The habenular commissure, is a brain commissure situated in front of the pineal gland that connects the habenular nuclei on both sides of the diencephalon. The habenular commissure is part of the habenular trigone; the trigonum habenulæ contains groups of nerve cells termed the ganglion habenulæ. Fibers enter the trigonum habenulæ from the stalk of the pineal gland, the habenular commissure. Most of the trigonum habenulæ's fibers are, directed downward and form a bundle, the fasciculus retroflexus of Meynert, which passes medial to the red nucleus, after decussating with the corresponding fasciculus of the opposite side, ends in the interpeduncular nucleus. NIF Search - Habenular commissure via the Neuroscience Information Framework
Tobacco smoking is the practice of smoking tobacco and inhaling tobacco smoke. The practice is believed to have begun as early as 5000 -- 3000 BC in South America. Tobacco was introduced to Eurasia in the late 17th century by European colonists, where it followed common trade routes; the practice encountered criticism from its first import into the Western world onwards but embedded itself in certain strata of a number of societies before becoming widespread upon the introduction of automated cigarette-rolling apparatus. German scientists identified a link between smoking and lung cancer in the late 1920s, leading to the first anti-smoking campaign in modern history, albeit one truncated by the collapse of Nazi Germany at the end of World War II. In 1950, British researchers demonstrated a clear relationship between cancer. Evidence continued to mount in the 1980s. Rates of consumption declined. However, they continue to climb in the developing world. Smoking is the most common method of consuming tobacco, tobacco is the most common substance smoked.
The agricultural product is mixed with additives and combusted. The resulting smoke is inhaled and the active substances absorbed through the alveoli in the lungs or the oral mucosa. Combustion was traditionally enhanced by addition of potassium or nitrates. Many substances in cigarette smoke trigger chemical reactions in nerve endings, which heighten heart rate and reaction time, among other things. Dopamine and endorphins are released, which are associated with pleasure; as of 2008 to 2010, tobacco is used by about 49% of men and 11% of women aged 15 or older in fourteen low-income and middle-income countries, with about 80% of this usage in the form of smoking. The gender gap tends to be less pronounced in lower age groups. Many smokers begin during early adulthood. During the early stages, a combination of perceived pleasure acting as positive reinforcement and desire to respond to social peer pressure may offset the unpleasant symptoms of initial use, which include nausea and coughing. After an individual has smoked for some years, the avoidance of withdrawal symptoms and negative reinforcement become the key motivations to continue.
A study of first smoking experiences of seventh-grade students found out that the most common factor leading students to smoke is cigarette advertisements. Smoking by parents and friends encourages students to smoke. Smoking's history dates back to as early as 5000–3000 BC, when the agricultural product began to be cultivated in Mesoamerica and South America; the practice worked its way into shamanistic rituals. Many ancient civilizations – such as the Babylonians, the Indians, the Chinese – burnt incense during religious rituals. Smoking in the Americas had its origins in the incense-burning ceremonies of shamans but was adopted for pleasure or as a social tool; the smoking of tobacco and various hallucinogenic drugs was used to achieve trances and to come into contact with the spirit world. To stimulate respiration, tobacco smoke enemas were used. Eastern North American tribes would carry large amounts of tobacco in pouches as a accepted trade item and would smoke it in ceremonial pipes, either in sacred ceremonies or to seal bargains.
Adults as well as children enjoyed the practice. It was believed that tobacco was a gift from the Creator and that the exhaled tobacco smoke was capable of carrying one's thoughts and prayers to heaven. Apart from smoking, tobacco had a number of uses as medicine; as a pain killer it was used for earache and toothache and as a poultice. Smoking was said by the desert Indians to be a cure for colds if the tobacco was mixed with the leaves of the small Desert sage, Salvia dorrii, or the root of Indian balsam or cough root, Leptotaenia multifida, the addition of, thought to be good for asthma and tuberculosis. In 1612, six years after the settlement of Jamestown, John Rolfe was credited as the first settler to raise tobacco as a cash crop; the demand grew as tobacco, referred to as "brown gold", revived the Virginia joint stock company from its failed gold expeditions. In order to meet demands from the Old World, tobacco was grown in succession depleting the soil; this became a motivator to settle west into the unknown continent, an expansion of tobacco production.
