Exam Notes

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University of Toronto St. George
Cell and Systems Biology
Melanie Woodin

Exam Notes Monday, January 09, 2012 10:46 PM Experiments Tetanic Induced LTP in rabbit/rat HPC - Liss & Loebel - Lecture 12  tetanic stimuli to perforated pathway; record in granule cells of DG o synaptic response observed, amplitude jumps up 175%, outlasts stimulus by hours Associative LTP in Rat SC → CA1 - Lecture 12 o stimulate two distinct groups of presynaptic fibers in SC pathway; record in CA1 pyramidal cell o tetanus at I + II (but not I or II alone) resulted in associative LTP o no long-term change in I, II tetanus alone (some short term post-tetanic potentiation possible in single input stimulation) Spike-timing Dependent Synaptic Plasticity - Li & Poo - Lecture 13/14  used spike-timing induction protocols (vs. tet. stim.) with lower frequencies → paired pre/postsynaptic AP Positive spike-timing interval: EPSP then AP (pre → post) > LTP Negative spike-timing interval: EPSP after AP(post → pre) > LTD  find avg. strength of synapse~25min. @ post-synaptic amplitude recording → start induction protocol → measure change Aplysia LTP + Learning and Memory - Kandel - 2000 nobel prize -Lecture 13/14  aplysia learn non-declarative memory → sensitization of gill-withdrawal reflex  skin of siphon → sensory neuron → interneuron → motor neuron → Gill withdrawal  serotonin released by facilitating interneuron → binds to receptors (metabotropic) → activate G-proteins → adenylate cyclase → signal transuction cAMP → PKA → inactivate K+ channels → increase duration of A.P. in presyn. term. (takes longer to get back to RMP) → depolarized longer → ↑Ca2+ influx → more NTS released by sensory neuron results in more sensitized reflex  proved that synaptic plasticity underlies a change in behaviour Fast and Slow PSP in Sympathetic Ganglion Cells - Lecture 17  nicotinic - 100ms - fast deplorization, return to baseline quickly elicited by single stimulus to preganglionic input  muscarinic - 5 min - takes longer to reach peak but lasts longer requires trains of APs → now a single fast depolarization will give rise to a burst of APs can be mimicked with LHRH2 Response to B.P. changes are Detected in Carotid Sinus Stretch Receptors - Lecture 17  increase B.P. = increased A.P. firing of stretch receptors larger increases = even greater firing (as opposed to low levels, a change won't cause much firing)  recording 1924 - perfuse different animal blood into head of another animals increased pressure in head caused a fall in b.p. in trunk Olfactory Receptor is on Cilia of Olfactory Cells - Salamanders - Lecture 18  solution of odorant molecules and KCL applied to (1) cell body and (2) distal dendrite/cilia  cell body - rapid initial depolarization due to KCl, smaller slow current (odorant)  cilia - small rapid current but large/longer-lasting current (due to odorant)  region of sensitivity is at the distal dendrite and cilia  the prolonged time course is consistent with idea that conductance change is due to GPCR o if it was just ion channels, would be faster like the KCl H Bipolar Cell Receptive Field - Off Centre - Lecture 21  shine light around until RF found → now focus in on an area to characterize response  general: light → decrease Glut → decrease excitation → hyperpolarize  central illumination → hyperpolarize  Annula Illumination → depolarization ∴ OFF centre RF Motor Control 1. Simple Reflexes - sensory neurons synapse with motoneurons in the spinal cord to mediate simple reflexes 2. Central Pattern Generators - networks of interneurons in spinal cord and brainstem to corrdinate motor groups for locomotion, respiration etc. 3. Complex movment planned and refined by motor cortex, basal ganglia and cerebellum (conscious) o gradate activity to make smooth movements α MN - major MN of spinal cord (actually make your muscles contract) γ MN - small MNs that regulate the sensitivity of muscle spindles (control level of activity) Motor Unit - single α-MN and muscle fibers it innervates Motor Pool - all the MNs supplying a particular muscle (many α-MNs) small MNs easily excited so recruited first, then progressively larger motor units depending on stimulus Temporal vs. Spatial Summation  temporal - one afferent (presynaptic fiber) fires succesive A.Ps → ride on falling phase and increase depolarization to activate postsyn. partner  spatial - one MN has many converging 1a afferents → EPSPs will spatially summate to depolarize the membrane Agonists work together, antagonists are relaxed Extensor - open or extend the joints (away from midline) Flexor muscles - close the joints or pull limbs toward body (toward