Physiology of analyzer systems
1. Optic system of eyeball. Cornea allows light to enter the eyeball. nAqueous humor fills anterior and posterior chambers in front of lens. nCrystalline lens is a transparent elastic and biconcave lens, which refracts light nand focuses it on retina. Vitreous body is a transparent gel enclosed by nvitreous membrane, which fills eyeball behind lens.
2. Aqueous humor circulation. Ciliary processes in posterior chamber nsecrete aqueous fluid. It flows between the ligament of the lens and thethrough the pupil into the anterior chamber of the eye. Then fluid passes into nthe angle between the cornea and the iris. Through the meshwork of trabeculli naqueous humor enters the channel of Slemm, which empties into extraoccular veins. nFunctions of aqueous humor: 1) maintains intraoccular pressure; 2) maintains nshape of eyeball; 3) acts as refractory medium; 4) supplies nutrition; 5) ndrains metabolic end products.
3. Physical refraction and reduced eye. Refraction is bending of light nrays at surface between two media. Ratio of velocity of light in air to that ia medium is called refractive index of that medium. If all refractive surfaces nof the eye are added together and considered to be one single lens and shape of neyeball is perfectly spherical, eye may be simplified. This is model, which nshows refraction in eyeball – “reduced eye”. In this model total refractive npower is 59 diopters, when lens is accommodated for distant vision. It is nconsidered that single lens exists at 17 mm in front of retina. As a result in the nretina is formed image, which is inverted, true and reversed with respect to nthe object.
4. Clinical refraction. All variants of refraction, which are observed nin patients we call clinical refraction. These are emmetropia, hypermetropia nand myopia. Emmetropia is normal and ideal condition of eye, when parallel nlight rays from distant object are focused on the retina with ciliary muscle ncompletely relaxed. Such a condition is observed in perfectly spherical neyeball. In hypermetropia parallel light rays are focused behind retina because nof shortening anatomical axis of eyeball. It Concave lenses should correct it. nIn myopia parallel light rays are focused before retina because of long nanatomical axis of eyeball. Convex lenses should correct it.
5. Aberrations and astigmatism. In spherical aberration light rays pass nthrough peripheral parts of the eye lens and are not focused sharply. This is nbecause of more refractive power in central part of lens. Due to this effect nobject loose clear contour. Unequal deviation of light rays of different nwavelengths causes in this condition chromatic aberration. This is focusing of ndifferent colors at different distances behind lens. Due to this object get nrainbow contour. Diffractive aberration occur in case of small duck interfere nto light rays in clear mediums of eyeball (for instance foreign body). So point nobject looks like rounded by gray and white circles. Astigmatism is an errors nof refraction in which light rays do not all come to a common focal point. nOblong shape of cornea or lens causes it. nSo, cylindrical lenses may correct this defect of refraction.
6. Accommodation and its regulation. Accommodation is adjustment of eye nlens for various distances. Relaxation of ciliary muscle cause decrease of nrefractive power of eye lens and provides clear vision for long distance. nDecrease of parasympathetic influence to ciliary muscle controls it. In case of nparasympathetic stimulation of ciliary muscle, it contracts, lens ligament nrelax, lens get more spherical, refractive power increases and eye can see nclear near objects.
7. Defensive mechanisms in eye. Fibrous tunic of eyeball is composed by navascular connective tissue, which gives shape to eyeball and protect nstructures inside eyeball. Functional defensive mechanisms are presented by ncornea reflexes. Irritation of cornea receptors gives impulses to nparasympathetic center in medulla oblongata (Edinger-Westfal nucleus) and thain hypothalamus, which permits tears secretion. Limbic system also controls ntear secretion. Blinking reflex is controlled by n. trigeminus and n. facialis, nwhich innervate m. orbicularis oculi.
8. Pupillary reflexes. When light pass into eye, pupil contracts. Idarkness pupil dilates. This is pupillary light reflex, which helps to nadaptation to light conditions. Reflex arc: light receptors – optic nerve- noptic tract – pretectal area – Edinger-Westfal nucleus – parasympathetic fibers nof n. oculomotorius (from n. trigeminus) – n. ciliaris – m. sphincter pupillae n- decrease of pupillary diameter.
