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Introductory Neurobiology Week 4 Day 1 Notes

by: lucy allen

Introductory Neurobiology Week 4 Day 1 Notes Biol 3640

Marketplace > University of Denver > Biology > Biol 3640 > Introductory Neurobiology Week 4 Day 1 Notes
lucy allen
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Notes for Tuesday, 1/26/2016.
Introductory Neurobiology
Dr. John C Kinnamon
Class Notes
introductory neurobiology, neurobiology




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This 6 page Class Notes was uploaded by lucy allen on Sunday January 31, 2016. The Class Notes belongs to Biol 3640 at University of Denver taught by Dr. John C Kinnamon in Fall 2016. Since its upload, it has received 17 views. For similar materials see Introductory Neurobiology in Biology at University of Denver.


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Date Created: 01/31/16
ion channels: transmembrane pores that allow the passage of charged particles into and out of the cell via an electrochemical gradient -most are distinguished based on ion specificity/selectivity, their gating mechanisms What We Will Cover Today -ion channel structure -selectivity -modes of action -sensory transduction -ligand-gated ion channel -acetylcholine receptor -voltage-gated sodium channel -voltage-gated potassium channel -black mamba -inactivating potassium channel -inward rectifier potassium channel -calcium activated potassium channel -voltage gated calcium channel -other ion channels -channelopathes (when an ion channel 'goes bad') -remember: plasma membrane is the capacitor of the cell -proteins in the plasma membrane are partially made up of ion channels -vary in appearance and structure -generally composed of subunits -five subunits: pentamer, six: hexamer -same subunit: homo- prefix -different subunits: hetero- prefix -ex: all same subunit, 6 total, = homohexamer Channel Selectivity -nonselective cations -others are very selective -sodium leak channels and voltage gated sodium channels, potassium leak channels and voltage gated potassium channels -modes of activation -activation via physical changes in the cell membrane -review voltage-activated, stretch-activated, extracellular activation -activation via ligands -review extracellular and intracellular activation -acetylcholine channel is an example of an ligand-gated ion channel -intracellular activation of the TRPV1 channel allows for binding of capsaicin and thus the spicy sensation from chili peppers -can have a general conformational change, a blocking particle, or a conformational change in one region -depolarization allows opening for a millisecond, allowing about 7,000 sodium ions to move through, and then the blocking particle inactivates the channel until it is repolarized Neurotransmitters can act on ion channels directly or indirectly -ionotropic receptors: act quickly, contrasted with a metabotropic receptor -metabotropic receptor: usually involving a GPCR, which takes time (intracellular second messenger pathways) -opportunity for amplification of the signal Sensory Transduction -ion channels are involved in sense of taste -can be direct (salt from a potato chip, immediate depolarization) -stimulus blocks ion channels in other cases (bitter or acidic flavors) -movement of ions out causes hyperpolarization, blocking the movement causes depolarization -instead of positive ions moving in, preventing the passage of ions out -sweet, umami and bitter flavors involve a G protein coupled pathway with a second messenger -umami: Japanese for "wonderful delicious", fifth primary flavor -sweet, sour, salt, bitter and umami -umami is the difference between a Dorito and a Frito -savory flavor, increases appetite for the item -Frito has no umami -sense of smell -GPCRs involved, simulate enzymes that produce second messenger which then acts on ion channels Ligand Gated Ion Channel -transmitter binds the receptor, opening the ion channel Acetylcholine Receptor -ion channel that is called a receptor -receptors work with agonists, antagonists, toxins and antibodies rather than specific properties of the ion channel -nicotinic: in postsynaptic membrane of muscles and neurons throughout Nervous Systems of vertebrates and invertebrates -receptors are activated by ACH from presynaptic nerve terminals, cause opening of nerve terminal and passage of cations -called nicotinic because nicotine has the same effect -heteropentamer, five subunits, varying type -two alpha, a beta, a gamma and a delta subunit -Ach binds to the two alpha subunits -widest part of ion channels is about 8.5nm, about the same thickness of a cell membrane -extracellular portion extends about 5nm out of membrane -central core is about 7/10 of a nanometer, but big enough for passage of cations -agonist: mimics the effects of the Ach (nicotine) ***CORRECTION SLIDE 25: NOT CAFFEINE TOO JUST NICOTINE*** Voltage-Gated Sodium Channel -m gate and h gate model -at rest m gate closed, when depolarized m gate swings open for about one millisecond and then the h gate swings closed (after passage of about ~7,000 cations) -structure in detail shows that this channel is a homotetramer (4 domains made of six transmembrane subunits, S throu1h S ) 6 -voltage gated part of each of the domains is located on segment 4 (S4) -represented by +'s -selectivity loops located on extracellular loops that connect S5 and S 6 -does not allow other cations through -the inactivation gate is located between domains 3 and 4 -depolarization of a Voltage-Gated sodium channel causes opening but at different