Psych 2210 1st Edition Lecture 5 Outline of Last Lecture I. The Neuron DoctrineII. Cells of the BrainIII. 4 Neuron Zonesa. Inputb. Integrationc. Conductiond. OutputIV. Structure of the NeuronV. Electrical SignalingVI. Reasons for differential distribution of ionsa. Selective Permeabilityb. Diffusionc. Electrostatic Pressured. Sodium-Potassium PumpVII. SummaryOutline of Current Lecture I. Action Potential II. Local vs. Action PotentialsIII. Steps in Action Potential IV. Steps following arrival of action potential Current LectureI. Action Potential a. Rapid reversal of RMP (resting membrane potential), that is transmitted down axon toward the next neuron (now very positive)b. Changes in electrical potential lead to action potential i. Neurons receive chemical signals from nearby neuronsii. Excitatory signals depolarize the cell membrane (i.e. reduce polarization)—make inside less negativeiii. Inhibitory signals hyperpolarize the cell (increase the polarization)—makes inside of the neuron even more negativec. All inputs regulated integrated at axon hillockd. If net inputs inhibitory: no action potential e. If net inputs excitatory: action potential is triggeredThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.f. Action Potentiali. Rapid reversal of inside potential conveyed down the axon to the next neuron. ii. Triggered when membrane reaches the threshold (varies from neuron to neuron)—critical level of depolarization (about -40mV)iii. The membrane potential reverses and the inside of the cell becomes positive II. Local vs. Action Potentialsa. Locali. Graded potential: size of change in electrical potential coded by strength of input stimulus1. The greater the stimulus, the greater the change in membrane potential 2. Size diminishes as it moves away from the point of stimulation 3. Occurs at the dendritesb. Action Potentiali. The neuron fires at full amplitude or not at all—the size (amplitude) is independent of the stimulus sizeii. Rate law: info is encoded in changes in the number of action potentials—with increased stimulus strength more are produced but the size is the SAME. III. Steps in Action Potentiala. (1) Depolarization: gradual entry of positive ions due to input from other neuronsb. (2) Threshold: critical level of depolarization; causes all voltage—gated Na+ gates to open c. (3) Sodium-influx: Na+ rush in i. Pushed by diffusion and electrostatic forcesii. Membrane potential inside reversed: becomes positively chargedd. (4) Potassium-efflux: K+ ion channels open, allowing K+ to leavee. (5) Peak: point at which Na+ channels closef. (6) Repolarization: K+ still leaving axon: leads to membrane potential returning tothe negative state. g. (7) Hyperpolarization: K channels close, membrane slightly more negative than the resting membrane potential (RMP)h. (8) Sodium-Potassium Pump Kicks in: return to resting membrane potential. Action potentials spread along axon. i. Propagation: process in which depolarization travels along an axon like a wave. ii. Uni-directional: action potentials always move away from the cell body to the terminal buttonsiii. Saltatory conduction: action potential regenerated at the node of Ranvier—rapid conduction.iv. Multiple Sclerosis1. Slow or disrupted signaling due to degraded neuron2. MS—means damaged Myelin somewherev. At the end of an axon—chemical signaling through the synapsevi. Parts of the synapse1. Presynaptic membrane: on the axon terminal of the presynaptic neuron2. Synaptic cleft: a gap that separates the membranes3. Postsynaptic membrane: on the dendrite or cell body of the postsynaptic neuron.IV. Steps following arrival of action potentiala. Action Potential arrives at the presynaptic axon terminal b. Ca++ influx: voltage gated calcium channels in the terminal membrane open and calcium ions Ca2+ enter c. Exocytosis: release of neurotransmitteri. Calcium ions cause synaptic vesicles to fuse with the presynaptic membraneii. Vesicles rupture, releasing neurotransmitter into the synaptic cleft. d. Receptor binding: transmitters bind to specific postsynaptic receptor molecules, causing the opening of ion channels and leading to an EPSP (excitatory postsynaptic potential) or IPSP (Inhibitory postsynaptic potential). e. Postsynaptic potential: EPSP’s and IPSP’s spread toward the postsynaptic axon hillock—if threshold is reached, action potential will