Consensual pupillary light reflex: reaction of eye pupil to light nirritation of opposite eye. It is possible due to diverging of nerve fibers nfrom one pretectal nucleus to both Edinger-Westfal nuclei.
9. Age peculiarities in eye structure. In old age lens of eye loose nelasticity. So this condition, when lens become non-accommodating, called npressbiopia. It should be corrected by bifocal glasses with upper segment nfocused for far-seeing and lower segment focusing for near-seeing. Iewboranatomical axis of eyeball is shorter, comparing to adults.
10. Development of refraction. Iewborn eye is hypermetropic. Eyeball ngrows with age, and normally gets spherical at maturation period. This process nis called emetropisation. Grate visual load in childhood and maturation period nlead to increase of intraoccular pressure. It may result in increase of nanatomical axis of eyeball and myopia.
11. Compositioof retina. Layers of retina from outside to inside: pigmented layer; layer of nrods and cones; outer limiting membrane; outer nuclear layer; outer plexiform nlayer; inner nuclear layer; inner plexiform layer; ganglionic layer; layer of noptic nerve fibers; inner limiting membrane.
12. nPhysiological peculiarities of pigmented layer and photoreceptors. Light falls non retina on inner side i.e. on inner limiting membrane. It is a minute area of n1 mm2 in center of retina. It provides acute and detail vision. nCentral portion of macula called fovea centralis. This is composed entirely of ncones. Pigmented layer of retina contains black pigment, i.e. melanin. It nprevents light reflection through the globe of eyeball and stores vitamin A.
13. Photochemical reactions in retina. Outer segment of photoreceptors ncontain photochemicals. Inner segment contains nucleus, synaptic body and other norganelles. Photochemicals are light-sensitive chemicals that decompose oexposure to light and excite nerve fibers leading from eye to central nervous nsystem. Rhodopsin is present in rods. Scotopsin and 11-cis-retinal compose it. nIodopsin is photochemical pigment of cones. Photopsin and 11-cis-retinal ncompose it. Rhodopsin cycle: rhodopsin under the influence of light converts to nprelumirhodopsin – lumirhodopsin – metaphodopsin I – metaphodopsin II – opsin – nrhodopsin. Metarhodopsin II converts also to all-transretinal (vitamin A) – n(isomerase’s action) – II cis-retinal – rhodopsin.
14. Central division of visual analyzer. Impulses from retina pass to optic nnerve – optic chiasm (fibers from nasal halves of retina cross to opposite nside) – optic tracts – synapse in lateral genicular body – geniculocalcarine nfibers – pass through optic radiation or geniculocalcarine tract – primary nvisual cortex in calcarine fissure or medial aspect of occipital lobe.
15. Other connections of optic tract. In addition to nlateral genicular body, fibers from optic tract also pass to:
– suprachiasmatic nucleus of hypothalamus for controlling ncircadian rhythms;
– pretectal nuclei – for control of fixation of eyes on objects of nimportance and for pupillary light reflex;
– superior colliculus – for control of bilateral simultaneous movements of ntwo eyes;
– pulvinar – forms secondary visual pathway.
Corpus callosum causes exchange of visual information between right and nleft hemispheres.
16. Light and dark adaptation. If a person remains ibright light for a long time, photochamicals in rods and cones reduce to nall-transretinal and opsins. Most all-transretinal converts to all-transretinol n(vitamin A). So, sensitivity of eye to light gets decreased. This is light nadaptation. If a person remains in dark for a long time, all vitamin A convert nto 11-cis retinal and than to photochemicals. Sensitivity of eye to light gets nincreased. This is dark adaptation.
17. Theories of color perception. According to Jung-Helmgolc theory there nare three types of cones for three fundamental colors: cones for red color ncontain erythrolab; cones for green color contain chlorolab; cones for blue ncolor contain cyanolab. According to Gering theory there are couples of nopponent colors: green – red; yellow – blue; white – black. Subcortical neurons npercept it due to on- and off- centers mechanism.
