoreceptors are useful in sensing such things as texture or vibrations, whereas tonic receptors are useful for temperature and proprioception among others. Adapting: Slowly adapting mechanoreceptors include Merkel and Ruffini corpuscle end-organs, some free nerve endings. Adapting type I mechanoreceptors have multiple Merkel corpuscle end-organs. Adapting type II mechanoreceptors have single Ruffini corpuscle end-organs. Intermediate adapting: Some free nerve endings are intermediate adapting. Adapting: Rapidly adapting mechanoreceptors include Meissner corpuscle end-organs, Pacinian corpuscle end-organs, hair follicle receptors and some free nerve endings.
Adapting type I mechanoreceptors have multiple Meissner corpuscle end-organs. Adapting type II mechanoreceptors have single Pacinian corpuscle end-organs. Cutaneous mechanoreceptors with small, accurate receptive fields are found in areas needing accurate taction. In the fingertips and lips, innervation density of adapting type I and adapting type I mechanoreceptors are increased; these two types of mechanoreceptors have small discrete receptive fields and are thought to underlie most low-threshold use of the fingers in assessing texture, surface slip, flutter. Mechanoreceptors found in areas of the body with less tactile acuity tend to have larger receptive fields. Other mechanoreceptors than cutaneous ones include the hair cells, which are sensory receptors in the vestibular system of the inn