Indentured servitude became the primary labor force up until Bacon's Rebellion, from which the focus turned to slavery. This trend abated following the American Revolution as slavery became regarded as unprofitable. However, the practice was revived in 1794 with the invention of the cotton gin. Frenchman Jean Nicot introduced tobacco to France in 1560, tobacco spread to England; the first report of a smoking Englishman is of a sailor in Bristol in 1556, seen "emitting smoke from his nostrils". Like tea and opium, tobacco was just one of many intoxicants, used as a form of medicine. Tobacco was introduced around 1600 by French merchants in what today is modern-day Gambia and Senegal. At the same time, caravans from Morocco brought tobacco to the
Nicotinic acetylcholine receptor
Nicotinic acetylcholine receptors, or nAChRs, are receptor polypeptides that respond to the neurotransmitter acetylcholine. Nicotinic receptors respond to drugs, including the nicotinic receptor agonist nicotine, they are found in the central and peripheral nervous system and many other tissues of many organisms, including humans. At the neuromuscular junction they are the primary receptor in muscle for motor nerve-muscle communication that controls muscle contraction. In the peripheral nervous system: they transmit outgoing signals from the presynaptic to the postsynaptic cells within the sympathetic and parasympathetic nervous system, they are the receptors found on skeletal muscle that receive acetylcholine released to signal for muscular contraction. In the immune system, nAChRs regulate inflammatory processes and signal through distinct intracellular pathways. In insects, the cholinergic system is limited to the central nervous system; the nicotinic receptors are considered cholinergic receptors.
Nicotinic receptors get their name from nicotine, which does not stimulate the muscarinic acetylcholine receptor, but instead selectively binds to the nicotinic receptor. The muscarinic acetylcholine receptor gets its name from a chemical that selectively attaches to that receptor — muscarine. Acetylcholine itself binds to both nicotinic acetylcholine receptors; as ionotropic receptors, nAChRs are directly linked to ion channels. New evidence suggests that these receptors can use second messengers in some cases. Nicotinic acetylcholine receptors are the best-studied of the ionotropic receptors. Since nicotinic receptors help transmit outgoing signals for the sympathetic and parasympathetic systems, nicotinic receptor antagonists such as hexamethonium interfere with the transmission of these signals. Thus, for example, nicotinic receptor antagonists interfere with the baroreflex that corrects changes in blood pressure by sympathetic and parasympathetic stimulation of the heart. Nicotinic receptors, with a molecular mass of 290 kDa, are made up of five subunits, arranged symmetrically around a central pore.
Each subunit comprises four transmembrane domains with both the N- and C-terminus located extracellularly. They possess similarities with GABAA receptors, glycine receptors, the type 3 serotonin receptors, or the signature Cys-loop proteins. In vertebrates, nicotinic receptors are broadly classified into two subtypes based on their primary sites of expression: muscle-type nicotinic receptors and neuronal-type nicotinic receptors. In the muscle-type receptors, found at the neuromuscular junction, receptors are either the embryonic form, composed of α1, β1, γ, δ subunits in a 2:1:1:1 ratio, or the adult form composed of α1, β1, δ, ε subunits in a 2:1:1:1 ratio; the neuronal subtypes are various homomeric or heteromeric combinations of twelve different nicotinic receptor subunits: α2−α10 and β2−β4. Examples of the neuronal subtypes include: 32, 23, 23, α4α6β32, 5, many others. In both muscle-type and neuronal-type receptors, the subunits are similar to one another in the hydrophobic regions. A number of electron microscopy and x-ray crystallography studies have provided high resolution structural information for muscle and neuronal nAChRs and their binding domains.
As with all ligand-gated ion channels, opening of the nAChR channel pore requires the binding of a chemical messenger. Several different terms are used to refer to the molecules that bind receptors, such as ligand, agonist, or transmitter; as well as the endogenous agonist acetylcholine, agonists of the nAChR include nicotine and choline. Nicotinic antagonists that block the receptor include mecamylamine, dihydro-β-erythroidine, hexamethonium. In muscle-type nAChRs, the acetylcholine binding sites are located at the α and either ε or δ subunits interface. In neuronal nAChRs, the binding site is located at the interface of an α and a β subunit or between two α subunits in the case of α7 receptors; the binding site is located in the extracellular domain near the N terminus. When an agonist binds to the site, all present subunits undergo a conformational change and the channel is opened and a pore with a diameter of about 0.65 nm opens. Nicotinic AChRs may exist in different interconvertible conformational states.
