Week 2 Notes
Week 2 Notes psych 115
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This 9 page Class Notes was uploaded by rallen17 Notetaker on Friday April 8, 2016. The Class Notes belongs to psych 115 at University of California - Los Angeles taught by Kennedy, P.J. in Spring 2016. Since its upload, it has received 20 views. For similar materials see Principles for Behavioral Neuroscience in Psychlogy at University of California - Los Angeles.
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Date Created: 04/08/16
115 week 2 Monday Neurophysiology Generation, transmission and integration of neural signals - Neurons communicate by electrical signals (changes in electrical charge and chemicals in form of neurotransmitters) - Action potential: rapid electrical signal that transfers to target neuron Dendrites - Receive information through receptors located in cell membrane - Receptors: receive - Once signal is received, the signal is sent to cell body, which at axon hillock may or may not generate action potential - Electrical signal travels along axon, whichis myeinate or unmyelinated - Signal comes down to axon terminal - When electrical signal reaches terminal, turns into transmitter Overview of today - Resting membrane potential - Post-synaptic potential: what happens on receiving neuron. (receiving). This may or may not become action potential - Action potential Before understanding membrane potential, we must understand cell membrane Cell membrane - Lipid bilay: 2 layers of fatty moelcules, hydrophobic (it repels water) - Proteins: can be transporters, channels, receptors, - Channels: pores in membrane that can pass ions in membrane - Ion channels: pores that enable ions (small charged particles) - Transporters require energy Resting membrane potential - At rest: electrochemical forces - Ions: electrically charged molecules, anions are negatively charged cations are positively charged - Ions are dissolved in intracellular fluid, separated from extracellular fluid by cell membrane - Resting membrane potential: the electrical potential different. o Neuron at rest: positive potassium inside, negative inside o Ouside: Na+, Cl- o Greater potassium inside at rest, more sodium and chloride outside at rest o Resting potential is -70 microvoluts The difference in electrical charge between inside of neuron and extracellular space How can we measure this? Put electrodes in extracellular space and one inside neuron, voltage drops to -60. -60 is resting membrane potential What establishes resting membrane potential? 1. Concentration gradients 2. Electrostatic pressure 3. Membrane permeability 4. Active ion transport 1. Concentration gradients a. Particles want to move to lowly concentrated areas i. Diffusion ii. Chemical driving force b. Concentration gradient exist across membrane 2. Electrostatic pressure a. “opposites attract” i. Like charges repel each other ii. Opposite charges attract each other b. Sodium moves inside, chlrodide ..? She messed up, email her to clarify what moves where 3. Membrane permeanabillity a. Factors into these different forces b. Sensivite to the membrane potential, charges c. Ion channels open when membrane potential is moved from resting state d. At rest, sodium channels mostly closed, they require 50 mV to open e. At rest, sodium channels are closed, they require a more positive membrane potential f. At rest, potassium channels are open, g. At rest, cl- cannels are open (-70 mV or higher so approaching 0) 4. Active ion transport a. Na+/K+ pump counteracts i. Without it, K+ in cell would become depleated b. ATP provided by mitochondria c. Na+/K+ provides mechanism to counteract K+ leaving out What is really happening at rest: K+ - K+ wants to leave - Passive concentraton gradient (more K+ inside) - Pressure from concentration gradient is greater than pressure provided by electrostatic difference - Greater force pushes K+ out than what keeps it in What is really happening at rest with Cl- - Cl- is in equilibrium - Electrostatic pressure forces Cl- out (more – on inside) - As Cl- accumulates outside, passive concentration gradiuent moves it back inside - Cl- channels are open at rest so no resistance to them crossing the membrane What is really happening at rest: Na+ - Na+: wants to enter - Passive concentration gradient (more Na+ outside). Free movement of ions. - Even though greater force pushing sodium inside, it is pushed out with sodium potassium pump - At rest, channels closed - At rest o Electrostatic pressure, concentration gradients - Sodum: pushed out with pump Neuron-neuron communication - If positive ions eneter, membrane potential becomes more + - “post synaptic potentials” The synapse - Synapse: communication between axons and dendrites - Synaptic cleft: space between neural processes Electrical effects of receptor