18. Disorders of color perception. There are three fundamental colors: red, nwhich is marked “protos”; green – “dateros”; blue – “tritos”. So normal color nperception is called normal trichromasia. If a person has abnormal perceptioof some fundamental color, this is prot-, daiter- or tritanomalia. If a persopercept only some two fundamental colors, this is dichromasia. If a persodifferentiates only one fundamental color this is monochromasia. In case of nblack and white vision a person has color blindness.
19. Visual acuity. Ability of human eye to discriminate nbetween point sources of light is called visual acuity. Normally a person with nvision acuity 1,0 can differentiate two point objects, which lay under the nangle 1 minute from distance 5 m.
20. Field of vision is area that is seeing by an eye at a ngiven instant. It has nasal and temporal division. Determination of extent of nperipheral visual field and thereby diagnosis of blindness in specific portions nof retina, is called perimetry. Optic disc produces physiological scotoma in 15 ndegrees lateral to central point of vision in perimetry chart.
21. Binocular vision provides detection of distance and nthree-dimensional appearance of object in front of eyes. This is due to central nanalysis of fields of vision from both eyes. Final visual image is formed ivisual cortex.
1. Role of external ear. External ear consists of auricle and external nauditory meatus. Function of external ear is collection of sound waves. nExternal auditory meatus conducts sound waves from auricle to tympanic nmembrane. External ear also helps in protection of middle and internal ear. It nprovides constant temperature and humidity near tympanic membrane and nmechanical defense also.
2. Role of middle ear in sound perception. Middle ear occupies tympanic ncavity. Tympanic membrane forms lateral wall of tympanic cavity. Handle of nmalleus attaches to point of maximal concavity of tympanic membrane on its ninner surface. Other end of malleus is bound to incus by ligaments. Opposite nend of incus articulates with stem of stapes. Faceplate of stapes lies against nmembranous labyrinths in oval window, where sound waves are conducted into ncochlear. Auditory ossicles increase pressure exerted by sound waves on fluid nof cochlear. Thus provides impedance matching between sound waves in air and nsound vibrations in fluid of cochlear.
Tympanic cavity is filled with air. Besides auditory ossicles tympanic ncavity also contains tensor tympani muscle and stapedius muscle. There are two nwindows in medial wall of tympanic cavity, round window and oval window.
3. Attenuation reflex and adaptation to sound. It is a reflex that noccurs when loud sounds low frequency sounds are transmitted through ossicular nsystem into central nervous system. It occurs after latent period of 40-80 ms. Tensor tympani muscle pulls handle of malleus inwards. nStapedius muscle pulls stapes out of oval window. These two forces are opposite to each other. It causes nentire ossicular system to become highly rigid. This mechanism reduces nossicular conduction of loud or low frequency sounds. As a result intensity of nsound, which comes into inner ear reduces to 30-40 decibels.
5. Mechanism of conduction of sound waves. Sound waves strike tympanic nmembrane. Ossicular system conducts this sound. Faceplate of stapes moves ninward into scala media at oval window. So fluid moves inward ninto scala media. It causes vibration of basilar membrane. When basilar nmembrane bends upward to scala vestibuli, hair cells depolarize and generate naction potential to nerve fibers of cochlear nerve.
6. Endocochlear potential. An electrical potential of + 80 mV exists all nthe time between endolymph and perilymph. Perylimph is present in scala nvestibuli and scala tympani. Its composition identical to ncerebrospinal fluid. Endolymph is present in scala media. Stria vascularis of scala media secrets it. It contains K+ nin high concentration and Na+ in low concentration. Endocochlear potential nsensitizes the cell and thereby increases its ability to respond to light nmovement of hairs. This potential is positive inside scala media and negative noutside. Continual secretion of K+ ions into scala media supports it.