Binding of an agonist stabilises the desensitised states. In normal physiological conditions, the receptor needs two molecules of ACh to open. Opening of the channel allows positively charged ions to move across it; the net flow of positively charged ions is inward. The nAChR is a non-selective cation channel, meaning that several different positively charged ions can cross through, it is permeable to Na+ and K+, with some subunit combinations that are permeable to Ca2+. The amount of sodium and potassium the channels allow through their pores varies from 50–110 pS, with the conductance depending on the specific subunit composition as well as the permeant ion. Many neuronal nAChRs can affect the release of other neurotransmitters; the channel opens and tends to remain open until the agonist diffuses away, which takes about 1 millisecond. However, AChRs can spontaneously open with no ligands bound or can spontaneously close with ligands bound, mutations in the channel can shift the likelihood of either event.
Therefore, ACh binding changes the probability of pore opening. The nAChR is unable to bind ACh. The
The nucleus accumbens known as the accumbens nucleus, or as the nucleus accumbens septi is a region in the basal forebrain rostral to the preoptic area of the hypothalamus. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum; the ventral striatum and dorsal striatum collectively form the striatum, the main component of the basal ganglia. The dopaminergic neurons of the mesolimbic pathway project onto the GABAergic medium spiny neurons of the nucleus accumbens and olfactory tubercle; each cerebral hemisphere has its own nucleus accumbens, which can be divided into two structures: the nucleus accumbens core and the nucleus accumbens shell. These substructures have different morphology and functions. Different NAcc subregions and neuron subpopulations within each region are responsible for different cognitive functions; as a whole, the nucleus accumbens has a significant role in the cognitive processing of motivation, aversion and reinforcement learning. In addition, part of the nucleus accumbens core is centrally involved in the induction of slow-wave sleep.
The nucleus accumbens plays a lesser role in processing fear and the placebo effect. It is involved in the encoding of new motor programs as well; the nucleus accumbens is an aggregate of neurons, described as having an outer shell and an inner core. Major glutamatergic inputs to the nucleus accumbens include the prefrontal cortex, basolateral amygdala, ventral hippocampus, thalamic nuclei, glutamatergic projections from the ventral tegmental area; the nucleus accumbens receives dopaminergic inputs from the ventral tegmental area, which connect via the mesolimbic pathway. The nucleus accumbens is described as one part of a cortico-basal ganglia-thalamo-cortical loop. Dopaminergic inputs from the VTA modulate the activity of GABAergic neurons within the nucleus accumbens; these neurons are activated directly or indirectly by euphoriant drugs and by participating in rewarding experiences. Another major source of input comes from the CA1 and ventral subiculum of the hippocampus to the dorsomedial area of the nucleus accumbens.
Slight depolarizations of cells in the nucleus accumbens correlates with positivity of the neurons of the hippocampus, making them more excitable. The correlated cells of these excited states of the medium spiny neurons in the nucleus accumbens are shared between the subiculum and CA1; the subiculum neurons are found to hyperpolarize while the CA1 neurons "ripple" in order to accomplish this priming. The nucleus accumbens is one of the few regions that receive histaminergic projections from the tuberomammillary nucleus; the output neurons of the nucleus accumbens send axonal projections to the basal ganglia and the ventral analog of the globus pallidus, known as the ventral pallidum. The VP, in turn, projects to the medial dorsal nucleus of the dorsal thalamus, which projects to the prefrontal cortex as well as the striatum. Other efferents from the nucleus accumbens include connections with the tail of the ventral tegmental area, substantia nigra, the reticular formation of the pons; the nucleus accumbens shell is a substructure of the nucleus accumbens.