times for different channels Sodium Channel Toxins TTX -puffer fish toxin -blocks voltage-gated sodium channels -death within 4-6 hours, known range within 20 minutes and 8 hours -100 people in japan die per year from TTX poisoning Paralytic Shellfish Toxin -red tide -produced by a dinoflagellate that is concentrated in shellfish (ex: oysters) -toxin is a saxitoxin -saxitoxin blocks sodium channels -common in shellfish -clams, oysters, mussels when red tide is present -take in dinoflagellate and concentrate it, doesn't hurt them Local Anesthetics -procaine, cocaine Scorpion Toxin -sodium channels open at rest -all nerve and muscle cells depolarized -sodium channel inactivation disrupted -extended period of depolarization Batrachotoxin-Poison Dart Frog -toxin in its skin, cause early opening and delayed inactivation of sodium channels -similar toxins in lilies (veratridine) and buttercups -Colombian frog Conotoxin -cone shells on the beach, if you step on one: -one toxin blocks voltage gated calcium channels: responsible for NT release -another blocks voltage gated sodium channels, no action potentials -another blocks Ach receptors, paralyzing muscles -takes effect in minutes, not much you can do Ciguatera Fish Poisoning -ciguatoxin: opens sodium channels -produced by a dinoflagellate algae that is eaten by reef fish -don't produce it, eat it and concentrate it, once ingested by others (humans) you can get sick due to concentrated toxin -don't eat reef fish! Potassium Channel -leak channel (RMP) and voltage-gated channel (important for repolarization of the membrane back to its resting potential) -generic potassium channel -homotetramer -looks like an inverted tepee -passage of potassium ions through this channel -hydrated and 'sloshing about' outside ion channel -when they enter they're like 'billiard balls' hitting each other and pushing each other through -lose their hydration -ion channel itself provides something like hydration for them -carbonyl groups associated with each of the four subunits -bind with unhydrated ion -sodium ion is smaller than potassium ion but the sodium ion will not pass through this channel because it is not energetically favorable -because of bond formation of potassium ion with oxygen of carbonyl on the channel where as the sodium ion cannot do this Dendrotoxin- Black Mamba -can bring death within 20 minutes -often repeats attack when threatened -aggressive nature and great speed over the ground -called black mamba because of color of inside of their mouth Some Potassium Channels Inactivate -four blocking particles that can swing in and block the channel causing inactivation -two conditions -depolarized to +50 mV -opening of channel during depolarization, closed when repolarized -hyperpolarized to -120 mV -inactivates slowly -slide 63 -no current until stimulating voltage is turned off -because it is inactivated so quickly -inward rectifier K+ channel -only opens when membrane potential is hyperpolarized -at +50 mV it is closed, but at -120 mV there is an inward current of potassium Calcium Activated Potassium Channels -can be activated by pH as well -slide 70 -VG calcium channel opened by depolarization, calcium enters cell and binds via intracellular binding mechanism to VG potassium channel allowing for repolarization of the cell -slide 71 -acetylcholine binds the Ach receptor, calcium enters the cell (sodium as well), calcium binds calcium activated potassium channel allowing passing of potassium out of the cell Voltage Gated Calcium Channels -two important jobs -provide calcium so vesicles and exocytose their neurotransmitters -key to release of NTs -calcium dependent action potentials -see slide 74, lower action potential red line represents the extended depolarization duration "shoulder" on the action potential due to calcium-dependency Other Ion Channels -don't know structure, just existence -voltage gated chloride channels: help maintain RMP -inward rectifier subunit only open during hyperpolarization of the ion channel -purinergic receptor: opened by ATP, turns out in taste cells that respond to bitter, sweet and umami; the neurotransmitter released is ATP -glutamate receptors: opened by glutamate -cyclic nucleotide-gated channel: ex: cAMP can act as a neurotransmitter and go through the ion channel Diseases Associated with Ion Channel Dysfunctions -most are genetic -periodic paralysis: when a person has a sudden onset of weakness which gradually subsides only to return later -two forms -too much potassium -onset usually in childhood -high carbohydrate, low potassium diet -too little potassium -onset usually from childhood to adulthood -low carbohydrate, high potassium diet -dietary restrictions are the way to treat these channelopathies -each caused by different genetic mutations of a potassium ion channel -Myasthenia: group of related disorders, with regards to the defects of the Acetylcholine receptor -defects cause muscle weak ness and fatigue, can be life threatening -onset in infancy -treatment: includes drugs -Malignant Hyperthermia: Ryanodine receptor, deals with calcium -controls calcium movement within muscle -triggered by exposure to certain anesthetics or muscle relaxants -causes dangerous increase in rate of activity in the muscle, sharp body temperature rise, lead to cascade of crises: heart malfunction, swelling of brain tissue and death -TAKE HOME MESSAGE: universe of ion channels, hundreds of types of sodium and potassium channels -these today were just a few of the big players!


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