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Final

PSL300 Final Exam Review (Tweed, Wojtowicz).pdf

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Physiology
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PSL300H1
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Hae- Young Kee

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Kim PSL300 Final Exam Overview Introduction to CNS 1. Nervous System  CNS = brain (86 billion neurons) + spinal cord (1 billion) o protected by bone, meninges, and CSF ‒ meninges = dura mater + arachnoid membrane + pia mater ‒ subarachnoid space (SAS) contains cerebrospinal fluid (CSF)  CSF secreted by choroid plexus (specialized regions in walls of ventricles)  ependymal cells transport ions, vitamins, nutrients, water from blood  ventricles  CSF cushions brain (mechanical protection) & maintains a chemical env’t w/ ↓ pH, ↓ [K ], no blood cells, little protein  flows throughout SAS  is reabsorbed by arachnoid villi (finger-like projections of arachnoid membrane through dura, into venous sinus)  puts into venous blood  entire volume recycled 3 times per day  PNS = somatic NS + ANS o ANS includes enteric NS (100-600 million)  glia – as abundant as neurons o astrocytes help create BBB ‒ makes “foot processes” on capillary walls ‒ secrete PARACRINES that ↑ tight junction formation in endothelial cells ‒ ex. of implication of BBB: Parkinson’s disease – treated by L-DOPA b/c DA can’t cross BBB 2. CNS  fueled mainly w/ O + glucose 2 o brain gets 15% of body’s blood (despite being only 2.5% of body weight) o glucose transported by membrane transporters from plasma  interstitial fluid o 50% of body’s glucose consumption (but very efficient, doesn’t produce heat)  gray matter vs. white matter o gray matter in CNS = arranged in clusters or layers, nuclei (vs. ganglia in PNS) o white matter = myelinated axons running in bundles, tracts (vs. nerves in PNS)  tracing neural pathways in CNS o horseradish peroxidase (HRP) injected near axon terminals  brought back to soma thru endocytosis  reacts to yield fluorescent products  visualize neuron o genetically modify mice s.t. novel proteins which can be tagged by fluorescent antibodies are produced 3. Spinal Cord  arranged in 31 segments, each w/ a pair of SPINAL NERVES o dorsal root: incoming SENSORY signals o dorsal root ganglion o ventral root: outgoing signals from CNS  muscles, glands  Gray Matter o dorsal horn (sensory/afferent) = VISCERAL SENSORY NUCLEI + SOMATIC SENSORY N. o ventral horn (motor/efferent) = SOMATIC MOTOR N. + AUTONOMIC EFFERENT N.  White Matter o ascending tracts = afferent, descending tracts = efferent o propriospinal tracts convey info b/w diff levels of spinal cord, stay w/i spinal cord  spinal reflex o sensory input usually synapses on an interneuron before motor o e.g., knee-jerk reflex o brain has some influence o pull hands together  stretch reflex activated  knee-jerk reflex should be amplified 4. Brain  6 major divisions: o cerebrum has 2 hemispheres connected at CORPUS CALLOSUM (bundle of axons) ‒ GREY MATTER includes cortex + basal ganglia (help control movement) + limbic system Page 1 of 24 Kim ‒ there is cerebral lateralization (specialization of some f’ns on hemispheres)  right: touch, spatial visualization & analysis  left: writing, speech, language & math ‒ 4 lobes: frontal, temporal, parietal, occipital ‒ limbic system has cingulate gyrus & amygdala (emotion, memory, esp. fear), hippocampus (learning & memory) ‒ consists of sensory, motor, and association areas  ASS’N AREAS: sensory  perceptions, motor outputs (skeletal muscle, glands, viscera) o diencephalon = hypothalamus + thalamus + pituitary + pineal ‒ thalamus = “switchboard” that processes info going into and coming from cerebrum ‒ hypothalamus involved in behavioural drives, endocrine/autonomic homeostasis o midbrain controls eye movement ‒ aiming eye movements at visual targets (foveation)  CN IV originates here ‒ also a synapse point for aud. info o pons + medulla = brainstem ‒ CNs II – XII arise from brain stem (i.e., all but CNI olfactory) ‒ medulla contains tracts b/w cerebrum + spinal cord  somatosensory tract and corticospinal tract, 90% of fibres crossing midline at PYRAMIDS  involuntary f’ns: swallowing, vomiting, breathing, b.p. ‒ pons relays signals b/w cerebrum + cerebellum  coordinates breathing ‒ brainstem contains reticular formation = diffuse network of neurons that extends thru whole brainstem  sends many projections up into higher brain areas, and down into spinal cord  involved in AROUSAL + SLEEP, muscle tone, pain modulation o cerebellum processes sensory data & coordinates movement ‒ contains most of the neurons of brain  cranial nerves enter/leave CNS thru skull o mnemonic: “On Old Olympus’ Towering Top, A Fin And German Viewed Some Hops” ‒ I. Olfactory ‒ II. Optic ‒ III. Oculomotor – horizontal eye movement ‒ IV. Trochlear – vertical eye movement ‒ V. Trigeminal – facial sensation, chewing ‒ VI. Abducens – eye movement (REM, foveation) ‒ VII. Facial – taste; efferents for tears, saliva, facial exp. ‒ VIII. Auditory/vestibulocochlear – hearing, eq’m ‒ IX. Glossopharyngeal – afferents from mouth, blood vessels; efferents for swallowing, parotid ‒ X. Vagus – afferents & efferents for many organs, muscles, glands ‒ XI. Spinal accessory – motor to mouth, neck, shoulders ‒ XII. Hypoglossal – motor to tongue o plasticity: e.g., CN XII can be co-opted for VII (w/ surgical graft) 5. Diffuse Modulatory Systems  noradrenergic system (NE) originates from locus coeruleus in pons  cortex, thalamus + hypothalamus, olfactory bulb, cerebellum, midbrain, spinal cord o attention, arousal, sleep-wake cycles, learning, memory, anxiety, pain, mood  serotonergic system (5-HT) originates from raphe nuclei on brainstem midline  most of CNS o pain, locomotion, sleep-wake cycles, mood, emotional behaviours (e.g., aggression)  dopaminergic system (DA) originates from substantia nigra & ventral tegmentum in midbrain  cortex, limbic system o motor control, reward signals (e.g., addictive behaviours)  cholinergic system (ACh) originates from pons, midbrain, and base of cerebrum  cortex, hippocampus, thalamus o arousal, sleep-wake cycles, learning, memory, transmitting sensory data thru thalamus Introduction to the Senses 6. 5 special senses (vision, hearing, eq’m, taste, smell) + 4 somatic senses (touch, T, proprioception, nociception)  unconscious of other, visceral sense data such as b.p., plasma [glucose], pH, etc. 7. Receptors & Neurons  every sensory system begins w/ receptors (not proteins; 1 cell which receives sensory stimuli) o may or may not be neurons Page 2 of 24 Kim o transduces stimulus E into electrical signals (changes in MP) ‒ if a neuron, may fire AP; if not, may release NTs to excite the next neuron o has an adequate stimulus = FORM of E to which receptor is most sensitive (e.g., pressure waves for hair cells) ‒ but is usually responsive to other types of stimuli as well ‒ classifications  chemo-, mechano-, thermo-, photo-  simple neurons = neurons w/ FREE nerve endings o sense T, noxious stimuli o may or may not have myelination  complex neural receptors = endings are in connective-tissue capsules (e.g., Pacinian corpuscle sense TOUCH) o i.e., nerve endings are not free  most SPECIAL SENSE receptors are non-neuronal cells that release NTs onto sensory neurons (e.g., hair cell) 8. Transduction nd  stimulus  opens/closes ion channels directly or viamessenger o usually channel is opened (Na or other cations)  DEPOL + o sometimes, K leaves cells  HYPERPOL. o or can close channels, such as in vision: light  closes cation channels  hyperpol.  Receptor sensitivity o recepstr threshold: minimum amt. of stimulus that will activate a receptor (i.e., produce AP in neuronal receptor, or any 1 neuron in pathway) ‒ some can be very sensitive: a single photon or a single odorant molecule o perceptual threshold: minimum amt. of stimulus that will make you AWARE of sensation ‒ depends on attention 9. Sensory systems involve series of neurons st  1° (1 -order) sensory neurons  2°  etc.  at each stage, convergence may occur – integrates, but loses, info  sensory systems carry info about many aspects of stimulus o modality – what type of stimulus/form of E it is (e.g., light? sound? touch?) ‒ labeled lines used: individual pathways to diff areas of brain  i.e., activity is all the same (electrochemical transmission) but how to distinguish in perceptions? o coding 10. Coding Location  stimulus location represented in 2 diff ways: o (i) in AUDITORY system (odd one): uses diffs in loudness and timing of sound b/w 2 ears o (ii) in VISUAL & SOMATIC SENSORY SYSTEMS: localized based on receptive fields  Receptive Fields o convergence determines size of receptive field (RF) ‒ higher convergence  larger RF o two-point discrimination dependent on size of RFs for a given pair of stimuli ‒ note: only applies when talking about groups of cells  lateral inhibition in 2° cells o b/c 1° cells adjacent to stimulus can still be activated  lateral inhibition stops signal from going on further (i.e., to 3°) o inhibition done by the most active neuron o e.g., in vision 11. Coding Intensity and Duration  can represent stimulus INTENSITY in 2 diff ways: o # of neurons = population coding o rate of firing = frequency coding  duration simply coding by length of time that neurons are firing  tonic receptors keep firing as long as stimulus lasts o vs. phasic receptors, which ADAPT if stimulus is constant ‒ adaptation = decline in receptor’s firing rate + +  mechanism depends on type of receptor: K channels open, Na channels close, other biochemical pathways that alter receptor’s responsiveness ‒ resulting decline in PERCEPTION of stimulus = habituation ‒ 12. Higher Processing  most sensory pathways run via thalamus to cortex Page 3 of 24 Kim o except olfactory: goes thru olfactory bulb  cortex o eq’m pathways project mainly to CEREBELLUM  CNS infers what is happening in world from activity in sensory neurons o sensory info at any given moment is highly incomplete  CNS “fills in” the gaps based on past experience ‒ e.g., perceiving images 3-D objects when they’re actually 2-D images ‒ “pushing the plesiomorphic button” Somatic Senses 13. 