7. Central division of auditory analyzer. Hair cells are secondary sensitive cells, nwhich give receptor potential to neurons of spiral ganglion of Corti. Theimpulse puss to vestibulocochlear nerve – dorsal and ventral cochlear nuclei iupper medulla – trapezoid body – superior olivary nucleus – lateral lemniscus. nThen fibers divide into three parts, which go to:
– nucleus of lateral lemniscus;
– higher centers;
– inferior colliculi – medial geniculate nnucleus – auditory cortex through auditory radiation.
Auditory cortex lies in superior gyrus of temporal lobe and performs nfinal processing of auditory information.
8. Binaural hearing. Binaural hearing helps in determination of ndirection to sound origin. Binaural hearing provides detection of time-lag nbetween entry of sound into one ear and into opposite ear. Medial superior nolivary nucleus detects this information. Difference between intensities of nsound in two ears also is important for determination of direction to sound norigin. Lateral superior olivary nucleus detects it.
9. Age peculiarities of auditory analyzer. Aging process leads to nprogressive symmetrical perceptive hearing loss, which is called presbycusis. nOtosclerosis in aged persons also may occur. It is a condition, when spongy nbone formation in bony labyrinth causes immobility of joint of stapes, which nresult in conductive hearing loss.
10. Functions of nvestibular analyzer. It is analyzer system, which detects sensation concerned nwith equilibrium and determines normal orientation and body movement with nrespect to direction of gravity power or acceleratory forces. Information from nvestibular analyzer helps in proper autonomic and metabolic control of skeletal nmuscles, which support proper locomotion and body posture under the influence of nEarth Gravity power.
11. Peripheral ndivision of vestibular analyzer. It is located in bony tubes and chambers ipetrose portion of temporal bone. Membranous labyrinth is a system of soft ntissue tubes and chambers filling within bony labyrinth. There are three nsemicircular canals ant two chambers, i.e. utricle and sacule, which are filled nwith endolymph. Macula is sensory organ of utricle and saccule. It is covered nwith gelatinous layer. Cilia of hair cells lay there. Hair cells synapse with nsensory axons of vestibular nerve. Macula of utricle determines normal norientation of willi respect to direction of gravitational or acceleratory nforces. Macula of sacule detects certain tips of sounds and detects equilibrium nwhen head is not in vertical position. In the beginning or end of linear motioof the head or whole the body, otolith membrane moves because of its inertion. nSo, irritation of sensory hair cells occurs. Utricle detects horizontal ndirection of movement and sacule – vertical. There are CaCO3 crystals nembedded a gelatinous layer that covers macula. Ampula is enlargement at one nend of semicircular canal. It has a small crest on top of which is a gelatinous nmass known as cupula. Hair cells have two kinds of cilia – kinocilium and nstereocilia. Kinocilium is large cilium located at one end of hair cell. nStereocilia are small. When stereocilia are bent towards kinocilium, hair cell nis depolarized, i.e. stimulated. When stereocilia are bend away from nkinocilium, hair cell is hyperpolarized, i.e. inhibited. It occurs because nacceleratory force acts to flow of fluid in semicircular canals during circular nmotion of the head or whole the body. Hair cells are located along crista nampularis and protect their cilia in cupula. Hair cells are secondary sensor ncells, which synapse with neurons. Axons of these nerve cells compose nvestibular nerve.
12. Conductive nand central division of vestibular analyzer. Hair sensory cells give impuls to nvestibulocochlear nerve, vestibular nuclei and uvula and flocculonodular lobe. nSuperior and medial vestibular nuclei cause corrective movements of eyes and nappropriate movements of head and neck. Lateral vestibular nucleus controls nbody movements. Inferior vestibular nucleus sends signals to cerebellum and nreticular formation.
13. Vestibulosomatic nreactions. These are reactions of skeletal musculature as a result of nirritation of vestibular sensory organs. Vestibulosomatic reactions are npresented by distribution of muscle tone through the body, general motor nreactions or eyeball movements. Normally vestibulosomatic reactions provide nadequate control of body posture, position of the head and eyeball in orbita to nkeep proper field of vision when performing body movement. In case of assuasive nor unusual vestibular stimulation rapid uneven movements of both eyeballs noccur. This is nystagmus. If head is rotated to left, eyes move towards right nin order to prevent image from moving off fovea. When eyes have rotated as far nas they can, they are rapidly returned to center of socket. If rotation of head ncontinues, eyes move in direction opposite to head rotation.