activation - Two main electrical effects o Hyperpolarization: membrane potential becomes more negative o Depolarization: membrane potential becomes more positive Efflux of negative ions, influx of positive ions - Postsynaptic potentials (PSPs) are brief changes in the resting potential results from synaptic input - IPSP: produces a small hyperpolarization - EPSP: depolarizing effect – produces a small local depolarization - See written notes from ehre Week 2 Wednesday 115 lecture Neurophysiology II Action potential propagation, neurotransmitter binding Review - Neurons use electrochemical signaling to transmit - Electro= flow or ions, chemical= binding - The axon terminal is where electrical signal changed into chemical signal Parts for neuron - Axon: where integration happens - Neurons integrate inputs they receive (temporal and spatial summation) - All the postsynaptic inputs are all integrated o Determines if something fires or not - Absolute refractory period: neuron cannot fire another action pot in certain space - Relative refractory period: neuron can fire another potential, but requires more depolarization Ion channel activity - At rest: o Sodium closed o Leaky potassium channel open - Depolarization o Gain of + or loss of – - Threshold o Sodium opens, potassium still open o Influx of sodium-> depoarlization +50 mV - Descending o Potassium are leaky and voltage gates potassium open Drives membrane back down (+ are leaving) o Sodium channel inactive o Potassium slow to close-> continuous loss-> back to rest Propagation of action potential - Distance traveled related to - No degradation of action potentials, they are actively propagated Velocity of action potential - Affected by o Thickness o Myelination Insulation Think about electricity Think about wires (they are fast) Allows salutatory conduction (talked about later): this is at breaks in myelination. So action potential jumps various distances o Fastest at 200 miles per hour Cells of the Nervous System - Glial cells o Breakdown transmitters, produce myelin, exchange nutrients and other materials with neurons o ? - Astrocytes o Largest glial cell o Star shaped o Send projections to capillaries o Connect neurons to capillary systems that allow for maintainence of health of neurons o Take up and release neurotransmitters - Microglia o “super cool” o In response to injury o They will remove debris o Involved with forming scars o When injury occurs Microglia will invade site of injury and will clean up Associated with neural pain and synapse maintainence o Schwann cells VS oligodendrocytes Schwann: incapsulate the neuron Mytelination: speed up electrical signal Salutatory conduction: jumping or electrical signal from node to node - Propagation of action potential o In unmytelinated axon Slower (10 meters per second) We have channels all along this axon When sodium enters (due to depolarization), that depolarization spreads to adjacent regions, that entry It propages in one direction because of the refractory period o In myelinated axon Can propagate in 150 meters per second Nodes of ranvier occur every 1 mm so action potential can just jump over (not regenerated at every spot?) No ion channels- no leakage of potassium- further improves amount of depolarization Next node= large amount of ion channels Disorder Affecting Myelination - Disorder where immune system attacks myelin - Myelin is fatty and appears white - Loss of myelin, there are motor imparments, neuron death, possible death, weakness, paralysis Neuron-neuron communication - See diagram - Synaptic cleft: space between - Presynaptic neuron: packages - Action potential arrival-> vesicle release-> signal received Different types of configuaration - Axo-axonic: axon to dendrite (primary) o Can increase signal coming from descending neuron o Can affect amount of neurtrans? o Can decrease signal coming from the two cells as well - Axo-somatic: Imput location and strength - Inversely proportional - Signal diminishes as it travels (I thought this didn’t happen??) Neurontransmitter release-transmission at chemical synapses - Axon terminal: point at which electrical signal changed into chemical Neurotransmitters - Synthizes and released by neuron - Two categories o Large: made in cell body and sent to axon terminal for use o Smaller: (aceylcholine etc) made in terminals, enzymatic, - Release o Happens when a vescicle dumps into synaptic cleft - When the action potential arrives at axon terminal, that travelling depolarization causes opening of voltage gated - Influx of neurons allow it to fuse and release neurotransmitter - Neurotransmitter binds to post synaptic cell o Allows spread of EPSP or IPSP Exocytosis - Happens through fusion t - 1. Mobilized vesicles translocate to the terminal plasma membrane where they selectively dock close to the active