4 somatic senses: touch, temperature, proprioception, nociception  proprioception = awareness of position of body parts relative to one another  nociception detects tissue damage or threat of it = pain or itch 14. Receptors  are ALL neurons; located in skin/viscera  near surface: o FREE ENDINGS sense temperature + noxious stimuli o Meissner’s corpuscles sense flutter, stroking o Merkel receptors sense steady pressure and texture  in deep layers: o FREE ENDINGS at hair roots sense hair movement o Pacinian corpuscles sense vibration o Ruffini corpuscles sense skin stretch  diff rates of ADAPTATION o Meissner’s & Pacinian – adapt RAPIDLY, b/c most important to sense changes o Ruffini & Merkel – adapt SLOWLY o variable among free nerve endings  thermoreceptors = free nerve endings o RFs ~1mm o COLD RECEPTORS sense temperatures below body temp.; WARM RECEPTORS 37-45°C; ‒ we have more cold than warm (maybe b/c our env’t is almost always colder than body?) o > 45°C  PAIN RECEPTORS activated o Adaptation ‒ when in range 20-40°C, adapt slowly  but outside of this range, don’t adapt at all b/c important to keep sending signal due to risk of tissue damage o use a family of cation channels: transient receptor potential (TRP) channels  nociceptors = free nerve endings o membrane channel receptors (protein) called vanilloid receptors respond to heat, capsaicin o another kind of membrane receptors respond to cold, menthol + o nociceptors can be affected by chemicals released from damaged cells (K , histamine, prostaglandins) and serotonin released by platelets  activate nociceptors OR sensitize (by ↓ receptor threshold) 15. Pathways & Processing  3 main classes of somatosensory nerve fibres: o (1) A-β – large, myelinated (FAST, 30-70 m/s) ‒ signal mechanical stimuli o (2) A-δ – small, myelinated (intermediate speed, 12-30 m/s) ‒ signal fast pain and cold o (3) C fibers – small, unmyelinated (SLOW, 0.5-2 m/s) ‒ signal slow pain, heat, cold, mechanical stimuli  somatosensory afferents cross the midline o 2° neuron axons do the crossing: ‒ coarse touch, nociception, temperature in SPINAL CORD ‒ fine touch, vibration, proprioception in MEDULLA o 3° cells in thalamus  SS cortex  topographical representation of SS cortex o close spatial organization, but distorted (e.g., fingers and lips get disproportionately large SS cortical areas dedicated) o sensory homunculus  Nociception Page 4 of 24 Kim o FAST PAIN (sharp, localized; A-δ fibers) vs. SLOW PAIN (dull, diffuse; C fibers) ‒ ITCH conveyed by subtype of C fibers o pain and itch mutually inhibit one another ‒ scratching  mild pain that relieves itch ‒ opioids  block pain, but may cause itchiness o nociceptive signals evoke responses in CNS ‒ trigger withdrawal reflex (= spinal) ‒ limbic system, hypothalamus: emotional distress, nausea, vomiting, sweating ‒ descending pathways thru thalamus can block nociceptive cells in spinal cord (e.g., to ignore pain) o pain can be modulated by the gate control mechanism ‒ C fiber  2° neuron  an INTERNEURON tonically suppresses signal C fiber  2° neuron signal ‒ when noxious stimulus activates receptor neuron  receptor (1°) neuron activates 2° neuron, and simultaneously inhibits interneuron (i.e., disinhibition) ‒ but, if we get non-noxious signals (e.g., touch thru A-β) in the same area, it can re-activate the interneuron, stopping disinhibition, and thus allowing inhibition to take place again  no/reduced pain perceived o pain can be felt in other organs besides skin: skeletal muscles = deep somatic pain (e.g., muscles “burning” during exercise) ‒ can also result from ischemia  ↓ [2 ] o referred pain – caused by convergence of nociceptors on a single ascending tract ‒ e.g., liver, gallbladder pain  right shoulder ‒ heart  left arm ‒ appendicitis  general abdominal area ‒ ureters (e.g., kidney stones)  testicles o ANALGESIC SUBSTANCES work by various mechanisms ‒ acetylsalicylic acid (aspirin) – inhibits prostaglandins (↓ inflammation), slows transmission of pain signals ‒ opioids (morphine, codeine) – block pain perception by ↓ NT release from 1° sensory neurons, and by inhibiting postsynaptic 2° sensory neurons ‒ body makes natural painkillers: endorphins, enkephalins, dynorphins Smell & Taste 16. chemoreception = evolutionarily old  may have evolved into chemical synaptic communication 17. Smell  receptors = 1° neurons  olfactory bulb’s 2° neurons  cortex, amygdala, hippocampus o descending modulatory pathways from cortex to bulb o 1° olfactory receptor neurons sit in olfactory epithelium (3 cm ) ‒ each has 1 dendrite + 1 axon ‒ have to go thru fenestrations in skull to reach olfactory bulb ‒ turnover