14. nVestibulosensoric reactions. This is subjective sensation of dizziness and nillusions about body location in surroundings. In case of assuasive or unusual vestibular nstimulation diverging of impulses to limbic structures cause such a reaction. nIn adequate stimulation, participance of limbic system helps in control of nproper nutrition and metabolic rate in contracting muscles.
15. nVestibuloautonomic reactions. Diverging of impulses to autonomic subcortical nnuclei is necessary for proper distribution of blood supply and metabolic nactivity between visceral organs and contracting muscles. Inadequate nstimulation of vestibular receptors lead to improper autonomic stimulation, nwhich may result in changing of heart beat rate, arterial pressure, motoric of ndigestive tract so on.
16. Vestibular ntraining. Endurance to vestibular stimulation may be increased due to nvestibular exercises using active body movements, especially head and body nbending. This is active vestibular training. Using of special devices, which nmoves whole the body with dosed linear or angular acceleration is passive nvestibular training. Mixed vestibular training, which include both active body nmovements and outer acceleration are also used. Nevertheless importance of nhereditary specialties of vestibular reactivity is considerable.
17. Age npeculiarities of vestibular sensory system. Until the moment of birth human has nvestibular analyzer system developed well. All the conductive pathways are nmielinised. Vestibular reactivity has genetic basis and could not be changed nconsiderably through the life.
1. Physiological importance of pain. According to moderotion, pain is nsubjective perception of systemic processes, which include information about ntissue damage. Activation of pain receptors leads to starting different nprotective reflexes to avoid tissue damage. However, pain is unpleasant sense nand involve to pain reaction wide net of regulative and homeostatic systems of nhuman organism. The important specialty in reaction to pain in human is nparticipation of brain cortex and limbic system, which leads to severe nemotional experience and autonomic reactions.
Nociceptive reactions are accompanied by motion reactions of entire body ntowards avoidance the pain. In human organism such motion reactions for the nsome part presented by unconditioned reflexes with short reflector arc formed nby neurons of spinal cord and brain stem. But majority of that are behavioral nand emotional reactions, which based on conditional reflexes. That is why nreflector arc includes besides neurons of spinal cord and brain stem structures nof limbic-reticular complex and brain cortex. Also different changes in humaorganism followed by pain are observed: increase of muscle tone, accelerated nheartbeat, increase of blood pressure, intensification of sweating, dilatatioof pupils and elevation of glucose and cuprum level in plasma, activation of nhemostasis. It considered to cause the majority of both visceral and nbiochemical reactions by excitation of sympathetic nervous system, which is npresented by neurons of hypothalamus, hypophisis and cells in medullar nsubstance of adrenal glands. In fact tissue damage and pain triggers the stress nreaction – common reaction of an organism, which leads to stimulation all the nfunctions, especially motion and that is why blood circulation due to ncardiovascular system, metabolism, transport of gases due to activation of nbreathing. Stimulation of pituitary-adrenal axis increases secretion of nadrenocorticotropic hormone from the anterior pituitary, and thus there is nincreased secretion of glucocorticoides from the adrenal cortex. That is why nfunctions of organism activate to defend one. But long lasting stress reactiois rather dangerous for organism. Adrenalin in high concentration may produce ndecreasing of blood supply in visceral organs, which leads to metabolic ndisorders and disturbances of its function. Besides that nociceptive nerve nendings in damaged tissues produce a lot of nervous impulses, which spreading ninto central nervous system activates wide net of nervous cells. This nconsiderable excitation leads to disturbances iervous regulation of all nfunctions in human organism.
2. Ranks of pain. There are nseveral ranks of pain:
Subjective sensations in pain may be presented emotional experience as nterror, worry, visual hallucination, dizziness, which appears before of nfollowed the pain.
