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Human Neurobiology: Exam 1 Study Guide

by: Jamie Burns

Human Neurobiology: Exam 1 Study Guide BISC 3320

Marketplace > George Washington University > Neuroscience > BISC 3320 > Human Neurobiology Exam 1 Study Guide
Jamie Burns
GPA 3.93
Human Neurobiology
Dr. Jeremic

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About this Document

A thorough compilation of the important topics covered in class // major concepts from each chapter. Includes important figures from book/ powerpoint slides. Extremely comprehensive : 11 pages long.
Human Neurobiology
Dr. Jeremic
Study Guide
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This 10 page Study Guide was uploaded by Jamie Burns on Wednesday October 14, 2015. The Study Guide belongs to BISC 3320 at George Washington University taught by Dr. Jeremic in Fall 2015. Since its upload, it has received 27 views. For similar materials see Human Neurobiology in Neuroscience at George Washington University.


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Date Created: 10/14/15
Chapter 1 Nervous System 1 Local Graded Potentials 2 Action Potential generated by extrinsic stimuli Generated by LGP light sound or touch Propagate rapidly over long distances Signals are graded Fixed in amplitude 01V and Locaize to the site of origin duration 1ms that rapidly propagates Their spread depends on the along nerve fibers 120ms without passive properties of nerve cell dissipation Intensity of stimulus is a coded by 1 frequency of ring 2 number of neurons being activated Excitatory and inhibitory synaptic potentials Depolarization hyperpolarization Synapse types 1 Chemical Majority of neurons communicates with chemicals 90 neurotransmitters which trigger influx or outflux of ions anions going inside cell ie Chloride 2 Electrical Chapter 2 Ion Channels Measurements of Channel Electric Activities Patch Clamp tells you magnitude of flux frequency of channels opening direction of flux duration time of channels opening mean opening time 9 all this info tells you what channel it is ca vs kna which ions want to come in out mean opening time ID channel Driving Force Vm Ek Channel Conductance and Permeability tSOmM K39 inout Ohm s Low yV t 39 f 39 lcurrent pA Vvoltage mV ychannel Conductance pS M W r 7 m J I39M h xlmilml im I Single channel electric activity Current versus Voltage curve Channel conductance depends on 1 Channel permeability qualitative 2 ion concentration quantitative Current cation OUT positive current cation IN negative current anion OUT negative current anion IN negative current potassium equilibrium potential 87mV m to right of Ek 393li K oulSIde potassium ows out QCmM K insde Equilibrium Potential to left of Ek potassium ows into cell H r m Compare graph F to previous slide in real cell at 0 Voltage there r is large net ux of K Ek A out of cell 35pA Vm Er Driving Forcerfor lon Movement 311 due to COHC l atrh potential im39 gradient L Imnml current pm K EqUi39ibrium POtentia39 Ex K CurrentVoltage Relation i Depends only on the ion concentration on either side of the membrane 4 From OmV to 2 5mV 9 net ux out ux from gradient is accelerated by electrical gradient 35pA to 45pA Current is positive From OmV to 75mV K still ows out of cell but the ux is decelerated by electrical gradient Current is positive At 75mV no net ux of K Gradient chemical Gradient electrical Current 0 Below 75mV electrical gradient overpowers conc gradient and K ows into cell Current is negative current generated by conc gradient remains constant at 35 pA any deviance from 35pA comes from electrical gradient Conc gradient pushes K outquotlt Ek equilibrium potentialquot voltage required to cancel out conc gradient Where current 0 Each graph is unique to the starting concentrations of K in and out of cell9 Nernst Equation 3mM90mM 30X gradient 1mM90mM 90X gradient 9mM90mM 10X gradient Nernst Equation EfRTZF 39 WK 9 ALL MONOVALENT IONS 5625 In KOKi 9 MAKE NEGATIVE FOR ANIONS e DEPENDS ONLY ON TRANSMEMBRANE 5K 58 Iog KCKi ION CONCENTRATION Channels stretchactivated ligandactivated voltageactivated CHAPTER 3 Ion Channels A LigandActivated Channels 35 subunits in cyclical fashion to create secluded environment one subunit transmembrane with extra and intramembranous regions Channel Selectivity Acidic amino acids at extracellular domain to attract sodium