time of 2 months  adult neurogenesis: stem cells in basal layer of epithelium continuously divide to produce new neurons  each new neuron’s axon must find its way up to olfactory bulb  odorant receptor proteins = G-protein coupled o largest gene family in vertebrates (1000 genes, 3-5% of genome) – humans express only 400 o odorant molecule binds receptor protein  olfctivated  ↑ [cAMP]  cAMP opens cation channels  depol./AP o each 1° neuron responds to 1 type of odorant molecule (i.e., expresses only 1 type of receptor protein) ‒ all cells w/ same receptor protein converge on a few 2° neurons in bulb ‒ brain combines info from hundreds of olfactory neurons to distinguish thousands of smells (combos of smells)  pheromones o rodents have vomeronasal organ (VNO) = accessory olfactory bulb ‒ involved in sexual behaviours o only vestigial traces of VNO in humans, if any; may be “human pheromones” – highly controversial 18. Taste  involves at least 5 sensations: sweet, sour, salty, bitter, umami + + o H = sour; Na = “salty”; sugars = “sweet”; thutamate = “umami”; toxins = “bitter” o may also have receptors for long-chain Fas (“6 dimension” of taste?) o taste receptors mainly on taste buds clustered on dorsal surface of tongue Page 5 of 24 Kim ‒ a taste bud has 50-150 taste cells, support cells, and regenerative basal cells  taste cells (receptors) = polarized epithelial cells ≠ neurons o Type 1 (support) cells: sense salty ‒ ION CHANNELS: Na enters T1 cells thru epithelial Na channel  depol. o Type II (receptor) cells: sense sweet, bitter, umami ‒ release ATP, which act on neurons and T3 cells ‒ exp. G PROTEIN-COUPLED RECEPTOR PROTEINS  sweet and umami: T1R receptors (T1R2/T1R3 for sweet; T1R1/T1R3 for umami)  bitter: ~30 diff T2R receptors  these receptors associated w/ G protein gustducin  signal transduction involving ↑ [Ca ], triggering release of ATP  ATP then acts on neurons and Type IIIs o Type III (presynaptic) cells: sense sour ‒ called presynaptic b/c the only type of taste cells that directly synapse on 1° gustatory neurons ‒ NT = serotonin + ‒ ION CHANNELS: not sure whether H acts on membrane surface receptor or inside of cell; may be both  any one “taste cell” senses just one taste (1:1 like olfactory receptor cells) o small patch of membrane covered w/ villi protrudes into oral cavity thru “taste pore”  gustatory afferents travel via CN VII, IX, X (facial, glossopharyngeal, vagus)  synapse in MEDULLA  thalamus  gustatory cortex  besides the mouth, there are CHEMORECEPTORS on walls of mouth, and gut o nerve endings in mouth have TRP receptor proteins activated by capsaicin, menthol, cinnamon, mustard etc. (not among the main “tastes” but “flavours” we can sense)  CN V (trigeminal) o stomach & intestine: can sense food chemistry using similar receptors and signal transduction like in tongue Equilibrium & Hearing 19. Anatomy of Ear  EXTERNAL EAR: pinna; ear canal, sealed by the tympanic membrane (eardrum)  MIDDLE EAR: Eustachian tube connects ear to pharynx (air-filled)  INNER EAR contains the sensors: (1) vestibular apparatus for eq’m and (2) cochlea for hearing 20. Equilibrium  sense of eq’m detects MOTION and TILT of head relative to gravity o several senses contribute: proprioception (e.g., stretch receptors in neck), and vision  Vestibular Apparatus (= membranous labyrinth) o set of fluid-filled chambers ‒ semicircular canals (superior + posterior + horizontal): cristae sense ROTATIONAL ACCEL.  all at right angles (orthogonal angles) to each other  3D  horizontal: side-to-side rot.  superior & posterior: up-and-down and ear-to-shoulder  canals filled w/ endolymph  each canal ends in a bulge called ampulla, which contain its crista ‒ maculae of the 2 otolith organs (utricle + saccule) sense head’s TILT & TRANSLATIONAL ACCEL.  Vestibular Hair Cells ≠ neurons o CRISTAE contain mechanoreceptors = hair cells o have stiff cilia, stereocilia  extend into gelatinous mass, cupula, which seals off canal o when head turns  endolymph lags behind  pushes on cupula, bending cilia ‒ cilia bent in opposite direction of head turn o each cell has one long stereocilium, kinocilium on one side ‒ if other hairs bend toward kinocilium  DEPOL., release of NT  sensory neuron activated ‒ if bend away from kinocilium  HYPERPOL.  