The shell and core together form the entire nucleus accumbens. Location: The shell is the outer region of the nucleus accumbens, – unlike the core – is considered to be part of the extended amygdala, located at its rostral pole. Cell types: Neurons in the nucleus accumbens are medium spiny neurons containing D1-type or D2-type dopamine receptors. A subpopulation of MSNs contain both D1-type and D2-type receptors, with 40% of striatal MSNs expressing both DRD1 and DRD2 mRNA; these mixed-type NAcc MSNs with both D1-type and D2-type receptors are confined to the NAcc shell. The neurons in the shell, as compared to the core, have a lower density of dendritic spines, less terminal segments, less branch segments than those in the core; the shell neurons project to the subcommissural part of the ventral pallidum as well as the ventral tegmental area and to extensive areas in the hypothalamus and extended amygdala. Function: The shell of the nucleus accumbens is involved in the cognitive processing of reward, including subjective "liking" reactions to certain pleasurable stimuli, motivational salience, positive reinforcement.
That NAcc shell has been shown to mediate specific Pavlovian-instrumental transfer, a phenomenon in which a classically conditioned stimulus modifies operant behavior. A "hedonic hotspot" or pleasure center, responsible for the pleasurable or "liking" component of some intrinsic rewards is located in a small compartment within the medial NAcc shell; the D1-type medium spiny neurons in the Nacc shell mediate reward-related cognitive processes, whereas the D2-type medium spiny neurons in the NAcc shell mediate aversion-related cognition. Addictive drugs have a larger effect on dopamine release in the shell than in the core; the nucleus accumbens core is the inner substructure of the nucleus accumbens. Location: The nucleus accumbens core is part of the ventral striatum, located within the basal ganglia. Cel
Neurotransmitters are endogenous chemicals that enable neurotransmission. It is a type of chemical messenger which transmits signals across a chemical synapse, such as a neuromuscular junction, from one neuron to another "target" neuron, muscle cell, or gland cell. Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, where they are received by neurotransmitter receptors on the target cells. Many neurotransmitters are synthesized from simple and plentiful precursors such as amino acids, which are available from the diet and only require a small number of biosynthetic steps for conversion. Neurotransmitters play a major role in shaping everyday life and functions, their exact numbers are unknown, but more than 200 chemical messengers have been uniquely identified. Neurotransmitters are stored in synaptic vesicles, clustered close to the cell membrane at the axon terminal of the presynaptic neuron. Neurotransmitters are released into and diffuse across the synaptic cleft, where they bind to specific receptors on the membrane of the postsynaptic neuron.
Most neurotransmitters are about the size of a single amino acid. A released neurotransmitter is available in the synaptic cleft for a short time before it is metabolized by enzymes, pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor. Short-term exposure of the receptor to a neurotransmitter is sufficient for causing a postsynaptic response by way of synaptic transmission. In response to a threshold action potential or graded electrical potential, a neurotransmitter is released at the presynaptic terminal. Low level "baseline" release occurs without electrical stimulation; the released neurotransmitter may move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an inhibitory or excitatory way; this neuron may be connected to many more neurons, if the total of excitatory influences are greater than those of inhibitory influences, the neuron will "fire".
It will create a new action potential at its axon hillock to release neurotransmitters and pass on the information to yet another neighboring neuron. Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations by Ramón y Cajal, a 20 to 40 nm gap between neurons, known today as the synaptic cleft, was discovered; the presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, in 1921 German pharmacologist Otto Loewi confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is credited with discovering acetylcholine —the first known neurotransmitter.
Some neurons do, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another. There are four main criteria for identifying neurotransmitters: The chemical must be synthesized in the neuron or otherwise be present in it; when the neuron is active, the chemical must produce a response in some target. The same response must be obtained. A mechanism must exist for removing the chemical from its site of activation. However, given advances in pharmacology and chemical neuroanatomy, the term "neurotransmitter" can be applied to chemicals that: Carry messages between neurons via influence on the postsynaptic membrane. Have little or no effect on membrane voltage, but have a common carrying function such as changing the structure of the synapse. Communicate by sending reverse-direction messages that affect the release or reuptake of transmitters; the anatomical localization of neurotransmitters is determined using immunocytochemical techniques, which identify the location of either the transmitter substances themselves, or of the enzymes that are involved in their synthesis.