potassium calcium permeability 9 further selectivity based on charge size sodium v calcium 9 electrostatic interactions are not enough to explain channel selectivity9 size of opening geometric constraints Transmembrane domains hydrophobic Extra amp Intercellular domains hydrophilic Extracellular bind neurotransmitters Intercellular Bind second messengers cAMP ATP GTP eg Insulin ATP binds to intercellular domain of K channel closes it9 depolarization Bl VoltageGated Channels Structurally similar to ligandgated channels BUT Nterminus amp C terminus are intercellular no need for extracellular domain 1 subunit with 4 domains huge domains Large intracellular domains suggest use onI101 messenger binding site Common tetramer structural motif 4 domains or 4 subunits One Subunit Kinases add phosphate groups Phosphatase remove phosphate groups VoltageGated Channel Chapter 4 Transport Primary Transport Dependant on ATP hydrolysis Eg Ca2ATPase Secondary Transport No ATP hydrolysis Utilize electrochemical gradient dependant on primary transport Cotransporter KCl 9 electroneutral both go out Fuel letting k out Antiporter Na Ca2 exchanger 3na in ca2 out ca passively diffuses in all the time Fuel letting na in Brings positive charge in favorable forward cyclequot facilitated by hyperpolarization quotReversed cyclequot when cell is depolarized FOR EXAM how transporters operate connect primary and 2ndary biological significance If you block primary transporter would you expect neurotransmission will continue No 9 you need a gradient to power coupling Will blocking secondary transporter a ect primary transport 9 initially No Eventually yes9 indirectly you will change charge d erential amp conc gradient across membrane Transport of Neurotransmitters Uptake by the Cell 9 coupled to Na gradient Na pulls NT in with Na Uptake by Synaptic Vesicles 9 coupled to H gradient 2H out NT in NT first enters cell then enters synaptic vesicles Inside vesicles pH is low5 Cytoplasm pH7 H want to leave vesicle so it s couple with inport of NT Proton pump makes vesicles acidic primary transport requiring ATP Primary and Secondary Transporter Structure Similarities COOH inside regulatory domain intracellular open to modifications to regulate transporter activity increase or decrease All have transmembrane domains bc ions must cross hydrophobic membrane Differences Some lack extracellular loop far smaller binding sites needed for ions than for NT Some have extracellular loops needed to selectively capture neurotransmitters binding sites Transportclassi cation 1 Primary active transport 2 Secondary active transport use E provided by hydrolys5 ofATP use electrochemical gradient of certain Na39K exchanger 3Nar2KATpase Ion to move other Ions across the memb Ca2ATpase NalCa exchanger CUNa etc Charge eectrogenic NalK exchanger eectroneutra CI transporters Chapter 5 Resting Membrane Potential Equilibrium Potential Eh Depends only on ion concentration on either side of membrane Signi cance of Changes in Membrane Potential F 0 Regulation of synaptic function generation and transduction of action potential 39 Transient changes in MP mediates signaling between cells in nervous system Channel current pA J 0 Stabilization of MP by CI currents is important for controlling cell excitability Ek Genetics defects that affects channel conductivity are causing several 1 Vm 39 Er WW 3 39 quot quot mm diseases vClcystic brosis Ach myasthenia gravis Patch potential mV Resting membrane potential is sensitive to changes in 16 but not Cl39 concentrations Chapter 6 Action Potentials Hodkin Huxley and Katz I cK cn conductance Relatlonshlp between lon conductance and AP I Variation of Ohm s Law V membrane potential Ion Permeability Current Driving Force Em equiibrium potential Gk INa Vm39ENa Vm E driving force Gk Ik VmEk K Ion currents Current channel permeability X driving force Membrane Currents During Depolarization Early and late currents during membrane depolarization 39539 I n 9 I 39 I i E E J 4 n IX nanAlum V g 77 IE 2 3 j t TE 1 r 39 Tr xr llmn r l 116 turn39n m E 5 quot E E or 5 E larix uI39nnl a 1 r 5 39 4 39 t Na replaced with choline mu m H m I quot quot Earl current Na in ux Effect of toxms In V Y Late current K efflux Ill N0 I I 17X gNaI 1 a TEA gK I 2 IE39 I I quot 397 Figuring out what uxes are responsible for ACTION POTENTIAL Negative early current means initially a cation