Psyc 6 week 2
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This 4 page Class Notes was uploaded by Sabrina Straus on Monday September 19, 2016. The Class Notes belongs to PSYC 6 at Dartmouth College taught by Catherine Cramer in Fall 2016. Since its upload, it has received 4 views. For similar materials see Introduction to Neuroscience in Psychology (PSYC) at Dartmouth College.
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Date Created: 09/19/16
4. 9/16/16 Class Notes NEURONS IN ACTION I. n vitro stimulation studies Hyperpolarization: put in negative current and makes the cell more negative Depolarization: positive current/move cell closer to zero> threshold at around 55> action potential> after potential (hyperpolarized region) graded potentialssize affects amount of current you put in (degrade overtime) action potentials: makes nervous system work ~rest: 60 II. Properties of action potentials (APs) ~same shape: threshold> hyperpolarize> back to same shape A. Threshold: cell will produce action potential if met B. Size of APs: allornone: doesn’t degrade over time C. Frequency of APs absolute refractory periodcannot fire another action potential relative refractory period: hyperpolarized and takes more depolarizing input to get the cell through threshold III. n vivo neural functioning A. Propagation of APs down the axon B. Graded potentials excitatory postsynaptic potential (EPSP): depolarizing response inhibitory postsynaptic potential (IPSP): one cell has an action potential measured in axon but at synapse with another cell there is a hyperpolarization ~both at same time: cancel out >add up EPSP and IPSP spatial summation: graded potentials degrade over distance//inputs on ends of dendritic tree have less of an impact than those closer to axon hillock temporal summation: has to overlap in time IV. Ionic bases of axonal transmission: based on excitable channels A. Sequence of events in the generation of an action potential 1. Voltagegated Na+ channels open w/ stimulant and action potential is reached > inflow of Na+ because electrostatic and diffusion pressure > peak of action potential And potential becomes 62 Eion (dynamic equilibrium) but gate closes quickly 2. Voltagegated K+ channels open > outflow of K+ > hyperpolarization to 80mV}after potential 3. Resting potential restored V. Propagation of the AP along an axon progressive depolarization by progressively opening sodium channels followed by hyperpolarizing the channels (progressive due to unmyelinated axon in nonvertebrates) factors affecting rate of conduction: myelin> can jump node to note (where the voltage channels are/ moves as a graded potential through myelin and action potentials at nodes aka nodes have to be close together) diameter of axonmakes a difference in unmyelinated axon>more surface area=faster myelination saltatory conduction (graded potential and action potentials) ~action potentials are the only way neurons can send signals over long distances Chapter Notes Chapter 4: Action Potential/spike/nerve impulse/discharge ~signal that conveys info over distances *at rest the inside of the neuronal membrane is negatively charged but the action potential reverses this properties >Ups and downs of action potential ● At rest: voltmeter is 65mV ● Action potential: oscilloscope ○ Rising phase: rapid depolarization of the membrane 40mV ○ Overshoot: inside of neuron is positively charged ○ Falling phase: rapid repolarization ○ undershoot/ afterhyperpolarization: the inside is more negative than the resting potential >generation of action potential ~pain is felt when action potentials are generated in certain nerve fibers in which a gated sodium channel opens when the nerve ending is stretched> Na+ crosses the membrane through channels and depolarizes the membrane making the inside less negative (generator potential)> critical level or threshold> action potential Causes of depolarization: ● Entry of Na+ through specialized ion channels sensitive to membrane stretching ● Interneurons: caused by Na+ entry through channels that are sensitive to neurotransmitters released by other neurons ● Injecting electrical current through a microelectrode >generation of multiple action potentials through passing a continuous depolarizing current ● Rate depends on magnitude of current (firing frequency) ● Absolute refractory period: max firing frequency (1000Hz) > min period 1msec ● Relative refractory period: time in between action potentials >optogenetics: introduces into neurons foreign genes that express membrane ion channels that open in response to light ~photopigments=light energy absorbed by proteins action potential in theory: redistribution