TeLODP See if CONSCIOUS POSITION SENSE: Joint angle specified by: as 1) joint receptors (discharge at extremes DC ARAL. system of flexion and extension) = / ee 2) muscle spindles (intrafusal fibers) Ge “s nee ea Se A SAD) | Ny = deficits in conscious position sense J Spe GTO: rapidly adapting ~ - impaired locomotion (sensory ataxia) ‘unconscious position sense: ‘only if theyre joint ‘oceptors! more sensitive all receptors inact ‘0 changes in angle than CEREBELLUM = SF eee DILLY = | — _skinjoint afferents eliminated by local dumags causes: : sete Bearer eer ceereten) aS 2 2 “5 jolt sition sense depends on “Clndoling has no efece : 77 egomarc Ca eee ge a 2 = cerebellar ataxia le ——— a i Uw Ine veity (a (rec) = a copy of every muscle command is sent to a Candin de syitem bor chyed se a ae eres reticle Loe = pe Ne ees, Sa Se = thus inthe absence of sensory fedback gd | ee (eayater a lateral dre! rhzotom) Cas A has an estimate of position sense is still available E Sale S View bens } eae mk CMT Show} ee rae herd) eh JA vemay |e y LAGVETAL YOSTTIOMING areas Sand7 + damage causes astereognosis — inability 0 recognize objects through integration of proprioceptive * parietal damage on right side causes neglect syndrome denial of injury or defct on contralateral side of body = patient fils eo recognize his own limbs “Ignores stimulation contralateral to lesion - double simultaneous stimulation, one side s ignored even though it would normally be perceived alone constructional apraxia - inability to draw half ofa ‘objects (apraxia = loss of skilled movement) ** hemiatrophy - children suffering from parietal damage hhave a hemiparetic side that doesn’t grow normally °* asomatognosia - loss of body sense; similar to finger agnosia (inability to pointlidentfy fingers) * Balint’s syndrome - “sticky fixation”; can only attend to one thing ata time = optic ataxia ~ difficulty reaching for objects using vision Ceorinatte ‘example: see someting (eye coordinates), reach for it (arm coordinates), drink ie (head coordinates) ALL MUST BE INTEGRATED! VB. Mountcastle and R.A. Anderson: - discovery of “gain field” — neuronal output is modulated by activity of other neurons =a neuron may respond differently, depending upon the fixation point, to same retinal stimulation = evidence of coordinate transformations = response was highly modulated by the position of the eyes = PPC provides instruction to frontal lobes, basal ganglia, and cerebellum ~ it is involved in behavioral goals, 0 it must integrate info from different coordinate systemspair BUD (ly ip) tape calle (@ VAL) we pei, (mat ot Pav dlp wibee cas) oe s tT SIGS wy Ke dosast teste alle (in rh jek (50-160) «dd Lee as Brcote 2 (18 oot bod aia ) J ( * taste receptor cells are broadly tuned to : = fey ghee cae (GO) deal Ke aqevin ee ce ee) = response of a single call is ambiguous ae = distributed coding throughout a population of cells SS 90% of Se oe = 90% of taste calls are response to 2 or more Napa rl “Comp, CE basic tastes (lee sla fine J Aen? ing! Cee errs is ee 6 Hagee) creen cheese. Feench east Ten gpecttand Me ere SAT ee pasee. sce peau cee = Ht from acids passes through fee ey amiloride-block channels amiloride-sensitive sodium channels ic = not voltage sensiive - always open = H+ blocks potassium channels = pose curren depolrizes cell & Mecseattare seen itsnice Seen Yoke “iver "Opening Cat channels, eresering fi “desde Cat channels, triggering NT release Niictriaaienctoene If [ff myecornetmtin the more i inhibi the salty taste eS chad Ge Slagle “Ginstie onal Slant BIMeER « bitter substance (quinine, calcium) RB /TIE@ - bitter substance binds to G-protin Cason) | sy YZ) blocks K+ channel (ia) [p@.,~ Sprorein aces PLC be x Sate, subsequent depolarization joie sack, RCS] ~ PIP, > IP, & DAG causes influx of Ca++ and NT release! es «IP, causes release of calcium from = bieter substances have 3 ‘ incernal stores ees NO, grous (O-ddogey a2) Gopahs - sucrose binds to G-protein Upanene “ “protein actraces aderyiyl cyclase 1S.0"7 ZZ), amino acids bind vo Cat+ and Nat channels = ATP --> cAMP fomirey> influx of cations depotarizes cell ~ CAMP activates PKA U * - Ca++ influx and NT release ensues =PKA phosphorylates K+ channels, ule “Junc..