{"id":4507,"date":"2018-10-07T01:34:13","date_gmt":"2018-10-07T05:34:13","guid":{"rendered":"https:\/\/www.amyork.ca\/academic\/zz\/?p=4507"},"modified":"2018-10-07T01:44:47","modified_gmt":"2018-10-07T05:44:47","slug":"other-sensory-systems","status":"publish","type":"post","link":"https:\/\/www.amyork.ca\/academic\/zz\/biological-basis-of-behaviour\/other-sensory-systems\/","title":{"rendered":"Other Sensory Systems"},"content":{"rendered":"<h2>Audition<\/h2>\n<h3>Sound and the Ear<\/h3>\n<p>Physics and Psychology of Sound<\/p>\n<ul>\n<li>Amplitude \uf0e0 a sound wave-s intensity (lightning bolts)<\/li>\n<li>Loudness \uf0e0 sensation related to amplitude but not identical to it (rapidly talking person sounds louder than slow music of same physical amplitude)<\/li>\n<li>Frequency \uf0e0 number of compressions per second (measured in Hz)<\/li>\n<li>Pitch \uf0e0 related aspect of perception; higher frequency sounds are higher in pitch<\/li>\n<li>Height of each way corresponds to amplitude and then number of waves per second corresponds to frequency<\/li>\n<li>Most adults hear sounds ranging from ~15Hz \u2013 ~20,000HZ; children hear high frequencies than adults because ability to perceive high frequencies decreases with age and exposure to loud noises<\/li>\n<\/ul>\n<p>Structures of the Ear<\/p>\n<ul>\n<li>Functioning of the ear is complex enough to resemble <u>Rube Goldberg-s<\/u> device<\/li>\n<li>The Outer Ear, Middle Ear, and Inner Ear<\/li>\n<\/ul>\n<p><strong>o <\/strong>Pinna \uf0e0 structure of flesh and cartilage attached to each side of the head; by altering reflections of sound waves, it helps us locate source of a sound (every person has a different shape) <strong>o\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong>After sound waves pass through auditory canal, they strike tympanic membrane (eardrum; vibrates at the same frequency as the sound waves that strike it) in the middle ear<\/p>\n<ul>\n<li>Connects 3 tiny bones that transmit vibrations to the oval window (membrane of the inner ear); 3 bones are hammer (malleus), anvil (incus), and stirrup (stapes)<\/li>\n<li>Tympanic membrane ~20 times larger than footplate of stirrup, which connects to oval window<\/li>\n<li>Vibrations of tympanic membrane transform into more forceful vibrations of the smaller stirrup<\/li>\n<li>Net effort converts sound waves into waves greater pressure on small oval window<\/li>\n<li>Transformation is important because more force is required to move viscous fluid behind oval window than to move the eardrum (has air on both sides)<\/li>\n<\/ul>\n<p><strong>o\u00a0\u00a0\u00a0 <\/strong>Inner ear contains snail-shaped structure called cochlea<\/p>\n<ul>\n<li>Cross section through cochlea shows 3 long fluid-filled tunnels (scala vestibuli, scala media, and scala timpani)<\/li>\n<li>Stirrup makes oval window vibrate at entrance to scala vestibuli \uf0e0 setting in motion the fluid in the cochlea<\/li>\n<li>Hair cells \uf0e0 auditory receptors lie between basilar membrane of cochlea on one side and the tectorial membrane on the other (they are modified touch receptors)<\/li>\n<li>Vibrations in fluid of cochlea displace hair cells (thereby opening ion channels in its membrane)<\/li>\n<\/ul>\n<h3>Pitch Perception<\/h3>\n<p>Frequency and Place<\/p>\n<ul>\n<li>Place theory \uf0e0 basilar membrane resembles strings of a piano in that each area along membrane is tune to specific frequency; according to theory, each frequency activates hair cells at only one place along basilar membrane, and the NS distinguishes among frequencies based on which neurons respond<\/li>\n<li>Frequency theory \uf0e0 basilar membrane vibrates in synchrony with a sound, causing auditory nerve axons to produce action potentials at same frequency (ex; sound at 50Hx cause 50 AP-s\/second)<\/li>\n<li>For low-frequency sounds, basilar membrane vibrates in synchrony with sound waves in accordance with frequency theory, and auditory nerve axons generate one AP per wave; soft sounds activate fewer