is owing into cell Figured out that Na ux responsible for AP used solution with reduced Na content result was a very small action potential also replaced na with choline only late current occurred 9 had to be Na Effect of Membrane Potential on Ion Currents Early and late currents A 3 PUG k It lt current mAcm Out l mk m rly current 20 H mV 52 26 1 mAcm2 393quot l 1 llLLlllILJJ I 50 100 mV 0 10 b Peak early Timems H h current l l ca k Id to current A at 85 no movement of k or na 9 equilibrium potential for k no net movement no current conc gradient electrical gradient Otherwise more and more e ux of k once the current gets larger and larger trying to get it back to 85 driving forcequot B sodium really wants to move at 85 in B but there is still not current in A because channels are not open Peaks at 10mV around 50mV na current 0 Equilibrium potential Chapter 7 Action Potential Propagation AP will travel in all directions towards soma amp axon terminal AP in soma has no effect there s no myelin nak atpase ushes it out Once it propagates down axon it may not switch direction Refractory Period Hyperpolarization of cell following AP another AP may not be generated Significance prevents reversal of direction of AP If allowed to reverse AP would not reach terminal amp signal would not be transmitted Myelination amp AP Propagation rmmembrane resistance riinternal resistance A I ll 12 Lambda length how far AP can propagate O t D 0 7 D m i to preserve 13 of original strength p we 39 axon 39 fiber 9 predicts speed of conduction Range 0608 Membrane Resistance Myelin prevents ion leakage speeds AP Internal Resistance Inversely proportional to size of axon ion ow Small diameter smaller signal 9 larger internal resistance SLOWER Large diameter larger signal9 smaller internal resistance FASTER Diameter of fiber diameteraxon diametermyelin Optimal ratio making up fiber diameter9 30 myelin 70 axon diameter Average 100200 layers of myelin wrapped around axon can t wrap around 100000x because diameter of fiber is constant at 7 would force axon diameter to decrease which slows signal 69 Summary Larger Membrane resistance more myelin9 speeds AP Smaller Internal Resistance large diameter9 speeds AP Electrical Signaling Between Cells Nodes of Ranvier myelin enhance AP High conducting area myelin nearly blocks leakage of ions slow attenuation of signal If no nodes signal would deteriorate very slowly to above 40mV Nodes allow regeneration of ap they re rich in Na amp K channels Saltatory Conduction no actual jumping more like a spark Electrical signaling vs Chemical Signaling 90 tranmissions are chemical 10 are electrical Synaptic plasticity while chemical takes longer it is more specific9 can be attenuated with more or less NT as opposed to on off transmission from electrical signal it s also more regulated Electrical signal Ca amp na ow into next cell9 Gap junctions faster because there s no quotmiddle man gtgtgt chemical transmission has more steps takes longer Less electrical dysfunction than in chemical transmissiongtgtgtgt mutated NT receptors mutated production of NT etc Gap junctions are made of conexons proteins that interact from apposing cells PM to form aqueous channel and thus to connect cytoplasm of neighboring cells conductance is maintained by the free ow of ions from one cell to the next via gap junctions Chapter 8 Glial Cells Excitability of Glial Cells not triggered by activiation of Na amp Ca channels Like neurons excited by neurotransmitters Glial membranes express channels transporters and pumps Contain NT receptors ion pumps voltageactivated K Ca channels etc CNS PNS Qlig Q EQE9 I I make myelin supportive Schwann cells make myelin Microglia protective supportive Astrocytes communication and processing Chapter 9 Synaptic Transmission Two Types of postsynaptic transmission A Excitatory EPSP B Inhibitory IPSP Two types of synaptic transmission A Electrical Synapse B Chemical Synapse direct or indirect Ionotropic Receptor aka ligandgated ion channels9 transmembrane ion channel proteins which open to allow ions like Na K Ca Cl DIRECT TRANSMISSION Metabotropic Receptor 2nd messenger channel linked to second messenger on intracellular side results in cascade INDIRECT TRANSMISSION Vr depends on the relative channel permeability for various ions and their individual equilibrium potentials In excitatory synapses Vr is MORE POSITIVE