* = may also be G-protin-coupled mechanism closing them leads to depolarization and NT release = sweet = organic compounds that do not ionize G-protein = gustducin gustducin KO mice lack behavioral and neurophysiological responses to bitter and sweet tastesOlfaction-~ + occurs ofcroryepthlum (10cm?) rere 2000 ‘olfactory tubercule _—> thalamus (MDN) \ (i es v £0 2 enim pate” 4S orbitofrontal cortex “22 ae ‘\y to olfactory cortex oF temporal { |, ollactory receptor eatublperlonsti btctory rere %p__ lobe (entorhinal cortex) true neuron cls (tera ih) ctactory bulb ‘ “hires APs / \ » Sregenerate 2 genes targee receptor tral and tufted PAS every 1-2 mos. ee cells (2nd order yd is (2nd ord parahippocampal gyrus proteins to their corresponding Sfiactory neurons) basal cell ‘glomeruli (secretes mucus) ~ ~ ean differentiate into = olfactory receptor TEMPORAL CODING a, (Copoend to cells activation of olfactory bulb cells changes. oo (1) activation of olfactory bulb cells changes predictably over the time course of stimulus presentation (2) individual neurons respond with specific spiking patterns to different stimuli SPATIAL CODING termination of olfactory response: “olfactory map” 1) odorants cifuse away ame 2) enzymes break down odorants 3) cAMP activates other pathways 4) adaptation to odorant G, ~ protein (1000 varieties - Buck & Axel, 1991) if 7 transmembrane alpha-helices Central pathways Anterior olfactory nucleus —> feedbacl tp bulb Primary olfactory cortex orbietroneal tence conscious perception & discr Amygdala Entorhinal cortex SS memories ‘emotion, endocrine, visceralEtat de ote a “ ‘more than a modality x ee \ 4 ee re Nist ed \\ “the effects of pain depend on their context eee | 2 \ more dan the strength of dhe stimulus Spe p “more of an experience than a sensation SA Pe aspect Decithe (sitit mcg?) sf Pain is transduced by free nerve endings (AS ~) ©) Ae AS <> type k:mechanical stimuli ee ee ¢ type limechanical & thermal stilt | [| 3 sensitive to chem, stimulation | ~ Both sensitive to chem. stimulation || | C (75% of fibers in peripheral nerve) polymodal: responds to M, T, and C stimulation silent: become active in inflamed tissue Revered! (Bin SENSING TEMPERATURE Riordan 2 een ses, Y/, ladder => back forded eld jaw bone —-> teeth/ears 2 sppendidds —> naval | abdominal cavity --> right s | lower quad. of abdomen = & Goin! Rett ANTERocpTERAL. SYSTEM ‘con oe ote (ee ee oe vy a release of substance neon PeSre. soins 1 Ack in lange quancies) ee Wall: ) Powna Rawanes ay ©) 20. simul = peasant warn Te * eel of pan not ret correlated I eee with C fiber activation rst ase oe | Pe ralneeoionretetiatoimeceed ste eotnd se ree Sara eee SS AS Chew > pain can arise in the absense of | sowour sna ass Fatologi pin rodeprnspecticneron Fao ic wide dynamic range neuron anesthesia dolorosaCEMTCAL Régulation’ OF PAIA/ Melek ad Wall's gate contre | theory Aeserdny ceguldin J = explains counter-irritation efffect Bi Cnubins y PAG AUTOMATIC GAIN CONTROL 2v6 ~ acsivaced by supraspinal serucures as well as ascending immpuaes from che ancerclacral syuern Capers ho) DORSAL HORN (substansia gelatinosa) ie ay [rece ore] gatekeeper keeps Pain cell under ha OPIOID RECEPTORS He { tonic inhibition ood = injection of opiates into PAG and PVG cause analgesia (2) when nociceptive afferents are stimulated, c—_porseariatt. - antagonist = Naloxone they inhibie the gatekeeper yey nocipetive afferents activate the P cell US eu ese ‘rubbing the leg activates large-diameter axons, [Deanl bem | NEGATIVE FEEDBACK which stimulate the gate-keeper ff Sparel gad t Jectrical stimulation of 2) Acbeta stimulate the P cell PVG, PAG, or Raphe nuclei ae ‘ é leads to long-lasting analgesia prediction: electrical simulation of dorsal eh dine fects are blocked by ‘columns also reduces pain by pecs le, ale Naxolone antidromically activating the = Naxolone also blocks the non-nociceptive afferent axon and placebo effect. synapse 4 = actually occurs, but not necessarily by this mechanism * im the presence of great amounts of pain, synapse 4 is ineffective, but synapse 5 functions —> leads to secondary hyperalgesia = secondary hyperalgesia is immediately eliminated by anesthetizing nociceptive afferents Thalmaic Nuclei MGN: hearing PL: pain/touch