neurons, and stronger sounds activate more<\/li>\n<li>At low frequencies, frequency of impulses identifies pitch, and number of firing cells identifies loudness; high frequencies, neuron might fire on every 2<sup>nd<\/sup>, 3<sup>rd<\/sup>, 4<sup>th<\/sup>, or later wave (its AP-s are phase-locked to peaks of sound waves \uf0e0 occur at same phase in sound waves)<\/li>\n<li>Volley principle \uf0e0 pitch discrimination; auditory nerve as a whole produces volleys of impulses for sounds up to 4,000\/second (no axon approaches frequency)<\/li>\n<li>When we hear very high frequencies, we use mechanism similar to place theory<\/li>\n<li>Basilar membrane varies from stiff at base (where stirrup meets cochlea; oval window), to floppy at other end (apex); highest frequency sound vibrate hair cells near the base, and lower frequency sounds vibrate hair cells father along membrane<\/li>\n<li>Responses depend on psychical parameters of cochlea (stiffness, friction, and properties of hair cells)<\/li>\n<li>Amusia \uf0e0 ~4% people have this; impaired detection of frequency changes (\u201ctone-deafness\u201d); have trouble recognizing tunes, singingoff key, don-t detect \u201cwrong\u201d note in melody; most probably genetic basis <strong>o <\/strong>Associated with thicker than average auditory cortex in right hemisphere but fewer than average connections from auditory cortex to frontal cortex<\/li>\n<\/ul>\n<h3>Auditory Cortex<\/h3>\n<ul>\n<li>As information from auditory system passes through subcortical areas, axons cross over in midbrain to enable each hemisphere of forebrain to get most of its input from opposite ear<\/li>\n<li>Primary auditory cortex (area A1) \uf0e0 in the superior temporal cortex; important for auditory imagery (becomes active when someone watches short silent videos that suggest sound)<\/li>\n<li>Resembles visual cortex \uf0e0 \u201cwhat\u201d pathway sensitive to patterns of sound in anterior temporal cortex; \u201cwhere\u201d pathway sensitive to sound location in posterior temporal cortex and parietal cortex<\/li>\n<li>Superior temporal cortex includes areas important for detecting visual motion and motion of sounds \uf0e0 patients with damage to area become motion deaf (hear sounds, but don-t detect that a source of sound is moving)<\/li>\n<li>People who are deaf from birth, axons leading from auditory cortex develop less than in other people<\/li>\n<li>Visual and auditory systems differ in this respect: whereas damage to area V1 leaves someone blind, damage to area A1 doesn-t produce deafness; people with damage to A1 hear simple sounds, unless damage extends into subcortical brain areas (main deficit is inability to recognize combinations\/sequences of sounds) \uf0e0 cortex is not necessary for all hearing, only for advanced processing of it<\/li>\n<li>Tonotopic map \uf0e0 auditory cortex provides kind of map of sounds<\/li>\n<li>Most cells respond to complex sound (dominant tone and several harmonics)<\/li>\n<li>Just as visual system starts with cells that respond to simple lines and progresses to cells that detect faces and other complex stimuli, same is true for auditory system<\/li>\n<li>Cells outside area A1 respond best to auditory \u201cobjects\u201d (animal cries, machinery noises, music, and other meaningful sounds)<\/li>\n<\/ul>\n<h3>Hearing Loss<\/h3>\n<ul>\n<li>Conductive deafness (middle-ear deafness)\n<ul>\n<li>Diseases, infections, or tumorous bone growth can prevent middle ear from transmitting sound waves properly to cochlea <strong>o <\/strong>People with this impairment have normal cochlea and auditory nerve, therefore able to hear their own voices through bones of the skull directly to cochlea, bypassing the middle ear<\/li>\n<\/ul>\n<\/li>\n<li>Nerve deafness (inner-ear deafness)\n<ul>\n<li>Damage to cochlea, hair cells, or auditory nerve; can occur in any degree and may be confined to one part of cochlea<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>(someone hears certain frequencies and not