Immunocytochemical techniques have revealed that many transmitters the neuropeptides, are co-localized, that is, one neuron may release more than one transmitter from its synaptic terminal. Various techniques and experiments such as staining and collecting can be used to identify neurotransmitters throughout the central nervous system. There are many different ways. Dividing them into amino acids and monoamines is sufficient for some classification purposes. Major neurotransmitters: Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid, glycine Gasotransmitters: nitric oxide, carbon monoxide, hydrogen sulfide Monoamines: dopamine, epinephrine, serotonin Trace amines: phenethylamine, N-methylphenethylamine, tyramine, 3-iodothyronamine, tryptamine, etc. Peptides: oxytocin, substance P, cocaine and amphetamine regulated transcript, opioid peptides Purines: adenosine triphosphate, adenosine Catecholamines: dopamine, epinephrine Others: acetylcholine, etc. In addition, over 50 neuroactive pepti
International Standard Serial Number
An International Standard Serial Number is an eight-digit serial number used to uniquely identify a serial publication, such as a magazine. The ISSN is helpful in distinguishing between serials with the same title. ISSN are used in ordering, interlibrary loans, other practices in connection with serial literature; the ISSN system was first drafted as an International Organization for Standardization international standard in 1971 and published as ISO 3297 in 1975. ISO subcommittee TC 46/SC 9 is responsible for maintaining the standard; when a serial with the same content is published in more than one media type, a different ISSN is assigned to each media type. For example, many serials are published both in electronic media; the ISSN system refers to these types as electronic ISSN, respectively. Conversely, as defined in ISO 3297:2007, every serial in the ISSN system is assigned a linking ISSN the same as the ISSN assigned to the serial in its first published medium, which links together all ISSNs assigned to the serial in every medium.
The format of the ISSN is an eight digit code, divided by a hyphen into two four-digit numbers. As an integer number, it can be represented by the first seven digits; the last code digit, which may be 0-9 or an X, is a check digit. Formally, the general form of the ISSN code can be expressed as follows: NNNN-NNNC where N is in the set, a digit character, C is in; the ISSN of the journal Hearing Research, for example, is 0378-5955, where the final 5 is the check digit, C=5. To calculate the check digit, the following algorithm may be used: Calculate the sum of the first seven digits of the ISSN multiplied by its position in the number, counting from the right—that is, 8, 7, 6, 5, 4, 3, 2, respectively: 0 ⋅ 8 + 3 ⋅ 7 + 7 ⋅ 6 + 8 ⋅ 5 + 5 ⋅ 4 + 9 ⋅ 3 + 5 ⋅ 2 = 0 + 21 + 42 + 40 + 20 + 27 + 10 = 160 The modulus 11 of this sum is calculated. For calculations, an upper case X in the check digit position indicates a check digit of 10. To confirm the check digit, calculate the sum of all eight digits of the ISSN multiplied by its position in the number, counting from the right.
The modulus 11 of the sum must be 0. There is an online ISSN checker. ISSN codes are assigned by a network of ISSN National Centres located at national libraries and coordinated by the ISSN International Centre based in Paris; the International Centre is an intergovernmental organization created in 1974 through an agreement between UNESCO and the French government. The International Centre maintains a database of all ISSNs assigned worldwide, the ISDS Register otherwise known as the ISSN Register. At the end of 2016, the ISSN Register contained records for 1,943,572 items. ISSN and ISBN codes are similar in concept. An ISBN might be assigned for particular issues of a serial, in addition to the ISSN code for the serial as a whole. An ISSN, unlike the ISBN code, is an anonymous identifier associated with a serial title, containing no information as to the publisher or its location. For this reason a new ISSN is assigned to a serial each time it undergoes a major title change. Since the ISSN applies to an entire serial a new identifier, the Serial Item and Contribution Identifier, was built on top of it to allow references to specific volumes, articles, or other identifiable components.