of electrical charge across the membrane in which depolarization of the cell during the action potential is caused by the influx of sodium ions across the membrane, and repolarization is caused by the efflux of potassium ion >membrane currents and conductances ~idealized neuron protein molecules in membrane 1. Sodiumpotassium pumps 2. Potassium channels 3. Sodium channels ~pumps work continuously to establish and maintain concentration gradients 1. K+ inside and Na+ outside 2. K+ moves outside as an electrical current ~I ion = g ion (V m E ion ). >ins and outs of action potential ● Membrane of ideal neuron is only permeable to K+(fall) but if you open the pump Na+ (rise) goes to the inside which depolarizes the neuron (reversing membrane potential) ~summary: When the membrane is depolarized to threshold, there is a transient increase in g Na (depolarizes the neuron) and allows entry of Na+>action potential>Restoring the negative membrane potential w/ increase in g K during the falling Phase (K+ leaves) Action potential in reality ~voltage clamp: measures membrane conductance at different potentials >voltagegated sodium channel: protein forms a pore (selective to Na+) which opens and closes based on changes in membrane voltage ● Sodium channel structure: single long polypeptide (4 domains clump together to form a pore)> pore is closed at negative resting potential> depolarized and pore opens to Na+ ○ Functional properties of the sodium channel: 1. Open with little delay 2. Stay open for 1msec 3. Cannot be opened again until membrane potential returns to negative value near threshold ○ Effects of toxins on sodium channel ■ blocks the sodium channel ● Tetrodotoxin ● Saxitoxin ■ Effect opening of channels ● Batrachotoxin channels open at more negative potentials and stay open for longer ● Veratridine ● Aconitine ■ Inactivation of channel ● Voltagegated potassium channels: Delayed rectifier ~terms: • Threshold : membrane potential at which enough voltagegated sodium channels open so that the relative ionic permeability of the membrane favors sodium over potassium. • Rising phase : inside of the membrane has a negative electrical potential>driving force on Na >Na rushes into the cell through the open sodium channels>depolarization • Overshoot: membrane potential goes to a value close to E Na (greater than 0 mV) • Falling phase: voltagegated sodium channels inactivate >voltagegated potassium channels open (triggered to do so 1 msec earlier by the depolarization of the membrane)(driving force on K when the membrane is strongly depolarized)>K rushes out of the cell through the open channels>membrane potential =negative again. • Undershoot: The open voltagegated potassium channels add to the resting potassium membrane permeability>membrane potential goes toward E K> hyperpolarization relative to the resting membrane potential until the voltagegated potassium channels close again. • Absolute refractory period : Sodium channels inactivate when the membrane becomes strongly depolarized (cannot be activated again) + another action potential cannot be generated until the membrane potential becomes sufficiently negative to deinactivate the channels. • Relative refractory period : The membrane potential stays hyperpolarized until the voltagegated potassium channels close (more depolarizing current is required to bring the membrane potential to threshold) action potential conduction down the axon ~When a patch of axonal membrane is depolarized sufficiently to reach threshold, voltagegated sodium channels pop open, and the action potential is initiated rate = 10m/sec ● Orthodromic conduction: action potentials conduct in one direction (soma to axon terminal) ● Antidromic conduction: backward propagation >factors influencing conduction velocity: two paths/ increases with increasing axonal diameter 1. Down the inside of the axon 2. Across the axonal membrane: if axon is narrow and many pores ~smaller axons require greater depolarization to reach action potential threshold >myelin and saltatory conduction: wraps axon/ consists of many layers of membrane ● Schwann cells: peripheral nervous system ● Oligodendroglia: central nervous system ~facilitates current flow down the inside of the axon=increasing action potential conduction velocity ~sodium channels are in nodes> allows for saltatory conduction (skipping node to node) action potentials, axons, and dendrites ● Spikeinitiation zone: axon hillock of soma where the axon originates ○ Usually occurs near sensory nerve endings ~depolarization of dendrites and soma from synaptic input leads to action potentials >synaptic transmission: transfer of info from one neuron to another