Reflected pain is caused by irritation of visceral organs. Such events as strong nconstriction of smooth muscles; disorders of blood supply; tension of vessels, nstomach, intestines result in pain in certain parts of body. It is determined nsensor neurons to connect through interneurons with autonomic and motor neurons nin spinal cord. In such a way, viscerosomatic autonomic reflexes are realized. nDue to mentioned intracellular contacts, human capable to locate nociceptive nsensation. These zones of human body where impulses from certain visceral norgans are reflected called as Zacharjin-Ged zones. For example, in stomach ndisorders a human fells pain around navel. Acute pain caused by blood supply ndisorders in heart muscle reflected to the left shoulder, left shoulder blade nand left epigastria.
3. Pain reception. Damage stimuli perception created by the brain from nelectrochemical nerve impulses delivered to it from sensory receptors. These nreceptors transfuse (or change) different influences of both internal processes nin organism and surrounding environment into the electric impulses.
3. Nociceptive structures in central nervous system. Afferent nociceptive impulses are collected into central nervous nsystem by two kinds of nervous fibers: quick a-delta myelinated nerve fibers nand C-fibers without myelin. The ascending fibers are included in spinothalamic ntract, which passes through the spinal cord and reach medulla oblongata. Here nthere are second order sensory neurons of spinomesencephalic tract. Fibers of nspinothalamic tract synapse with third-order neurons in the thalamus, which iturn project to the postcentral gyrus of the contralateral cerebral hemisphere. nInformation about the pain from head, face and mouth cavity ascend to central nnervous system by sensory fibers of cranial nerves, for instance facial, nglossopharyngeal, vagus and trigeminus nerves.
Central nociceptive neurons lay iucleus of thalamus, hypothalamus, nmidencephalon central gray substance, reticular formation and somatosensoric nfields of brain cortex.
The reticular formation is a complex network of nuclei and nerve fibers nwithin the medulla, pons, midbrain, thalamus, and hypothalamus that functions nas the reticular activating system. Because of its many interconnections, the nreticular activating system is activated in a nonspecific fashion by any nmodality of sensory information. Nerve fibers from the reticular activating nsystem, in turn, project diffusely to the cerebral cortex; this results inonspecific arousal of the cerebral cortex to incoming sensory information.
There are special “paiucleus” in thalamus, which situated iventroposterolateral parts. Only extreme stimulation their firing activity cacause.
The main role iociceptive sensation belong to brain cortex, where nrealizing of pain is form. Activation of hypothalamus and limbic system is nresponsible for all variety of emotional reactions to pain and autonomic nreflexes. Several brain regions whose activity is somehow changed by the nabsence of sensation from the amputated limb cause appearance of phantom paiphenomenon. It was at first described by a neurologist during a Civil War. A nveteran with amputated legs asked for someone to massage his cramped leg nmuscle. It is now know that this phenomenon is common in amputees, who may nexperience complete sensations from the missing limbs. They perceive the phantom nas been very real, especially with their eyes closed, and they sans it moving nin accordance with the way the limb would naturally move if it were real. These nsensations are sometimes useful; for example, in fitting processes into which nthe phantom has seemingly entered. However, pain in the phantom is experienced nby 70 % of amputees, and the pain can be serve and persistent.
One explanation for phantom limbs is that the nerves remaining in the stamp ncan grow into nodules called neuromas, which generate nerve impulses that are ntransmitted to the brain and interpreted as arising from the missing limb.
However, phantom limbs may occur in cases where the limb is not amputated, nbut the nerves that normally enter from the limb are severed in an accident. Or nit may occur in individuals with spinal cord injuries above the level of the nlimb, so that the sensations from the limb do not enter the brain. In these ncases, the phantom limb phenomenon requires a different explanation. Current ntheories propose that the source of the phantom may arise in several brairegions.
