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Psyc 220 Week 3 Notes

by: Lynde Wangler

Psyc 220 Week 3 Notes PSYC 220

Lynde Wangler
GPA 3.836

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Chapter 2: Synapses and Synaptic Transmission, Neurotransmitters, etc.
Meghan Jones
Class Notes
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This 3 page Class Notes was uploaded by Lynde Wangler on Sunday January 31, 2016. The Class Notes belongs to PSYC 220 at University of North Carolina - Chapel Hill taught by Meghan Jones in Spring 2016. Since its upload, it has received 17 views. For similar materials see Biopsychology in Psychlogy at University of North Carolina - Chapel Hill.


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Date Created: 01/31/16
PSYC 220 WEEK 3 Lecture 1/27/16 (review) Nerve Cells& Nerve Impulses  Molecular Basis of the Action Potential:  Resting membrane potential (-70mV); maintained by sodium- potassium pump; more internal potassium and external sodium  Leaky potassium channels are open and some sodium channels are open allowing the membrane to depolarize slightly  BUT THEN  The threshold of excitation is reached and the neuron depolarizes when voltage-gated sodium channels allow sodium to flood into the cell  Membrane potential continues to rise and reaches reversal of potential (overshoot) when the relative charge of the inside is more positive than the outside  At this point voltage-gated potassium channels open and K+ floods out into the extracellular space repolarizing the cell; also at this point sodium channels are DEACTIVATED (not closed)resulting in absolute refractory period  K+ continues to leave the neuron resulting in an undershoot and sodium channels reset (relative refractory period); another action potential can be generated but greater stimulation is required  Resting potential is restored  Manipulating Action Potentials: o Scorpion venom keeps sodium channels open; excess sodium is toxic o Local anesthetics block sodium channels preventing an action potential from occurring  Sodium-Potassium Pump: maintains resting membrane potential; exchanges internal sodium for external potassium (think salty banana – potassium in the cell and sodium in the extracellular fluid)  The All-or-None Law: the magnitude of the action potential is not dependent upon the strength of the stimulus; once the threshold of excitation has been met, an action potential will fire with an invariable magnitude that will not decay as it travels down the axon due to saltatory conduction when action potentials jump from node (of Ranvier) to node  Why Don’t Action Potentials Travel Backward? – voltage-gated sodium channels in the membrane where the cell has already been depolarized are inactivated for just long enough that there are no longer any sodium ions to (re)depolarized the neuron; absolute refractory period  Propagation of an Action Potential: thicker axon = faster conduction; myelination = faster conduction Lecture 1/29/16 Synapses  Myelin Sheath – increases membrane resistance (ions do not leak out across the membrane from the inside); decreases membrane capacitance; allows action potential to jump from node to node without losing magnitude  Synapses – chemical (as opposed to electrical) transmission was not widely accepted until the 1950s Charles Sherrington coined the term synapse in 1906: o Studied reflex arc-circuit (consists of sensory neuron, interneuron, and motor neuron); 3 observations:  Reflexes are slower than conduction along an axon (something was slowing the information to the muscles)  Weak, subthreshold stimuli could cause a reflex when combined together (EPSPs & IPSPs by temporal and/or spatial summation)  One set of muscles is excited while one is inhibited (studied dogs’ flexor and extensor muscles of the legs and found that when one flexed, the other three extended and the flexor muscles relaxed)  Characteristics of Electrical Signals of Nerve Cells Action Conduction Overshooting All-or-none First Na+ Voltage- Potential along axon then K+ gated channels EPSP Transmissio Depolarizing Graded Na+ K+ Chemically n between regulated neurons IPSP Transmissio Hyperpolarizi Graded K+ Cl- Chemically n between ng regulated neurons o EPSPs and IPSPs alter the spontaneous firing rate of neurons (neurons are always active)  Otto Loewi – proved that chemical communication occurs across synapses; stimulated the vagus nerve of a frog heart and then put a different heart in the solution that the first heart was in and observed the same effects cannot harness loose electricity so it must have been chemical  Steps of Synaptic Transmission:  1) Neurotransmitters are synthesized in the presynaptic cell and packaged in vesicles  2) Action potential causes Ca2+ to enter prompting exocytosis of the vesicles, releasing the neurotransmitters into the synaptic cleft  3) Neurotransmitter binds to receptor on postsynaptic cell causing a variety of effects (depending on the neurotransmitters and receptors)  4) Neurotransmitters release from receptors and is taken back to the presynaptic cell by transporter proteins  5) Postsynaptic cell releases retrograde transmitters signaling the presynaptic cell to limit release of further neurotransmitters  6) Negative feedback sites on presynaptic cell respond to retrograde transmitter  Neurotransmitters: chemicals that travel across the synapses to affect the postsynaptic cell o Amino Acids – glutamate (+), GABA (-), glycine(-), aspartate, etc.; modified amino acid  Ach (acetylcholine) o Monoamines – serotonin; dopamine, norepinephrine, epinephrine (catecholamines) o Neuropeptides – endorphins, substance P, neuropeptide Y, etc . o Purines – ATP, adenosine o Gases – NO (nitric oxide) NOT nitrous oxide (laughing gas)  Neurotransmitter Release: most neurotransmitters are synthesized in the synaptic terminal and are then stored in vesicles influx of calcium causes the vesicles to undergo exocytosis and release the neurotransmitters into the synaptic cleft o MAO inhibitors – monoamine oxidase breaks down transmitters into inactive chemicals  Activating the Postsynaptic Neuron: effect on postsynaptic cell depends on the neurotransmitter and that transmitter’s receptors; there are either ligand- gated or transmitter-gated channels o Ionotropic Receptors: neurotransmitter causes protein channel to change its shape and allow ions to flow in; faster but effects are short- lived; mostly rely on Glutamate (+) and GABA (-) o Metabotropic Receptors: initiate a sequence of metabolic reactions; slower but longer-lasting effects; acts through a second messenger (like cAMP) activated by a G-protein


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