zone - 2. Docked vesciles then undergo a priming step, during which ? - ? - ? - Postsynaptic potentials are graded - Actioni potential is all or none - The more action potentials, the more neurotransmitter release - Requency of action potential controls volume of signal Ending Neurotransmission - You want cells to be able to have open communication - In synaptic cleft o Enzymes released and clean out excess neurotransmitter o There is also neurotransmitter removal Transporters reuptake excess neurotransmitter o Diffusion Neurotransmitters simply move out of the synaptic cleft; minor mechanism in CNS Preventing neurotransmitter release - Normal behavior requires precise timing - Synthesizing enzymes help make neurotransmitter - When neurotransmitters are realese, there are autoreceptors - Autoreceptors: bind neurotransmitter that has been released and the can alter calcium and alter exocytosis - Autoreceptor activation; breaking mechanism Neurotransmitter action on the post synaptic neuron - Neurotransmitter release and recognizes and bind to receptors to open on post synaptic cell - These signals are stopped by these neurotransmitters on the receptors being degraded Transmitter receptors - 2 types o 1. Ionotropic receptors Ligrand gated ion channel Can recognize and bind to another molecule (other molecule is receptor) Fast transmtion Neuro? ? o 2. Metabotropic receptors Indirectly linked with ion channels Slower than ionotropic! Sampel: GPCR’s Slower Members of complex recognize and bind to ? located in vicinity Slower due to second step Second messenger: slow acting signaling moelcuel that amplifies and prolongs the effects of synaptic activity Slower to come on and also slower to turn off The effects of the neurotransmitter needs inaciviation of G protein and degradation of second messenger Can be amplified G protein coupled receptor activation - G proteins before activated are alpha, beta, gamma subunit o Alpha coupled to gdp - When neurotransmitter binds o GDP traded for GTP, these involved in metabolic reactions This causes alpha and beta to separate and then interact with their targets These are affectors - It is an affector Review - Ionotropic: fast - Metabotropic: slower o Secondary mechanism Transmitter reeptors- recognition - “key and lock” o Can have different effect depending on type of thing it binds to - Ex: Ach o Indogenous (produced in body) o In PNS, motor neurons, throughout brain o When ACH binds to recognition domain, - Knee jerk reflex (with Ach) o Sensory neuron, synapse, motor neuron requires o 40msec response time o Unipolar (only one projection) o Synapses in ventrical horn o aCh activates muscls - Curare o Exogenous ligand, recognizes and blocks cholinergic receptors (receptor antagonist) o Binds and prevents indogenous Ach, making neurotransmitter unable to perform function o Leads to paralsysis Neurotransmission- electrical synapse - Allows for populations of cells to activate at same time - Ions flow freely - 0 time delay Measuring electrical activity in the brain - EEG - Electroencephalogram - Used to diagnose certain types of brain injury - Measures changes in populations of neurons - Seizure o Massive activation across the brain o Neurons firing at very high frequencies o Some forms are result of problems with ion channels (genetic mostly) o During seizure, consciousness can be lost, violent muscle contraction o Patient might scream right before Muscles seize Aura: right before, they see or smell something In vivo electrophysiology- featuring bernard - Allows us to see how brain comutes experience - Bernard runs around an environment looking for sprinkles, o One neuron fires when he is in certain spots - Fire in tiny pockets of space - Single hypocampal neuron, EEG biofeedback - Train your brain - Person asked to use brain not touching anything to play videogame, they get rewarded when they are trained to do certain things Menipulating neuronal activity - Optogenetis o Alters electrical signalsing (alters ion channels) o Opsin: ion channels or pumps that can e activated in response to light, found in eyes, packaged up in o Sensory photoreceptors: found in some algae - Channel rhodopsin: receptor that passes + ions o Sensivite to blue (opens with blue light) - Halo rhodopsin: allows entry of chloride which inhibits neuron - Manipulating neuronal activity o Optogenetics o By using laser LED, we can artificially activate them o Think about the mouse direction of walking can turn right or left Manipulatig neuron activity - Chemogenetics- uses designer receptors exclusively activated by designer drugs (DREADDs) - CNOxide: - Can activate or inhibit neuorns - Can only activate in presence of plausopine or oxide - When CNO in system, neurons are either inhibited or activated o
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