than AP threshold Electrical Synapse Electrical signaling is mediated by direct current ion flow from cell to cell via gap junctions connexons Chemical Synapse Chemical synapse is established at the junction of presynaptic ending and postsynaptic density Neurotransmitters released from presynaptic site activates receptors on the postsynaptic membrane Chapter 10 Indirect Synaptic Transmission Direct more efficient no phosphorylation Indirect less efficient less regulated but signal is amplified Metabotropic Receptor Indirect Transmission One subunit with 7 transmembrane domains Nterminal extracellular binds ligand Transmembrane domains do not form pore They bind G proteins Versus ionotropic channels that have 45 subunits forming circular channel GProteins Ligand binds GDP phosphorylated to form GTP Releases beta gamma dimer to target downstream molecules Direct Gproteinchannel interaction dissociated G protein complex directly binds to amp activates a channel Indirect Gproteinchannel interaction dissociated G protein complex activates second messengers like cAMP Activation only lasts so long termination eventually stops signal must reset complex so it can receive stimulation signal GTP loses Pi becomes GDP reassociates alpha with beta gamma dimer Termination depends on hydrolysis of GTP Suppressed hydrolysis complex stays dissociated prolongs signal Example Achetocholine Direct Interaction ACh binds metabotropic channel GDPalpha beta gamma is phosphorylated to GTPalpha which kicks off beta gamma dimer This dimer binds to K channel and opens it E ux of K causes hyperpolarization of cell 1 rpmphi mu er nt Y 392 l L 39 rumpl ulegr n In mxi t 21 mm hamwl l l nlunhlr n Lile 1 HAHJIIIl39lz39 MIN A III A JM l I39lm phmiu h39l1 439 I lnh ln s t dl39 W 39 39 39nt39 PIMI 39LLI 39 I R I 139 quotitAMl mkprmirm ptvtnnn Lnuw lumhu 39V 1 39L39N39h t39ll39 prult39m MI JM39 Fl nplaxmn Gas upregulates Ac 9 increase in CAMP 9 increase channel activity Gai downregulates Ac 9 decrease in cAMP 9 decrease channel activity Gaq12 Phospholipase C PLC 9 cleaves PIP2 9 DAG Ca see following slides don t need to know all the dirty deets Example Phospholipase C PLC Pathway Indirect Norepi binds receptor Gprotein complex dissociates binds to Phospholipase C PIP2 becomes DAG 1P3 DAG9 Protein kinase 1P3 activates Ca2 release9 protein kinase Result decreased Ca2 release Example Adenylyl W pathway Indirect Interaction Binding of ligand norepi increases ca2 permeability by 2x INDIRECT Dissociated complex binds adenylyl cyclase catalyzes cAMP Ca eine blocks phosphodiesterase upregulates CAMP increase in ux of ca in brain heart muscles Kinase phosphorylation Phospodiesterase dephosphorylation Chapter 11 Mechanism of Neurotransmitter Release Action potential triggers release of NT at end of presynaptic terminal Synaptic delay 12ms crossing cleft fusion of vesicles Action Potential Calcium 9 NT Release OR just Calcium 9 NT Release Calcium required for AP to trigger NT release Artificial release of Ca2 without AP still triggers NT release Quantal Release Ach is released from presynaptic terminals in multimolecular packets quanta quotQuantum Contentquot number of quanta release VARIES quotQuantum Sizequot number of molecules in each quantum FIXED Ach 7000 molecules quantum V Number of Channels Activated by a Quantum PNS Receptors are invaginated to increase surface area therefore ussszzz azziesza 1Sigquot231312raided thew channels available to be A B activated 1000 C Q CNS Receptors are small only 1556 39 channels to be activated amplitude of signal is fixed Synaptic Integration Many synapses end on same receptor in order to Quantal events at peripheral synapses Quantal events at central synapses increase Signal Large uctuation in amplitude Little uctuation in amplitude l Synaptic Integration Methods of Transmitter Release Vesicle Hypothesis Vesicles containing NT are released from presynaptic terminal via exocytosis fusion of vesicles with membrane Uptake via endocytosis on postsynaptic neuron Kiss and Run Hypothesis For expedited signaling vesicles w NT hang out partial fusion with postsynaptic neuronal membrane to release fastdiffusing NT closes amp quotreloadsquot with NT o ll lk dl Dist hnrgv 39 o o A o o j C C lt quot 30 o o o o f y Optr LION I a I Q I I I ll 3ltC I3 r 4 391 3quot J o 3 a o L39 w 9


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