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Notes 1/11-1/15

by: Joseph Merritt Ramsey

Notes 1/11-1/15 nsci 4340

Joseph Merritt Ramsey
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1/11 - Neuron Properties 1/13 - Action Potential 1/15 - Neurotransmitters
Neurobiology of Disease
Dr. James Cronin
Class Notes




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This 22 page Class Notes was uploaded by Joseph Merritt Ramsey on Tuesday January 19, 2016. The Class Notes belongs to nsci 4340 at Tulane University taught by Dr. James Cronin in Spring 2016. Since its upload, it has received 46 views. For similar materials see Neurobiology of Disease in Neuroscience at Tulane University.


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Date Created: 01/19/16
January 11, 2016 Membrane Physiology: A Review  Brief Neuron Breakdown and Review o Overall Diagram  Contains an Integrative, Conductive, and Output Region o Electrode Diagram and Components  Differential Amplifier  Reference Electrode  Oscilloscope  Time Plotted vs. Voltage  Manipulator (in mV)  External Electrode  Maintenance of Membrane Potential o Potentials Creating a “Steady State”  A function of the Electrical Gradient coming to balance the Chemical Gradient  Diagram – the flow is steadied only with a charge present o Potassium Example and the Nernst Equation  The Nernst Equation can be used to describe Ion Potential (Eion)  Potassium’s example shows the linear relationship of concentration differences and Membrane Potential (V ) m  Voltage Clamping Experiments – the voltage can be clamped so the Membrane Potential is at a different level to see how ion flow changes  Diagram o Ohm’s Law and Membrane Potential  Seen through Current Clamping – here the current is manipulated and changed to see how the Membrane Potential (Vm), which is Voltage, changes  Ohm’s Law ???? = ???????? Or ∆???? = ????∆????  Diagram – shows how the response to the stimulus is proportionate until action potential is reached  Therefore: Ohm’s Law only describes passive properties of cellular response  What is Steady State? o Ion Potentials (E ion from Nernst Equation ENa 56mV EK -102mV E -76mV Cl ECa 125mV o Goldman-Katz Equation  Permeability is also important though  If a particular ion is more permeable, then it will contribute more to the overall Voltage of the cell  Goldman-Katz takes into account permeability of the given ion to determine the V of the cell m  The membrane is most permeable to Potassium (K)  Equation ???????? ????([????] ???? + ????([????????] ???? + ????([????????]????) ???? (????([????] ) + ????([????????] ) + ????([????????] ) ≈ = 62???????? ???? ???? ????  What Does Elevated Potassium do to the Cell System? o Hyperkalemia – excess Potassium is present causing an overall depolarization of the cell o The increases presence of K changes the Concentration/Chemical Gradient  With more K outside, less K will leak outward through Leak Channels  Leak Channels are incredibly important to maintaining the delicate Steady State of the Cell  Fewer K Ions leaking out of the cell causes an increased number of positive ions inside the cell  Effects of Capacitance and Resistance o Capacitance: measured with the Time Constant (τ)  Capacitance is displayed as the Shape of the Wave in the Cellular Response  Independent of Distance (at a given point), how much time for the charge to degrade by 63%?  Asking how much charge can be stored at a given point?  Measured with Membrane Capacitance and Membrane Resistance o Resistance: measure with the Distance Constant (λ)  Resistance is displayed as Amplitude in the Cellular Response  Independent of Time, how much distance for the charge to degrade by 63%?  Asking how much charge is lost as the charge travels?  Measured with Axial Resistance and Membrane Resistance January 13, 2016 Action Potential: A Review  Axon Recording o Original Recording  Analog Sine Function – recorded with every two milliseconds o Overall Diagram o Some Popular Techniques  1) Voltage Clamping – the voltage is held at a given point (Command Voltage, V )cand the amplifier records the counter current to observe the cell’s response  2) Patch Clamping – a single “patch” (can be one channel, can be multiple) is manipulated with a microelectrode  Discovery of Action Potential Components o Using Voltage Clamping to Initially Discover the Action Potential  Diagrams o Various Manipulations to Demonstrate the Underlying Currents  1. Removal of Ions  2. Current and Conductance Components (show the delays)  3. Various Voltage Clamps (Different Membrane Potentials) o Summary of Conductances  Na: fast acting (onset and offset), two gates for activation and inactivation  K: slow acting (onset and