Separate ISSNs are needed for serials in different media. Thus, the print and electronic media versions of a serial need separate ISSNs. A CD-ROM version and a web version of a serial require different ISSNs since two different media are involved. However, the same ISSN can be used for different file formats of the same online serial; this "media-oriented identification" of serials made sense in the 1970s. In the 1990s and onward, with personal computers, better screens, the Web, it makes sense to consider only content, independent of media; this "content-oriented identification" of serials was a repressed demand during a decade, but no ISSN update or initiative occurred. A natural extension for ISSN, the unique-identification of the articles in the serials, was the main demand application. An alternative serials' contents model arrived with the indecs Content Model and its application, the digital object identifier, as ISSN-independent initiative, consolidated in the 2000s. Only in 2007, ISSN-L was defined in the
Reins are items of horse tack, used to direct a horse or other animal used for riding. They are long straps that can be made of leather, metal, or other materials, attach to a bridle via either its bit or its noseband. Reins are used to give subtle commands or cues known as rein aids. Various commands may ask for a slower speed, request a halt or rein back. Rein aids are used along with leg aids, shifting of body weight, sometimes voice commands. On some types of harnesses there might be supporting rings or "terrets" used to carry the reins over the animal's back; when pairs of equines are used in drawing a wagon or coach it is usual for the outer side of each pair to be connected to the reins and for the inside of the bits to be connected between the pair of horses by a short bridging strap or rope. The driver carries "four-in-hand" or "six-in-hand" being the number of reins connecting to the pairs. A single rein or rope may be attached to a halter to guide a horse or packhorse. A long rein called a longe line may be used to allow the horse to move in a circle for training purposes, or for the purpose of a clinical lameness evaluation by a veterinarian.
On certain designs of headgear, a third rein may be added to the paired reins, used for leading, longeing, or other specialized or stylistic purposes. The best-known example of a third rein used in the USA is the leading rein of the mecate of the classic bosal hackamore. Types of reins include: Closed reins, or loop reins: reins that are either a single piece or that buckle together at the ends. English riders use closed reins. Western riders in timed rodeo events use a single closed rein. A closed rein helps prevent the rider from dropping the reins. Double reins: The combined use of two pairs of reins, a curb rein and a snaffle rein; this is two single reins, though sometimes split reins may be seen on western-style bridles. Double reins are used with a double bridle, with bits such as the Pelham bit and, less on some gag bits used for polo. Draw reins and running reins: long reins made of leather or nylon webbing, that attach to the saddle or the girth, run through the bit rings, back to the rider.
Several design variations, they add mechanical advantage to the rider's hands and may the horse's ability to raise its head. Used in conjunction with a snaffle rein by English riders used alone by western riders. Lead rein: A third rein used on bridles, not to be confused with the single lead rope of a halter nor the direct rein aid known as the "leading rein". In North America a third rein is most seen as part of the mecate of a hackamore. In Mongolia it is integral to the bridle, tied to either a bit ring or a chin strap. Long reins, longlines, or driving lines: exceptionally long reins which allow the rider to control the horse from a cart, or from the ground, with the handler walking behind the horse. Mecate: a style of rein seen on a bosal style hackamore made of a single piece of rope that encompasses both a closed rein and a leading rope. Romal reins: a rein style from the vaquero tradition that incorporates a closed rein with a long quirt at the end. Side reins: used when longeing a horse, attached from the bit to the saddle or surcingle, they are not meant to be held by the rider.
Split reins: a rein style seen in western riding where the reins are not attached to one another at the ends. They prevent a horse from tangling its feet in a looped rein when the rider is dismounted, they are longer than closed reins. Two reins—reins used on bridles with two reins: Snaffle rein: Usually a laced rein that buckles at the center, used on the bradoon of a double bridle, or the upper ring of a pelham bit. Curb rein: The rein used at the end of the shank of a curb bit or pelham. Modern curb reins buckle together at the ends, though reins of the classical curb were sewn together at the ends to create a single rein. In popular culture, to rein in means to hold back, slow down, control or limit. Sometimes the eggcorn, reign in, is used. Usage of the opposing free rein dates back to Geoffrey Chaucer and means to give or allow complete freedom, in action and decision, over something. Horse tack Neck rein Riding aids Study of rein tension on side reins, The Veterinary Journal, Volume 188, Issue 3, June 2011, Pages 291–294 Equine and Comparative Exercise Physiology, August 2005 Rein Check, June 2011