In clinical observation the “gates theory of pain” is mentioned. It is nobserved that pain can be relieved by another pain, touching the skin or nmassage accordingly area of body. Such phenomenon probably can be explained by nmechanism of lateral inhibition in gelatinous substance in spinal cord. Those nsensory neurons whose receptive fields are stimulated most strongly inhibit nsensory neurons that serve neighboring receptive fields. In physiological conditions nlateral inhibition similarly plays a prominent role in the ability of sensory nsystems and brain to discriminate the most important stimulus in variety of nexternal influences. Transmission of nnervous impulses takes place iociceptive system due to special chemicals nmediators and modulators of central nervous system: substance P, kinines, nkalidine, enterotoxine, histamine, serotonine, prostaglandin E6, neurotensin, nmetabolism products, ions K+, H+, inflammatory products and others. Such nchemicals appear in peripheral and central nociceptive structures, in skin, nglands and also in poison of bees, wasps and scorpions.
4. Anti-nociceptive system. To antinociceptive neuro-endocrine system nbelong nervous structures, which are concentrated, obviously, in brain stem. nHigh intensity of pain stimuli permits activation of these structures, which ncontaieurons capable to release endogenous opioids. To such structure nbelong, for instance, prefrontal cortex, hypothalamus, central gray substance, nmedial thalamic nuclei and limbic system.
The discovery in 1973 of opioid receptor proteins in the brain suggested nthat the effects of well-known opium and morphine might be due to the nstimulation of specific neuron pathways. The ability of opium and its analogues nto relieve pain (promote analgesia) has been known for centuries. Morphine, for nexample, has long been used for this purpose. nThis implied that opioids might resemble neurotransmitters produced by nthe brain.
It is well known, that anesthetics have effect to ion gates, namely GABA n(gamma-amino- buttery acid) and glycinic receptors, which cause increase of Clˉ nconduction.
Substance P is polypeptide, which is composed from 11 amino acids and nlocated in intestines, peripheral nerve endings and different parts of central nnervous system. Substance P is one from six known polypeptides, called as ntachykinins.
There are three tachicininic receptors; two of which binding to substance P nand neurocinin K are cloned. It is determined that both are combined with nG-proteins. Activation of substance P receptors cause phospholipase C nactivation and increase both of inozitolthreephosphate and diacylglycerol.
Substance P in large concentration is contained ierve endings of primary nafferent neurons of spinal cord and perhaps is transmitter in first synapses inociceptive passwais of dull pain. Besides that, this substance is revealed inegro-streatum system, where its concentration is in proportion to dopamine none. Substance P also is determined in hypothalamus, where it may take certaiplace ieurohumoral regulation. In injection, substance P causes blushness nand edema. Evidently, it is transmitter, producing ierve endings during naxon-rephlex. Substance P takes part in peristaltic of intestines. Recently it nascertained, that central active antagonist natural killer-I at experiment ianimals has not cause any changes in monoamine exchange in brain.
5. Role of opioid peptides. In brain and digestive tract are located receptors, nwhich bind to morphine. Investigation endogenous ligands of these receptors ngive ability to reveal two similar pentapeptides, called encephalines, which nbind to opioid receptors: met-encephalin and ley-encepfalin. Such chemicals are nknown as opioid peptides. Encephalines are containing ierve endings of ndigestive tract and many parts in brain. It function as neurotransmitters. nThese peptides are present in gelatinous substance. In injecting into braistem, opioid peptides manifestate analgetic effect. Encephalines also may slow ndown intestines peristaltic.
Opioid peptides are synthesized in composition of precursor, from which nsignal peptide is separated. Proencephalin firstly was revealed in adrenal ngland. It also is precursor of met-encephalin and ley-encephalin in brain. nProopimelanocortin is revealed in anterior hypophisis and brain. In contains nß-endorphin in composition of which at aminogroop-end met-encephalin is ncontaining. Precursor gives origin also for adrenocorticotropic hormon and melanocyte nstimulating hormon. There are special special encephalin and ß-endorphiproducing neuron systems. Hypophisis secretes into blood ß-endorphin. nAnother molecule-precursor is prodinorphin. Dinorphin 1-17 is located iduodenum; dinorphin1-18 – in posterior pytuitary and hypothalamus. Encephalines nare metabolised mainly by two peptidase: encephalinase A and encephalinase B.