others) <strong>o\u00a0\u00a0\u00a0\u00a0 <\/strong>Can be inherited, or can develop from disorders <strong>o\u00a0\u00a0\u00a0\u00a0 <\/strong>Exposure to loud sounds produces long-term damage to synapses and neurons of auditory system (lead to ringing of ears, sensitivity to noise, or other problems <strong>o <\/strong>Nerve deafness produces tinnitus \uf0e0 frequent\/constant ringing in ears (due to phenomenon like phantom limb); if brain no longer gets normal input, axons representing other parts of body may invade brain area previously responsive to sounds (especially high-frequency sounds)<\/p>\n<h3>Sound Localization<\/h3>\n<ul>\n<li>Sound localization less accurate than visual localization<\/li>\n<li>One cue for location is difference in intensity between ears; high-frequency sounds, the head creates sound shadow (making sound louder for closer ear)<\/li>\n<li>Second cue is difference in time of arrival of two ears (most useful for localizing sounds with sudden onset)<\/li>\n<li>Third cue is phase difference between ears (each sound wave has phases with 2 consecutive peaks 360<sup>o<\/sup> apart)<\/li>\n<li>Humans localize low frequencies by phase differences and high frequencies by loudness differences; localize sound of any frequency (speech sounds) by its time of onset if it occurs suddenly enough<\/li>\n<\/ul>\n<h2>The Mechanical Senses<\/h2>\n<h3>Vestibular Sensation<\/h3>\n<ul>\n<li>Sensations from vestibular organ detect direction of tilt and the amount of acceleration of the head; critical for guiding eye movements and maintaining balance<\/li>\n<li>Vestibular organ consists of saccule, utricle, and 3 semicircular canals; vestibular receptors are modified touch receptors<\/li>\n<li>3 semicircular canals \uf0e0 oriented in perpendicular planes; filled with jellylike substance and lined with hair cells<\/li>\n<li>AP-s initiated by cells of vestibular system travel through part of 8<sup>th<\/sup> cranial nerve to the brainstem and cerebellum (8<sup>th<\/sup> cranial nerve contains both auditory component and vestibule component)<\/li>\n<\/ul>\n<h3>Somatosensation<\/h3>\n<ul>\n<li>Somatosensory system \uf0e0 sensation of body and its movements; it-s not one sense but many, including discriminative touch (identifies shape of an object), deep pressure, cold, warmth, pain, itch, tickle, and position\/movement of joints<\/li>\n<\/ul>\n<p>Somatosensory Receptors<\/p>\n<ul>\n<li>Touch receptor may be a simple bare neuron ending (many pain receptors), modified dendrite (Merkel disks \uf0e0 respond to light touch), an elaborated neuron ending (Ruffini endings and Meissner-s corpuscles), or a bare ending surrounded by other cells that modify its function (Pacinian corpuscles)<\/li>\n<li>Stimulation of a touch receptor opens sodium channels in the axon \uf0e0 starting AP<\/li>\n<li>Pacinian corpuscle \uf0e0 detects sudden displacements or high-frequency vibrations on the skin<\/li>\n<li>Inside the outer structure is neuron membrane; outer structure provides mechanical support that resists gradual\/constant pressure \uf0e0 insulates the neuron against most touch stimuli; if a sudden or vibrating stimulus bends the membrane, enabling sodium ions to enter, depolarizing the membrane<\/li>\n<li>Heat receptors responds to capsaicin (chemical that makes jalapenos hot)<\/li>\n<\/ul>\n<p>Input to the Central Nervous System<\/p>\n<ul>\n<li>Information from touch receptors in head enters CNS through cranial nerves; information from receptors below the head centers spinal cord and passes toward the brain through the 31 spinal nerves <strong>o <\/strong>Includes 8 cervical nerves, 12 thoracic nerves, 5 lumbar nerves, 5 sacral nerves, and 1 coccygeal nerve<\/li>\n<li>Each spinal nerve innervates to a limited area of the body called dermatome; each overlaps one third to one half of next dermatome<\/li>\n<li>The insular cortex (secondary somatosensory cortex) responds to light touch as well as variety of other pleasant emotional experiences<\/li>\n<li>Various areas of somatosensory