offset), slow nature gives rise to undershoot, one gate for activation  Results in Refractory Periods  Absolute – the sodium gates are closed (inactivated) because of voltage interactions, so an AP cannot occur  Relative – after a given voltage, the sodium gates will open back up, theoretically allowing for an Action Potential, but Potassium’s slow nature continues to hyperpolarize the cell, demanding a stronger signal to fire again  Action Potential Propagation o Diagram: Active vs. Passive Signals Passive Displays a Time Delay and a Fading of Strength Active Displays a Time Delay and the Same Strength o Application: Physiatry o Propagation  1. Process  The interaction of active and passive signals that move down the axon  It’s a regenerative process  The gates prevent antidromic movement of the charge up the axon  2. Speed – two factors  I. Diameter – a thicker diameter allows for an increased capacitance, which retains the charge for a longer time  II. Myelin – gives rise to Saltatory conduction with the signal jumping from node to node o C5ers (pain neurons) are unmyelinated o Lacking Myelin decreases resistance drastically and demands a huge capacitance for anything to happen  Channels o Here Patch Clamp Techniques are used to see channel effects  Diagrams (microelectrodes are always used and a slight suction is applied to fully clamp) o Various Modifications  1. Single Channel  Frog oocytes are often used for easy access  Use PicoAmps (10 -1) to record  The reading is a bunch of steps, each one revealing the linear and constant nature of a single channel  2. Multiple Channel  When multiple channels are present, a stairstep sort of composition is made  Summating the entire cell’s channel makeup results in the smooth signature curve o Channel Components  Numerous transmembrane components January 15, 2016 The Synapsel: A Review  Synapses o Electrical – direct connection  Incredibly rapid, almost instantaneous (Diagram)  This is a more primitive form of a synapse due to the lack of ability to modulate in different manners  So gap junctions are more prevalent in reflexes and older neurological structures  Their modulation occurs by opening and closing based on environmental ion concentrations, so not as specific or narrow as Chemical Synapses  Comprised of Six Connxins that make up a Connexon  A collection of connected cells forms a Syncytium  Dye coupling can be used to view the Gap Junction and which cells utilize electrical synapses because the dye simply diffuses through o Found in smooth muscles (heart, intestines) o Chemical – outside actor  Diagram  11 Steps For Synaptic Transmission (and Diagram)  1. Transmitter Synthesized  2. AP Arrives at Presynaptic Terminal  3. Depolarization Open the Voltage-Gated Calcium Channels  4. Influx of Calcium into the Cell  5. Intracellular Calcium Causes Vesicles Fusion with Presynaptic Membrane  6. Transmitter is Released Into Synaptic Cleft  7. Transmitter Binds to Receptor Molecules  8. Receptors are Ligand-Gated Channels or Start Signal-Transduction Cascade  9. Post-Synaptic Current Causes IPSP or EPSP  10. Retrieval of Vesicular Membrane from Plasma Membrane  11. Transmitter is Inactivated  Drugs that Attack at each stage  1. Transmitter Synthesized o Methionine Sulfoximine Inhibits Glutamine Release (step in synthesis of Glutamate and GABA) o Carbidopa inhibits the synthesis of Dopamine in the periphery so L-Dopa treatment reaches the CNS for Parkinson’s  2. AP Arrives at Presynaptic Terminal o Novacaine is a Sodium Channel Blocker, so AP doesn’t propagate into the Terminal (local anesthetic)  3. Depolarization Open the Voltage-Gated Calcium Channels o  4. Influx of Calcium into the Cell o  5. Intracellular Calcium Causes Vesicles Fusion with Presynaptic Membrane o Alpha-Latrotoxin from the Black Widow causes Ca independent firing with (causes convulsions)  6. Transmitter is Released Into Synaptic Cleft o Tetanus Toxin blocks GABA release so inhibition is lessened (causes convulsions)  7. Transmitter Binds to Receptor Molecules o Mirapex Binds and activates Dopamine receptors (Parkinson’s Treatment) o Diazepam (Valium) is a GABA agonist, so it enhances inhibition, helps with anxiety and epilepsy o Clozapine is serotonin receptor agonist used as an antipsychotic  8. Receptors are Ligand-Gated Channels or Start Signal- Transduction Cascade  9. Post-Synaptic Current Causes IPSP or EPSP  10. Retrieval of Vesicular Membrane from Plasma Membrane  11. Transmitter is Inactivated o SSRI’s inhibit Serotonin reuptake which helps treat depression o Cholinesterase inhibitors retain certain levels of AcH in the cell  Mechanisms of Neurotransmitter Release o Calcium Dependent  Calcium is crucial to AP firings and transmitter