less/no NT released o are tonically active at rest, releasing NT onto 1° sensory neurons o but endolymph can CATCH UP  no longer lag ‒ head rotation at constant v for ~20 s  no more lag ‒ then stop suddenly  momentum causes cupula to be pushed in opposite direction of original rot. v. o in maculae, hair cells extend stereocilia into a gelatinous otolith membrane ‒ on membrane surface are particles of C3CO + protein = otoliths (“ear stones”)  these are primarily acted upon by gravity, which drags the membrane with them, bending the hairs ‒ when head is UPRIGHT: macula of utricle = horizontal; macula of saccule = vertical ($) Page 6 of 24 Kim  Eq’m pathways project mainly to CEREBELLUM o hair cells activate 1° neurons of CN VIII (vestibulocochlear) o either go straight to cerebellum o or synapse in MEDULLA  cerebellum OR up thru reticular formation, thalamus to cortex 21. Hearing  sense receptors for sound in cochlea o cochlear hair cells ≠ neurons ‒ activate 1° neurons of cochlear branch of CN VIII  Sound = pressure waves o frequency  PITCH ‒ most people can hear 20 – 20,000 Hz; acuity highest 1000 – 3000 Hz o amplitude  LOUDNESS ‒ loudness ~ sound intensity, f’n of amplitude measured in decibels (dB)  10x ↑  10 dB ↑  normal conversation ~60 dB; > 80 dB can damage hearing o sound E conveyed to cochlea by middle ear bones = malleus  incus  stapes ‒ sound  shakes eardrum + attached malleus  i.e., eardrum transduces sound waves into vibrations ‒ stapes seals off oval window ‒ the 3 bones amplify vibration ‒ this is turn produces fluid waves in cochlear perilymph  bend the cochlear duct (containing endolymph), activating hair cells  activate neurons of CN VIII  path of waves: OVAL WINDOW  perilymph in vestibular duct  perilymph in tympanic duct  out thru round window  PERILYMPH = similar to plasma  ENDOLYMPH = similar to intracellular fluid, w/ high [K ], low [Na ]  Cochlear duct contains organ of Corti o it sits on top of (i) basilar membrane and under (ii) tectorial membrane o auditory hair cells each has 50-100 stereocilia, which extend into TECTORIAL membrane ‒ fluid waves of PERILYMPH deform these 2 membranes, bending cilia back and forth  Hair Cells o at rest, weakly activates sensory neuron ‒ stereocilia w/i a cell attached by protein bridges, tip links, which open and close ion channels in cilia membrane ‒ at rest, ~10% of channels open o when cilia bend toward longest cilium, more channels open + 2+ + 2+ ‒ cations (mainly K and Ca , not Na ) enter cell  depol.  opening of voltage-gchannels  NT release onto 1° neuron o when cilia bend away from longest cilium, channels close  Coding Pitch & Location o Basilar membrane responds to diff freq. at diff pts. along its length ‒ high freq.  maximally displace stiff area near round, oval windows ‒ low freq.  maximally displace flexible area near helicotrema (tip of cochlea) o aud. signals pass from each ear to both sides of membrane ‒ cochlear nuclei in medulla   midbrain  thalamus (and cerebellum)  auditory cortex o recall: loudness coded by firing freq. ‒ loudness codes location of sound source ‒ the EXTERNAL EAR filters sound in a complex way we don’t yet understand  Hearing Loss o 3 types ‒ conductive hearing loss: sound can’t be transmitted thru external or middle ear  e.g., malfunction of 3 middle ear bones ‒ central hearing loss: damage to cortex or neural pathways from cochlear to cortex (i.e., neural damage) ‒ sensorineural hearing loss: damage to hair cells or elsewhere in INNER EAR  cause of 90% of hearing loss in elderly (presbycusis) o cochlear implants are effective in restoring hearing ‒ tiny microphone + processor + transmitter to fit behind ear ‒ convert sound  electrical impulses  radio waves  send radio signal to receiver and electrodes under skin ‒ these signals relayed to cochlea or auditory nerve (CN VIII), bypassing damaged areas Page 7 of 24 Kim Vision 22. Anatomy of Eye  lens divides eye into 2 chambers: o anterior chamber, filled w/ aqueous humor (plasma-like) and o vitreous chamber, filled w/ vitreous body (clear gelatinous matrix; maintains shape of eyeball)  lens is suspended by ligaments, zonules 23. Focusing Light  light enters eye thru cornea (continuous w/ white of the eye, sclera) = transparent, dome-shaped bulge o cornea + lens together focus light on retina o cornea to lens: need to pass thru PUPIL, whose size controlled by smooth pupillary muscles ‒ bright  PARASYMPATHETIC  constriction of circular pupillary muscles ‒ dark  SYMPATHETIC  contraction of radial muscles (orthogonal to pupillaries) o pupillary (consensual) reflex tested as part of neurological exam ‒ light shone into 1 eye  signals travel via CN II to thalamus, then to midbrain  parasympathetic fibers (b/c bright) of CN III (oculomotor) to constrict pupils of both eyes  Depth of Field o when pupil tightly constricted  FULL DEPTH OF FIELD (i.e., everything we see is in focus) ‒ when dilated  SHALLOW depth of field  only objects @ focal length are in focus ‒ “pinhole” = perfect “lens”… but we have a lens, not pinhole, b/c pinholes allow in very little light  Refraction of light o at every interface of diff media: ‒ air  cornea  aq. humor  lens  vitreous humor o 2/3 of total refraction occurs at cornea; 1/3 at lens ‒ but lens is the only part that can ADJUST shape to alter refractivity  purpose: to focus image right on the retina o angle of refraction depends on 2 factors: (1) diff b/w densities of 2 media [Snell’s Law], (2) incidence angle ‒ in turn, the incidence angle depends on shape of lens, and direction of light ray  Concave (scatters) vs. Convex (converges) lenses  Clear vision: focal point must fall on RETINA