thalamus send impulses to different areas of primary somatosensory cortex (located in parietal lobe)<\/li>\n<li>Various aspects of body sensation remain at least partly separate all the way to the cortex (the somatosensory cortex acts as a map of body location)<\/li>\n<li>The activity corresponds to what you experience, not what has actually stimulated your receptors<\/li>\n<li>Damage to somatosensory cortex impairs body perceptions (trouble putting clothes on correctly)<\/li>\n<\/ul>\n<h3>Pain<\/h3>\n<ul>\n<li>Prefrontal cortex (important for attention) responds only briefly to any new light, sound, or touch; with pain it continues responding as long as pain lasts<\/li>\n<\/ul>\n<p>Pain Stimuli and Pain Paths<\/p>\n<ul>\n<li>Pain sensation begins with bare nerve ending (acid, heat, or cold)<\/li>\n<li>Axons carrying pain information have little or no myelin and therefore conduct impulses relatively slowly; thicker and faster axons convey sharp pain; thinner ones convey duller pain (postsurgical pain) <strong>o <\/strong>Pain messages reach brain more slowly than other sensations, but the brain processes pain information rapidly; motor response to pain are faster than motor response to touch stimuli <strong>o\u00a0 <\/strong>Pain axons release 2 neurotransmitters in the spinal cord\n<ol>\n<li>Mild pain releases glutamate<\/li>\n<li>Stronger pain releases both glutamate and substance P (without substance P, mice don-t detect increased intensity)<\/li>\n<\/ol>\n<\/li>\n<li>Pain-sensitive cells in spinal cord relay information to several sites in the brain; one path extends to the ventral posterior nucleus of the thalamus and from there to the somatosensory cortex (responds to painful stimuli, memories of pain, and signals that warn of impending pain)<\/li>\n<li>Pain pathway crosses immediately from receptors on one side of the body to a tract ascending the contralateral side of the spinal cord<\/li>\n<li>Touch information travels up ipsilateral side of the spinal cord to medulla, where it crosses to the contralateral side<\/li>\n<li>Pain and touch reach neighboring sites in the cerebral cortex<\/li>\n<li>Painful stimuli activate path that goes through reticular formation of medulla and then to several of central nuclei of thalamus, amygdala, hippocampus, prefrontal cortex, and cingulate cortex \uf0e0 areas react to emotional associations<\/li>\n<li>\u201cSympathetic pain\u201d shows up mainly as activity in cingulate cortex<\/li>\n<li>People with damage to cingulate gyrus still feel pain, but no longer distresses them Ways of Relieving Pain<\/li>\n<li>Opioids and Endorphins<\/li>\n<li>Opioid mechanisms \uf0e0 systems that respond to opiate drugs &amp; similar chemicals; brain puts stop on prolonged pain<\/li>\n<li><u>Pert <\/u>and <u>Snyder<\/u> discovered opiates bind to receptors found mostly in spinal cord and periaqueductal gray area of the midbrain<\/li>\n<\/ul>\n<p>(researchers found that opiate receptors act by blocking release of substance P)<\/p>\n<ul>\n<li>Endorphins \uf0e0 attach to same receptors as morphine; a contraction of endogenous morphines; relieves different types of pain, released during sex, music<\/li>\n<li>Gate Theory \uf0e0<u>Melzack<\/u> and <u>Wall<\/u>; spinal cord neurons that receive messages from pain receptors also receive input from touch receptors and from axons descending from the brain (other inputs can close \u201cgates\u201d for pain messages)<\/li>\n<li>Why some people withstand pain better and why same injury hurts worse at some times than others<\/li>\n<li>Nonpain stimuli modify the intensity of pain (concentrate on something else when in pain)<\/li>\n<li>Larger diameter axons (unaffected by morphine), carry sharp pain; thinner axons convey dull postsurgical pain, and morphine inhibits them<\/li>\n<li>Placebos<\/li>\n<li>Placebo \uf0e0 drug or other procedure with no pharmacological effects (experimental groups receives potentially active treatment; control group receives placebo); often relieve pain<\/li>\n<li>Placebo