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Week 3- Behavioral Neuroscience

by: Celine Notetaker

Week 3- Behavioral Neuroscience PSYC 4183-001

Marketplace > University of Arkansas > Psychlogy > PSYC 4183-001 > Week 3 Behavioral Neuroscience
Celine Notetaker
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Detailed notes from lecture paired with helpful images and many example questions!
Behavioral Neuroscience
Nathan Parks
Class Notes
Behavioral Neuroscience
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This 7 page Class Notes was uploaded by Celine Notetaker on Sunday February 7, 2016. The Class Notes belongs to PSYC 4183-001 at University of Arkansas taught by Nathan Parks in Spring 2015. Since its upload, it has received 25 views. For similar materials see Behavioral Neuroscience in Psychlogy at University of Arkansas.


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Date Created: 02/07/16
Behavioral Neuroscience- Week 3 Review EXAMPLE QUESTION 1: Suppose we inject a bunch of Na+ into an axon. What will happen to the extracellular concentration of K+? Answer: It will increase EXAMPLE QUESTION 2: What best explains the movement of NA+ upon the opening of a NA+ ion channel? Answer: Na+ is driven into the cell by the force of diffusion and electrostatic force EXAMPLE QUESTION 3: True or false- Graded potentials are best recorded by an electrode placed in the axon terminal Answer: FALSE- its actually at the axon hillock EXAMPLE QUESTION 4: An action potential is triggered when? Answer: When graded potentials depolarize the axon hillock enough to trigger open voltage-gate Na+ channels Opening a Cl- or K+ channel will increase the Cell’s internal negativity -Some cells have no axons, some have very small axons Action Potential Continued… - Action Potential is the amplification and transmission of what’s summating in the soma and the dendrites -Action potentials will move down the entire axon -In an unmyelinated axon the voltage gates would have to be close together to create a constant chain down until it reaches the axon terminal. -In a Myelinated axon the voltage gated channels can be further apart on the length of the axon than if it were on an unmyelinated axon.  You don’t have to regenerate the AP as often and it’s only done at the nodes of ranvier  Therefore AP is faster with myelinated axons Myelination speeds the propogation of action potential  Saltatory conduction Refractory periods (also review from week 2 notes) - In the relative refractory period you have to overcome hyperpolarization as well as generate enough charge above the threshold to trigger another action potentials If Action Potential is always the same amplitude, how can it convey any information? RATE LAW: The larger the graded potential the FASTER the neuron will fire When an action potential arrives at the axon terminal it drives the release of neuroransmitters - so the more AP you have per second the more neuro transmitters released the bigger the graded potential in the next cell Synaptic T ransmission -The arrival of AP results in a synaptic transmission -tightly linked to rate law Types of synapses 1. Axodendritic (most common): Axon terminals form a synapse with dendrites 2. Axosomatic (2ndmost common): Axon terminal forms a synapse directly with cell body 3. Axoaxonal (rare): Axon terminal of one cell forms a synapse with the axon of another cell 4. Electical synapse: VERY UNCOMMON but bypasses the neuro transmitter communication Terminology Presynaptic cell: The cell that releases the neurotransmitter Postsynaptic cell: The cell that accepts the neurotransmitter Synaptic cleft: The space inbetween the pre- and post synaptic cells Synaptic vesicle: Spherical membranes containing neurotransmitters (like pre- packaged units of neuro transmimtter).  It fuses with the presynaptic membrane and releases the Ntrans. Into the synaptic cleft Neurotransmitter: Substance that transmits information between neurons Postsynaptic Receptors: Region of postsynaptic…..? HOW IT WORKS Depolarization of an axon terminal by the action potential triggers voltage-gated Ca++ channels to open and Calcium enters the cell Ca++ influx then causes synaptic vesicles to fuse with presynaptic membrane and release their neurotransmitters into the synaptic cleft Released Ntrans. In the synaptic cleft will then bind with postsynaptic receptors (2 kinds) 1. Ionotropic: The binding of ntrans. To these postsynaptic receptors causes the receptors’ ion channel to open Ions (Na+, K+, Cl-, or Ca++) flow in or out of the cell, producing EPSPs or IPSPs 2. Metabotropic: The binding of a ntrans. Indirectly causes an ion channel to open by means of a G-Protein. It can also change what the cell is doing metabolically and can keep the ion channel open for a longer period of time than it would in a ionotropic receptor Can drive longer neuronal changes in the membrane -Neurotransmitters must be cleaned out of the synaptic cleft  if it did not we would not function properly  Reuptake: neurotransmitter is removed from the synaptic cleft and into the presynaptic terminal by a transporter protein  Enzymatic Reactivation: Enzymes break down neurotransmitters in the synaptic cleft that way it can no longer bind to the post-synaptic receptors o In some cells they will do both Reuptake the neurotransmitter where the enzyme will then break it down inside the pre-synaptic cell. This controls the concentration of neurotransmitters. EXAMPLE QUESTION 5: How does myelin speed the transmission of the action potential Answer: Myelin insulates a large proportion of the axon requiring the action potential to be regenerated fewer times Major Neurotransmitter systems Amino acids - Glutamate – primary EXCITATORY neurotransmitter in the brain (EPSPs) - Gaba- Primary inhibitory neurotransmitter in the brain (IPSPs) -Acetylcholine Monoamines - Dopamine - Norepinephrine - Serotonin **Know the name of all these neurotransmitter systems, what they do, and how they’re cleaned up from the synaptic cleft Agonist: Facilitates the affects of a neurotransmitter on the postsynaptic cell Antagonist: Inhibits the effects of a neurotransmitter on the postsynaptic cell, it could also bind to the post-synaptic receptor to prevent the neurotransmitter from binding Sites of drug action EXAMPLES 1. L-DOPA = a drug that can cross the blood brain barrier and then turns into dopamine once inside. This would be an AGONIST because it supplies more of what’s inside the pre-synaptic cell 2. Black widow spider venom= can directly stimulate the voltage gated Ca+ channels on the cell (by passing the action potential process), causing vesicles to bind to the membrane and release Ach  over-excitation of cells and muscles will contrtact without release (too much can lead to death). This would also be an AGONIST GLUTAMATE Glutamate + GABA = foundation of brain function Glutamate= pimary excitatory neurotransmitter of the CNS  Involved in everything! Post-synaptic receptors AMPA receptor: Iontropic; Na+ Kainate receptor: Ionotropic; Na+ NMDA receptor: Ionotropic; Na+/Ca++ Metabotropic glutamate receptor Reuptake/deactivation Reuptake of glutamate is accomplished by glutamate transporters (GLT) on the presynaptic cell and astrocytes VGLUT- brings glutamate into the VESICLE Drugs Agonists: Glycine, Sarcosine Antagonists: Phencyclidine (PCP), Ketamine, Dextromethorphan GABA = the primary inhibitory neurotransmitter of the CNS Post-synaptic receptors GABA-a receptors: ionotropic; Cl- GABA-b receptors: Metabotropic; K+ Reuptake/deactivation Reuptake is accomplished by GABA transporters (GAT) on the presynaptic cell and astrocytes VGAT – is a transporter that brings GABA INTO the vesicle Drugs Agonist: Anxiolytics (Xanax); alcohol  Primary use of these are anti-anxiety Antagonist: Bicuculliine Acetylcholine Ach= the first neurotransmitter discovered Involved in: 1. PNS: muscle contraction 2. CNS: consciousness, attention, learning/memory


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