o distant objects – rays roughly parallel  lens flattens b/c don’t need to bend much to converge o close objects  lens becomes rounder (flat lens will aim the image behind the retina) ‒ process called accommodation  unconscious reflex: eyes reflexively focus on where your ATTENTION is directed ‒ closest point at which you can focus an object = near point of accommodation  this near point gets farther away w/ age… presbyopia (vs. presbycusis in hearing loss)  Lens Shape controlled by ring of smooth muscle: ciliary muscle o goes around the lens, attached by ZONULES o when ciliary muscle RELAXED  ring wide, ↑ tension in zonules  flattens lens o when ciliary muscle CONTRACTS  ring tighter, ↓ tension in zonules  makes lens rounder  Issues with Focusing o hyperopia (far-sightedness) – lens is TOO FLAT, focal pt. falls behind retina ‒ solution: CONVEX lens to help converge light rays more o myopia (near-sightedness) – lens TOO ROUND (or eyeball too long), focal pt. falls in front of retina ‒ solution: CONCAVE lens to help scatter rays more  Projected image is UPSIDE-DOWN on retina  brain’s higher processing interprets by flipping image back 24. Phototransduction  Visible light = electromagnetic (400 – 700 nm)  phototransduction = conversion of light E (photons) into electrical E o humans: occurs on retina, where photoreceptors (rods & cones) are ‒ photoreceptors most densely packed in macula, the center of which is called fovea ‒ medial to macula is optic disk, where optic nerve and retinal veins exit eyeball and arteries enter = blind spot  don’t notice blind spot b/c: (i) binocular vision, (ii) brain “fills in” the gaps  Retinal layers arranged “inside-out”? o optic nerve axons are the 1 to encounter light rays, and then ganglion cells, then bipolar cells, and lastly the photoreceptors (light reaches receptors b/c the other layers are transparent) o MELANIN in pigment epithelium helps absorb any light that escape photoreceptors to reduce reflection o CHOROID LAYER (outermost) contains blood vessels Page 8 of 24 Kim  2 main types of photoreceptors (= 1° neurons) o (1) cones – for high-acuity colour vision in bright light ‒ most densely packed in FOVEA (only cones, no rods here) o (2) rods – more sensitive, so can f’n in low light ‒ outnumber cones 20:1 ‒ distributed across retina – don’t look directly at a faint star to see it; look away so light gets to the rods outside of fovea o they have same basic structure: ‒ OUTER SEGMENT: membrane folds into disk-like layers (in rods: outermost disks detached from cell)  these disks contain pigments that transduce light into MP  makes contact w/ pigment epithelium here ‒ INNER SEGMENT: nucleus, organelles for ATP and protein synth. ‒ BASAL LAYER: synapses at bipolar cells, and uses Glu  Pigments o rods have 1 kind of pigment, rhodopsin, composed of 2 molecules: OPSIN (membrane protein) + RETINAL (VitA-deriv. which absorbs light) ‒ DARK  retinal binds opsin ‒ PHOTON  change shape in retinal, released from opsin = “bleaching”  alters MP o cones have 3 pigments, all similar to opsin ‒ “red”, “green”, “blue” cones ‒ brain deduces colour from activities of these 3 types of cones ‒ the pigments differ in absorption wavelength ranges, but w/ fair overlap (wide ranges) ‒ “primary colours” = human concept, not a physical phenomenon  Phototransduction involves 3 cation channels in photoreceptor membrane o DARKNESS: high [cGMP] in rod  (1) K channels & (2) cyclic-nucleotide-gated (CNG) channels open  rod slightly 2+ depol. -40 mV  (3) Ca channels open at terminal  glutamate released onto BIPOLAR CELLS o LIGHT  rhodopsin cleaved (bleaching)  OPSIN activates G protein transducin (= cGMP phosphodiesterase when bound to GTP)  ↓ [cGMP] due to hydrolysis  CNG channels close, slowing influx of cations (but K efflux continues)  -70 mV (hyperpol.)  less Glu released ‒ activated retinal diffuses out of rod and is transported into pigment epithelium (& kept there until light off) o RECOVERY PHASE: retinal recombines w/ opsin ‒ retinal back to inactive form in pigment epith., then returns into rod and recombines w/ opsin to make INACTIVE RHODOPSIN ‒ can take a while; e.g., eyes adapting slowly going from bright light into darkness 25. Visual Pathways  photoreceptors  BIPOLAR CELLS  ganglion cells o up to 45 photoreceptors may converge on 1 bipolar cell, which in turn converge on ganglion cells ‒ “data compression”: 100 million receptors  1 million ganglion cells o axons of ganglion cells form CN II (optic) o convergence highest in peripheral retina  large receptive fields of ganglion cells (low acuity) ‒ vs. least in fovea (1:1 receptor to bipolar)  small RECEPTIVE FIELDS of ganglion cells (high acuity)  at each level of synapse, other cells have influences on the synaptic transmission o amacrine cells synpases w/ bipolar and ganglion o horizontal cells synapses w/ both photoreceptors and bipolars  2 types of bipolar cells: o (1) ON bipolar cells – metabotropic Glu