decreases response in cingulate cortex but not somatosensory cortex<\/li>\n<li>Relieve pain partly by increasing release of opiates and partly by increasing release of dopamine<\/li>\n<li>Antiplacebos (nocebos) worsen pain by increasing anxiety (suggestions that pain will increase)<\/li>\n<li>Cannabinoids and Capsaicin<\/li>\n<li>Cannabinoids (related to marijuana) also block certain kinds of pain\n<ul>\n<li>Act mainly in periphery of the body rather than CNs like opiates<\/li>\n<\/ul>\n<\/li>\n<li>Capsaicin produces painful burning sensation by releasing substance P \uf0e0 release substance P faster than neurons resynthesizing it, leaving cells less able to send pain messages <strong>o <\/strong>High doses damage pain receptors<\/li>\n<\/ul>\n<p>Sensitization of Pain<\/p>\n<ul>\n<li>Damaged\/inflamed tissues releases histamine, nerve growth factor, and other chemicals that help repair damage but also magnify responses of nearby heat and pain receptors (anti-inflammatory drugs relieve pain by reducing release of chemicals from damaged tissues)<\/li>\n<li>Barrage of painful stimuli potentiates cells responsive to pain so that they respond more vigorously to similar stimulation in future\n<ul>\n<li>Painful stimuli also release chemicals that decrease release of GABA (inhibitory transmitter) from nearby neurons; brain learns how to feel pain, and gets better at it<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>Social Pain<\/p>\n<ul>\n<li>When someone is left out there is increased activity in the cingulate cortex, which responds to emotional aspect of pain; can relieve pain with Tylenol<\/li>\n<\/ul>\n<h3>Itch<\/h3>\n<ul>\n<li>Researchers identified special receptors for itch and special spinal cord paths conveying itch<\/li>\n<li>2 types: (1) mild tissue damage \uf0e0 skin releases histamines that dilate blood vessels, produce itching, need anti histamines; (2) contact with plants produce itch, rub capsaicin on it to help<\/li>\n<li>Spinal cord pathway conveys itch sensation; some axons respond to histamine itch, others to plants; these pathways also respond to heat<\/li>\n<li>Itch axons activate certain neurons in spinal cord that produce gastrin-releasing peptide \uf0e0 blocking the peptide decreases scratching<\/li>\n<li>Itch pathways respond slow; axons transmit impulses at slow velocity<\/li>\n<li>Itch directs you to scratch area and remove what-s irritating skin; can cause mild pain \uf0e0 relieves itch; opiates decrease pain \uf0e0 increase itch<\/li>\n<li>Inhibitory relationship between pain and itch is evidence that itch is not type of pain<\/li>\n<\/ul>\n<h2>THE CHEMICAL SENSES<\/h2>\n<h3>Chemical Coding<\/h3>\n<ul>\n<li>Labeled-line principle \uf0e0 each receptor would respond to limited range of stimuli, and the meaning would depend entirely on which neurons are active<\/li>\n<li>Across-fiber pattern principle \uf0e0 each receptor responds to wider range of stimuli, and a given response by a given axon means little except in comparison to what other axons are doing<\/li>\n<li>Nearly all perceptions depend on the patter across an array of axons<\/li>\n<\/ul>\n<h3>Taste<\/h3>\n<ul>\n<li>Taste and smell axons converge onto many of the same cells in an area called the endopiriform cortex<\/li>\n<\/ul>\n<p>Taste Receptors<\/p>\n<ul>\n<li>Receptors for taste not true neurons but modified skin cells (lasts ~10-14 days)<\/li>\n<li>Mammalian taste receptors are in taste buds located in papillae (surface of the tongue)<\/li>\n<\/ul>\n<p>How Many Kinds of Taste Receptors<\/p>\n<ul>\n<li>Adaptation \uf0e0 reflects fatigue of receptors sensitive to sour tastes<\/li>\n<li>Cross-adaptation \uf0e0 reduced response to one taste after exposure to another<\/li>\n<li>For other senses, the number of AP-s is what matters; in taste, the temporal pattern is more important<\/li>\n<li>One way to identify taste receptor types is to find procedures that alter one receptor but not others<\/li>\n<\/ul>\n<p>Mechanisms of Taste Receptors<\/p>\n<ul>\n<li>Neuron produces an AP when sodium ions cross its membrane<\/li>\n<li>Saltiness receptor detects Na, just allows Na ions on the tongue to cross the membrane.