midline) Myotactic Reflex AKA Stretch Reflex  Stretch Receptors (extensor) → Group 1A afferents a. contract αMN (agonists) b. interneuron → inhibit antagonists  Golgi Tendon Organs (tendon/muscle junction) → Group 1B afferents a. interneuron → inhibit agonists b. straight to antagonist MN → contraction Muscle Spindle - small intrafusal fibers (γ MN → spindle → Group I/II → Spinal Cord)  embedded in between extrafusal muscle fibers (α MN) Go Pathway: Cortex activates Neostriatum inhibits GP disinhibits thalamus → activates mvmnt  substantia nigra = net excitation of striatum  subthalamic n. = activates GPi → inhibit thalamocortical tract Parkinson's Disease - resting tremor; increased tone (activates antagonist); slow/decrease in mvmt  hard to initiate movements; slowness of movement once begun  DA neurons in S. Nigra degenerate - less striatal activity, less inhibition of GP, inhibits thalamus; less excitation of motor cortex Sensory Processing Short Receptors - sensory receptors located on sensory cells that have receptor potentials that spread passively to synaptic region  no A.P.s → only release NTS if depolarized  e.g. hair cell Long Receptors - receptor potentials give rise to A.P.s trains  duration - temporal information  frequency - intensity  e.g. olfactory cells Transduction - mechanical stimuli at skin/muscles/joints/→transduced to receptor potential  can be depolarizing or hyperpolarizing; increase intensity → increase R.P. → amplitude 3  amplification - fish can detect electrical fields of a few nV/cm Receptor Potential  increase stretch = increase amplitude (but not a linear response) o big response at low end, small reponse at larger values o why? advantage of providing amplitude coding over a wide-range of stimulus intensities  at very high levels, RPs saturate and cannot increase amplitude o if it remains high, the receptor potential adapts to a lower level  SAR - encode stimulus duration o responds at begging, but adapts and freq. decreases until it fires NO MORE  RAR - detect CHANGE o response is maintained throughout stimulus Sensory Receptors - determine the range of stimuli that can be detected  Adequate Stimulus - each is specialized o usually have cell body in middle (bipolar or pseudounipolar) Olfaction Smell and Memory  can elicit memories and emotions (involuntary)  100000 olfactory receptor neurons project to olfactory bulb  long cilia extend into nasal cavity and lie in mucus layers  new cells 1-2 months at basal cells of olfactory epithelium Transduction lateral olfactory tract → limbic system (amygdala, ERC, HPC, subiculum) → medial n. of thalamus then frontal cortex for recognition  sensory cilia → reach ganglion → olfactory bulb → CNS  odorants bind to GPCR → frees α-subunit → activate AC → cAMP → Ca/Na channels (depol.) → vgCl- current enhances this → PLC activated → IP →3directly on Ca2+ channel → depolarization  amplification of 1000x of intermediate products Odorant Specificity  olfactory receptor recognizes spectrum of odors  every odorant receptor is found in restricted area of epithelium from development (family of R genes in zones) Olfaction and Gender  sensitivity can be induced (can't smell, exposed, then can smell)  enhanced senstivity to odors they could already detect (increases 5x in females) o pair bonding, kin recognition, reproduction Anosmia  traumatic brain injury, virus (temp), or congenital anosmia, or Alzheimer's Disease  suffer from depression Taste similarity to olfaction  external chemical stimuli  75% of taste comes from smell  some tastants act on GPCRs o but some change membrane conductance directly  receptor neurons also regenerated throughout life (burn your tongue) Taste Receptors  ciliated neuroepithelial cells (short receptors)  chemical synapse onto afferent neurites in taste bud o microvilli project from taste cell into the taste bud where they are bound by tastants 1. Direct Action on ion channels: a. Salt → Na || sodium influx through apical membrane channels diffuse down gradient (way more salt in the food than in the cell) → depolarization b. Sour → H || cause proton block on K+ channels (can't leak out) or flow through directly leading to depolarization 2. Second Messenger: Bitter/Sweet/Umami (MSG a.a. taste) → GPCR o large molecules bound by GPCR specific for them → 2nd messengers → depolarization 3. Pain Fibers - Capsaicin → KAIN5 4. Nociceptive/Thermal Stimuli → nonspecific cation channels open signalling to CNS → damaged cells release chemicals (ATP) a subunit of ATPR (p2x) for immune response Vision  5 cell layers:[photoreceptors → Muller → horizontal → amacrine → ganglion] o plus pigment
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