release (Calcium channels blocked with Cadmium to see) o A View of Calcium on the Membrane  Vesicle Proteins: *synaptotagmin, synaptobrevin  Membrane Proteins: syntaxin, SNAP-25  Docking most certainly occurs before Ca binds to prepare the vesicle for release o Toxins Altering the Calcium Channel  1. Botulism – cleaves parts of synaptic membranes  Botulism cleaves membrane proteins which causes inefficient firing and thus droopiness and slurred speech  2. Tetanus - cleaves parts of Synaptobrevin  Tetanus blocks release of Inhibitory neurotransmitters specifically, causing overexcitation and convulsions  3. Alpha-Latrotoxin from Black Widow causes Calcium independent release and convulsions  Discovery of the Neurotransmitter o Otto Loewi’s Experiment  Two chambers with Frog Heart with Vagus Nerve in tact  Stimulate one chamber and the other had a response as well, with a slight delay  Determined it must be a Chemical actor  Looking at Types of Neurotransmitters (All Small Molecule Type) o 1. Biogenic Amines  Catecholamines  Pathway  Vesicular Monoamine Transporters (VMATs) o VMAT1 – Adrenal Cells o VMAT2 – Catecholamine and 5-HT Neurons o VMAT2 Inhibitors Block Catecholamine Transmission, reducing activation (Reserpine is a common drug)  Stops Dopamine from being transferred and becoming Epinephrine, ceasing excitation  This is used for high blood pressure and psychosis  Inactivation o 1. Diffusion o 2. Reuptake – catecholamine reuptake is relatively nonspecific, coupled to Na Gradient  DAT (Dopamine Transporter)  Cocaine increases extracellular Catecholamines and 5-HT  Clocks reuptake through DAT  NET (Norepinephrine Transporter)  Worked on by Tricyclic Antidepressants (Elavil, Tofranil) o 3. Enzymatic Inactivation  MAO’s (Monoamine Oxidase degrades transmitters)  MAO –ANE and 5-HT o MAO InhAbitors (Clorgyline) can be used as antidepressant  MAO – o-phenylethylamine (which B results in NE or Epi release) o MAO inhBbitors (Deprenyl) are used in Antidepressants as well  COMT (Catechol-O-methytransferase)  Deactivates DOPA  COMT inhibitors help increase Dopamine concentration in conjunction with L-Dopa Treatment  Serotonin  Pathway  Transport o VMAT2 transports 5-HT into the vesicles  Inactivation o 1. Reuptake – done through SERT (Serotonin Reuptake Transporter)  Drugs known as SSRI’s (Selective Serotonin Reuptake Inhibitors)  Antidepressants by stopping SERT from removing Serotonin, therefore prolonging the effects  Citalopram (Celexa, Cipramil, Emocal, Sepram)  Escitalopram oxalate (Lexapro, Cipralex, Esertia)  Fluoxetine (Prozac, Fontex, Seromex, Seronil, Sarafem, Fluctin)  Fluvoxamine maleate (Luvox, Faverin)  Paroxetine (Paxil, Seroxat, Aropax, Deroxat)  Sertraline (Zoloft, Lustral, Serlain) o 2. Enzymatic Inactivation (done by MAO ) A  Histamine  Pathway  Transport – done by VMAT  Inactivation o 1. Enzymatic Inactivation – done by MAO  Antihistamines which cross the Blood Brain Barrier (BBB)  Antagonists can also be used to counteract the Vestibular Hypothalamic Pathways o 2. Amino Acids  GABA  Pathway  Transport – Vesicular Inhibitory Amino Acid Transporter  Inactivation o 1. Reuptake – GAT (GABA Reuptake Transporter) o 2. Enzymatic Inactivation (Degraded by GABA-T (GABA transaminase))  GHB works on GABA-T to stop GABA degradation, which causes euphoria, memory loss, “date-rape” drug  Receptors – GABA receptors increase Cl- conductance, I GABA rMceptors increase K (through GIRK channels) o Benzodiazepines – GABA agonists, antianxiety o Barbituates – GABA agonists, anesthesia  Glutamate  Pathway  Transport – trnasported into vesicles by Vesicular Glutamate Transport (VGluT)  Inactivation o 1. Reuptake – done through EAAT (Excitatory Amino Acid Transporters)  Located on neurons and Glia  Receptors o 1. AMPA – o 2. NMDA – Voltage sensitive Mg block Na/K channels that also increase Ca conductance and memory o 3. Kainate o 4. Quisqualate  Astrocytes’ Contribution  1. Glutamate/GABA released during synaptic activity  2. Glutamate/GABA taken up by astrocytes (EAAT)  3. Glutamate/GABA broken down into Glutamaine  4. Glutamine released by Astrocytes  5. Glutamine taken up by neurons, converted back to Glutamate/GABA (VGluT or VIAAT) o 3. Acetylcholine  Pathway  Transport - moved into vesicles by Vesicular Cholinergic Transporter (VAChT)  Inactivation  1. Enzymatic Inactivaiton – done extracellularly through Acetylscholinesterase (AchE) o Breaks AcH into Choline which is taken back into the cell  Cholinesterase Inhibitors  1. Sarin – chemical warfare causing convulsions  2. Malathion – insecticide to control fruit fly and mosquito  3. Neostigmine – improves muscle tone and ability in patients with MG


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