<\/li>\n<li>Sour receptors detect acids<\/li>\n<li>Sweet, bitter, umami receptors resemble metabotropic synapses<\/li>\n<\/ul>\n<p><strong>o <\/strong>After molecule binds to one receptor, activate G-protein that releases 2<sup>nd<\/sup> messenger within cell <strong>o\u00a0\u00a0\u00a0\u00a0 <\/strong>Each receptor detects 1 type of taste, several receptors feed into next set of cells in taste system <strong>o\u00a0\u00a0 <\/strong>Each neuron responds to 2+ kinds of taste (depends on a pattern of responses across fiber)<\/p>\n<ul>\n<li>Bitter substances vary except that they are a bit toxic (25+ bitterness receptors) \uf0e0 detect many dangerous chemicals (but can-t detect low quantities of it)<\/li>\n<\/ul>\n<p>Taste Coding in the Brain<\/p>\n<ul>\n<li>Information from receptors in the anterior two thirds of the tongue travels to the brain along the chorda tympani (branch of 7<sup>th<\/sup> cranial nerve \uf0e0 facial nerve)<\/li>\n<li>Taste information from posterior tongue and throat travels along branches of 9<sup>th<\/sup> and 10<sup>th<\/sup> cranial nerve<\/li>\n<li>Nucleus of the tractus solitaries (NTS) \uf0e0 structure in medulla; taste nerves project to it<\/li>\n<li>From NTS, information branches out, reaching the pons, lateral hypothalamus, amygdala, ventral-posterior thalamus, and two areas of cerebral cortex <strong>o <\/strong>One of these areas, somatosensory cortex, responds to touch aspects of tongue stimulation <strong>o <\/strong>Other areas (insula) is primary taste cortex <strong>o\u00a0 <\/strong>Each hemisphere receives input mostly from ipsilateral side of tongue <strong>o\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong>One connection from insula goes to small portion of frontal cortex (maintains memories of recent taste experiences)<\/li>\n<\/ul>\n<p>Individual Differences in Taste<\/p>\n<ul>\n<li>Supertasters \uf0e0 have highest sensitivity to all tastes and mouth sensations; have strong food preferences (avoid strong-tasting\/spicy foods)<\/li>\n<li>Difference between tasters and supertasters depends on number of fungiform papillae near tip of the tongue (supertasters have largest number)<\/li>\n<li>Anatomical difference depends partly on genetics but also on age, hormones, and other influences<\/li>\n<\/ul>\n<h3>Olfaction<\/h3>\n<ul>\n<li>Olfaction \uf0e0 sense of smell; response to chemicals that contact membranes inside the nose<\/li>\n<li>Plays a role in social behaviour (smells of other people and rating desirability)<\/li>\n<\/ul>\n<p>Olfactory Receptors<\/p>\n<ul>\n<li>Olfactory cells \uf0e0 neurons responsible for smell; line the olfactory epithelium in the rear of the nasal air passages (in mammals, each cell has cilia that extend from cell body into mucous surface of nasal passage) <strong>o <\/strong>Olfactory receptors located on the cilia<\/li>\n<li>Each of these proteins traverses the cell membrane seven times and responds to a chemical outside the cells by triggering changes in<\/li>\n<\/ul>\n<p>G-protein inside the cell<\/p>\n<ul>\n<li>G-protein provokes chemical activities that lead to AP<\/li>\n<li>Given chemical produces major response in one or two kinds of receptors and weak responses in a few others<\/li>\n<\/ul>\n<p>Implications for Coding<\/p>\n<ul>\n<li>3 kinds of cones and 5 kinds of taste receptors<\/li>\n<li>olfaction processes airborne chemicals that don-t range along a single continuum<\/li>\n<\/ul>\n<p>Messages to the Brain<\/p>\n<ul>\n<li>When an olfactory receptor is stimulated \uf0e0 axon carries impulse to olfactory bulb<\/li>\n<li>Cells of olfactory bulb code identity of smells<\/li>\n<li>Olfactory bulb sends axons to olfactory area of cerebral cortex<\/li>\n<li>Olfactory receptors vulnerable to damage because they are exposed to the air (have survival times over a month)<\/li>\n<\/ul>\n<p><strong>o\u00a0\u00a0\u00a0 <\/strong>A that