Study Guides (248,633)
Canada (121,642)
Physiology (149)
PSL300H1 (104)

PSL300 Final Exam Review (Tweed, Wojtowicz).pdf

24 Pages

Course Code
Hae- Young Kee

This preview shows pages 1,2,3,4. Sign up to view the full 24 pages of the document.
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)
More Less
Unlock Document

Only pages 1,2,3,4 are available for preview. Some parts have been intentionally blurred.

Unlock Document
You're Reading a Preview

Unlock to view full version

Unlock Document

Log In


Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.