receptor, mGluR6, that hyperpolarizes cell when binds Glu ‒ i.e., light  ↓ Glu release  “less hyperpol.” = depol. (ACTIVE) o (2) OFF bipolar cells – ionotropic Glu receptor that depolarizes cell when binds to Glu ‒ i.e., dark  tonic Glu release  depol. (ACTIVE)  2 types of ganglion cells: o ganglion cell RFs are roughly circular, with “center” and “surround” o (1) on-center/off-surround ganglion cell – excited by light on center, inhibited by light falling on surround o (2) off-center/on-surround ganglion cell – inhibited by light falling on center, excited by light falling on surround o both are weakly active when light falls on both center and surround (modulated effect)  Ganglion cells can also be classified based on how their signals are used in brain: o (1) large, magnocellular ganglion (M) cells – movement of objects o (2) small, parvocellular ganglion (P) cells – form and fine detail (e.g., texture) o 80% of all ganglion cells are M or P cells (i.e., there are other minor types as well) Page 9 of 24 Kim ‒ (3) melanopsin ganglion cells may act as photoreceptors  contain MELANOPSIN  axons project to SCN  Axons of ganglion cells form optic nerve o some fibres cross midline at optic chiasm o most proceed to lateral geniculate in THALAMUS, where they synapse  primary visual cortex o lateral visual fields of EACH EYE projects to contralateral side of brain ‒ i.e., left visual fields of both left & right eyes project to right side of brain ‒ right visual fields of both left & right eyes project to left side of brain o binocular zone = region seen by both eyes ‒ brain deduces 3-D locations of objects  Glaucoma = degeneration of optic nerve o usually caused by ↑ intraocular pressure, sometimes caused by excess aqueous humor (e.g., canal of Schlemm gets blocks and can’t pump out fluids) o treatment: drugs to inhibit aq. humor production, or surgical reopening of canal of Schlemm o optic nerve damage may involve NO or apoptosis-inducing factors  visual pathways are organized TOPOGRAPHICALLY o found in lateral geniculate & visual cortex, as well as many higher visual processing areas Spinal Reflexes 26. Aside: NOTE for all Wojtowicz’s lectures  loosely refers to FLEXION and EXTENSION a lot  flexion: general term referring to the muscle actions involved in bending of a joint (e.g., curling your biceps)  extension: refers to straightening out of a joint (e.g., your leg in the stance phase) 27. Overview: Nervous system anatomy  PNS o basically all neurons/neuron parts residing outside of the brain, spinal cord  CNS o brain, spinal cord o Spinal Cord ‒ white matter = myelinated axonal tracts (on the periphery of spinal cord, and called “COLUMNS”)  dorsal column – ascending tracts that send sensory info to brain  lateral & ventral columns – contain both ascending & descending tracts ‒ grey matter = unmyelinated cell bodies (on the inside of spinal cord, and called “HORNS”)  dorsal horn – receives sensory input  intermediate zone – integrates sensory input  ventral horn – motor output3 28. Clinical Implications  neuronal stem cells in central canal of spinal cord  can we repair spinal cord damage?  back pain: result of abnormal synaptic plasticity o pain signals keep firing even when the stimulus is removed, b/c wired so strongly when the stimulus was there 29. Overview: Spinal Reflexes  simplest circuits in nervous system (very few synapses) o often a feedback loop for regulating position, force, etc. o ***stimulus  receptor  sensory neuron  to spinal cord (dorsal horn)  then to interneuron OR directly to  efferent (motor) neuron (ventral horn, α motoneurons)  effectors (= glands, organs)  response  sensory info entering spinal cord  output by spinal cord o action is taken w/o consultation of brain o but info gets sent up to brain anyway, and then brain may have modulating influences on outputs  begins when receptor detects change which needs to be acted upon o e.g., proprioceptors (tell something about position) ‒ (1) muscle spindle detects changes in muscle length  a stretch receptor which lies w/i EXTRAFUSAL FIBERS (responsible for contraction of muscles), and contain INTRAFUSAL FIBERS together  gamma motor neurons from CNS innervate intrafusal, and regulate sensitivity of muscle spindle; not necessary for movement, but used as ‘fine-tuning’ Page 10 of 24 Kim ‒ (2) Golgi tendon organ detects ACTIVE muscle contraction  initiates inhibition of the homonymous muscle (the same muscle which initiated the stimulus, i.e., contraction)  links muscle and tendon 30. Stretch Reflex  stretching of a muscle  reflexive contraction of that same muscle  monosynaptic o simplest, FASTEST reflex o 35 ms  muscle spindles activated by any motion of the joint (passive/active, doesn’t matter) o afferent  efferent  homonymous muscle  f’n: to stabilize limb postures (important for sitting and standing)  example: patellar (knee jerk) reflex o stimulus: tap to tendon stretches muscle  muscle spindle activation  afferent  