point, stem cell matures into new olfactory cell in same location as the first and expressed same receptor protein \uf0e0 axon then has to find its way to correct target in bulb<\/p>\n<ul>\n<li>Each olfactory neuron axon contains copies of olfactory receptor protein; if entire olfactory surface is damaged at once by blast of toxic fumes so it has to replace all receptors at same time, many fail to make same connections and olfactory experience doesn-t fully recover<\/li>\n<\/ul>\n<p>Individual Differences<\/p>\n<ul>\n<li>Smell detection depends on female hormones<\/li>\n<li>Deleting a particular gene that controls a channel through which most potassium passes in the membranes of certain neurons of the olfactory bulb (can enhance smell in mice)<\/li>\n<\/ul>\n<h3>Pheromones<\/h3>\n<ul>\n<li>Vomeronasal organ (VNO) \uf0e0 set of receptors located near (but separate from) the olfactory receptors\n<ul>\n<li>Specialized to respond only to pheromones (chemicals released by an animal that affect the behavior of other members of same species)<\/li>\n<\/ul>\n<\/li>\n<li>Each receptor responds to one pheromone; olfactory receptors respond to new odor but not to a continuing one (continue responding strongly even after prolonged stimulation)<\/li>\n<li>In humans, VNO is tiny and has no receptors (it is vestigial)\n<ul>\n<li>Part of human olfactory mucosa contains receptors that resemble other species- pheromone receptors<\/li>\n<\/ul>\n<\/li>\n<li>Behavioural aspects occur unconsciously (alters skin temperature and other autonomic responses and increases activity in the hypothalamus) <strong>o <\/strong>Smell of woman-s sweat (after ovulation) increases man-s testosterone secretions; smell of male sweat causes women to increase release of cortisol (stress hormone; not charmed by sweaty man)<\/li>\n<li>Human body secretions probably do act as pheromones (although effects more subtle than in most other mammals)<\/li>\n<\/ul>\n<h3>Synaesthesia<\/h3>\n<ul>\n<li>Synaesthesia \uf0e0 combination of more than one sense; experience some people have in which stimulation of one sense evokes perception of that sense and another one also (ex: one person sees each letter as having a color)<\/li>\n<li>People reporting synaesthesia have increased amounts of gray matter in certain brain areas and altered connections to other areas<\/li>\n<li>Genetic predisposition causes synaesthesia (people aren-t certainly born with letter-to-color or number-to-color synaesthesia)<\/li>\n<li>When people misperceive stimulus (as an illusion), the synesthetic experience corresponds to what the person thought the stimulus was, not was it actually was <strong>o <\/strong>Result implies phenomenon occurs in cerebral cortex (not in receptors or first connections to the NS)<\/li>\n<li>One hypothesis: some axons from one cortical area branch into another cortical area<\/li>\n<\/ul>\n","protected":false},"excerpt":{"rendered":"<p>Audition Sound and the Ear Physics and Psychology of Sound Amplitude \uf0e0 a sound wave-s intensity (lightning bolts) Loudness \uf0e0 sensation related to amplitude but not identical to it&hellip; <a class=\"continue\" href=\"https:\/\/www.amyork.ca\/academic\/zz\/biological-basis-of-behaviour\/other-sensory-systems\/\">Continue Reading<span> Other Sensory Systems<\/span><\/a><\/p>\n","protected":false},"author":4,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[114],"tags":[],"_links":{"self":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts\/4507"}],"collection":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/comments?post=4507"}],"version-history":[{"count":0,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/posts\/4507\/revisions"}],"wp:attachment":[{"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/media?parent=4507"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/categories?post=4507"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.amyork.ca\/academic\/zz\/wp-json\/wp\/v2\/tags?post=4507"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}