efferent paths (1) contraction of quadriceps, (2) relaxation of hamstring, allowing extension of leg (reciprocal inhibition) 31. Golgi Tendon Reflex  contraction of a muscle  reflexive relaxation of the same muscle  multisynaptic (disynaptic?) o GTO afferent (type Ib)  inhibitory Ib interneuron  efferent, α motoneurons ‒ inhibitory NT = glycine  f’n: if excessive load is placed, muscle contraction is inhibited as to prevent injury o load is dropped o acts in concert w/ stretch reflex to stabilize posture 32. Flexor Withdrawal Reflex  adverse stimulus  reflexive flexion in direction away from the stimulus o i.e., flexion of joints proximal to stimulus & extension distal to stimulus  Aδ, C nociceptors afferents  interneurons (in superficial dorsal horn)  motoneurons  multisynaptic o fast, but not as fast as stretch reflex o fast enough s.t. we are unaware of what happened until moments later  require divergent signal transmission: (1) excitatory interneurons (flexor muscles), (2) inhibitory neurons (antagonistic muscles)  reciprocal inhibition: basic property of intermediate zone o w/o it, arm would snap back into the adverse stimulus o activation of flexor motoneurons causes inhibitions of antagonist extensors o for co-contraction of antagonists, this circuit is suppressed (e.g., for joint stiffness; what happens perpetually in tetanus) 33. Crossed Extensor Reflex  for balancing when switching from bipedal stance to putting all weight on one foot o can be in concert w/ FWR ‒ when flexor withdrawn, need postural support for vestibular perturbation  opposite pattern of activation in contralateral limbs o signal by commissural interneurons  # of synapses not specified  divergence required for o (1) simultaneous flexor activation & extensor inhibition on ipsilateral side (for FWR) o (2) transmission of sensory info to CONTRALATERAL side: flexor inhibition & extensor activation (i.e., opposite pattern to that produced on ipsilateral side to adverse stimulus)  nociceptor  1° sensory neuron diverges in spinal cord  postural adjustment (CER) + ascending for sensation of pain + FWR 34. Extensor Thrust Reflex  pressure on sole of foot  reflexive activation of extensor motor nuclei o i.e., non-painful pressure on foot sole  POSITIVE FEEDBACK to put more pressure and plant foot down firmly o operates only during stance  Aβ mechanoreceptors  sensory neuron  excitatory interneuron  extensor motoneurons (extensor motor n.)  F’n: for maintaining stance  Babinski sign = indicator of working ETR o normal (antigravity) pattern: point toes forward upon pressure on foot o Babinski (flexion withdrawal) pattern: point toes up upon pressure on foot Page 11 of 24 Kim ‒ babies do this normally b/c reflex circuit not fully wired ‒ also occurs in adults w/ corticospinal tract damage 35. Vestibulospinal Reflex  perturbation in balance  reflexive compensation to maintain balance  receptor = vestibular system of inner ear o recall: SEMICIRCULAR CANALS – rotational, OTOLITH ORGAN – translational, head tilt  falling  activation of OOs  afferent  (interneuron?)  motoneurons  extensor muscles in arms & legs  head tilt  asymmetric activation of OOs    downhill limbs EXTEND, uphill limbs FLEX  note: visual postural reflexes readjusts body stance to maintain alignment w/ vertical axes in visual env’t, regardless of vestibular or proprioceptive inputs Central Pattern Generation 36. Central pattern generators (CPGs)  REFLEXES = insufficient to generate complex, rhythmic motor patterns (e.g., breathing, locomotion) o e.g., stretch reflexes cannot restore postural stability after a perturbation: a CENTRALLY COORDINATED response required o done by central pattern generators (CPGs) ‒ neural networks that make up these CPGs are distributed across many regions of nervous system (i.e., functional networks = complex integration) ‒ the ARRANGEMENT of neural networks determines: (i) nature of outputs, (ii) temporal sequence and (iii) periodicity of sequence repetition  Locomotion: Leg Step Cycle o programmed by network of neurons in intermediate zone of lumbar cord o 2 major characteristics that enable rhythmic activation: ‒ (1) pacemaker neurons: express specific ion channels  repetitive BURSTS of activity  feed-forward excitation – PMNs excite other PMNs ‒ (2) reciprocal inhibition (RI): inhibition of INTERNEURONS by other interneurons  (* distinct from RI of antagonistic motoneurons in spinal reflexes)  e.g., arm movement: when BICEPS (= flexor) active  TRICEPS (= extensor) inactive (& vice versa)  observable in muscle EMGs, but actually happening b/w the interneurons of spinal cord o Step cycle has 2 stages: (1) SWING phase (= flexion), (2) STANCE phase (= extension) ‒ similarly, the neural activity underpinning these stages are also in 2 distinct phases  (1) flexor burst generator (FBG)  flexor motor nuclei (swing)  (2) extensor burst generator (EBG)  extensor motor nuclei (stance)
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