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Brain & Behavior Week 4 Notes

by: Willow Frederick

Brain & Behavior Week 4 Notes Natural Science 2

Marketplace > New York University > CORE > Natural Science 2 > Brain Behavior Week 4 Notes
Willow Frederick

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These notes cover everything neuron-related. Lecture 7 and 8. Action potentials, local graded potentials, synaptic transmission, voltage, neurotransmitters, ligands, and the steps of neurodevelopme...
Brain and Behavior
Andre Fenton
Class Notes
neurodevelopment, synapse, Actionpotential, axon, dendrites, voltage, neurons, localgradedpotentials, ligands
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This 6 page Class Notes was uploaded by Willow Frederick on Friday September 30, 2016. The Class Notes belongs to Natural Science 2 at New York University taught by Andre Fenton in Fall 2016. Since its upload, it has received 34 views. For similar materials see Brain and Behavior in CORE at New York University.


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Date Created: 09/30/16
Brain & Behavior Week 4: 9/27­9/29 Lecture 7: Synapses: Circuits & Networks for Exchanging Drugs Synapses: building blocks for neural computations  Synaptic Circuits  Axo­dendritic synapse  Most synapses are formed by an axon stimulating a dendrite, but axons also sometimes  synapse on cell bodies or even other axons o Dendro­dendritic: In some cases, specialized dendrites synapse on other dendrites  The neuron with the ‘veto power’ could prevent the AP from happening by releasing an IPSP OR it could depolarize, activating an APCalcium rushes in  One neuron receives many different inputs – the visual system represented as a neural chain   Convergence: synaptic integration o Excitatory neural transmission: INCREASED probability of an action potential  (EPSP)  o Inhibitory neural transmission: DECREASED probability of an action potential  (IPSP)  Divergence: amplification o 5 different axons are hitting it – plus sign ones are excitatory (red) o if it depolarizes enough, at the axon hillock an AP will generate & will propagate  down the axon  o (middle photo): if the inhibitory neurons are at the same time as excitatory  neurons  that push n pull can generate info in the brain  only a small # of cells are able to fire­ how?  The inhibition might be less for that cell for a fraction of a second,  or maybe the excitation is strong/plenty enough to fire an AP  If the next neuron doesn’t generate an AP, that signal is lost  Summation  Temporal summation:  o If you get a lot of AP releases neurotransmitters at the same time, it can reach the  threshold o increasing the rate of AP’s is a way of signaling you ran into a wall, for ex.  Spatial summation o Synchrony is a big part of getting signals propagated in the brain  o 3 wimpy inputs that happen together in time can be effective! Prof’s Summary So Far  presynaptic­ neurotransmitter release  postsynaptic­ receptor binding  ion channels open  ionic current flows across membrane  postsynaptic membrane potential changes (graded, decrementing PSP)  postsynaptic cell is excited or inhibited (IPSP or EPSP)  summation of PSP determines if an AP is triggered  Short­Term (last less than a second) in Chemical Synaptic Transmission ~ “Plasticity”  rapid stimulation­ tetanus   the nervous system isn’t fixed­ activity across the synapses change the functions  Short­term plasticity mechanisms­   Facilitation  depolarization AP o 2  AP comes, there’s still residual calciumtriggers another AP o more Ca+ available more responses o calcium pump has to pump calcium out (requires energy) o but before it pumps it all out, next AP comes aka facilitation!  Depression  o The neurotransmitter is being released from the cell –receptors are not responding to the neurotransmitters bc there are no more n  These synapses are dynamic thru their use—changing their function  Chemical Neurotransmission (in a cell at rest)  Ionotropic Receptors (ion­feeding) o When a nt binds it, it makes a hole in the membrane positive ions can enter the  cell  o The driving force of sodium is about 6x greater o When cation channel opensmore depolarization   Metabotropic Receptors – there are tons of different kinds   o The G­protein itself changes shape, dissociates from receptor, moves in the  membrane, releases another metabolite   ion channel opens –for sodium OR potassium   the receptor & its properties determine what the response will be in the  post­synaptic cell   the receptor ‘designs the cell’s response’  the receptor is a protein, a product of the genome  Ligands (neurotransmitters): the thing that binds to another thing  agonist drugs: mimic an andogenous neurotransmitter or ligand—causes that receptor to  do more of what that receptor does   antagonist drugs: interferes w/what that receptor would do by blocking it  o can be competitive or non­competitive  the cells are not passive – cells can change their sensitivity to drugs by changing the # of  receptors they make in response to ‘experience’ o cell’s response to agonist (mimics ligand exactly)  down­regulation  o cell’s response to antagonist (blocks receptor)  up­regulation – make more or  less receptors?  2 types of receptors in post­synaptic membrane o ionotropic (fast)­ channel is normally closed, but when a ligand binds to it, the  receptor channel changes in shape/ opens only ions go thru & enter cell  o metabotropic (slow): NT binds to receptor, but there’s a G­protein (2  d messenger) activated,  G­protein goes to neighbor ion channel & opens it Lecture 8 (Kally):  Neurodevelopment or how to build something really complicated   Neural systems develop according to a genetic program that is refined by neuron­specific  experience   HoW? o Make a lot of neurons o Tell them where to go  o Tell them what type of neuron to be  o Connect them to each other o Organize their functions  Group them into function  Refine that w/experience   What drives patterning? –gene expression  What guides development?  ­organizer regions 1. PROLIFERATION: radial glia guide migrating cells  a. Cell differentiates into a neuron cell continues to undergo mitosis  2. MIGRATION: radian glia guide migrating cells  a. Inside out migration of neurons  b. Sister cells split up & part ways  3. DIFFERENTIATION: what types of neuron will they be? a. How is cell fate determined?  ­by location & the signals around that location, as  well as what they are exposed to! b. Your fertilized egg divides into 2, then into 4, into 8, so on until you have about  100 cells –looks like a ball w/a hollow center (frog blastula­stage—v early stage) c.   d. how is differentiation regulated? ­ by molecules in the local environment 4. SYNAPTOGENESIS (connect the cells to each other) a. Neurons have filopodia (little feet) b. Axon finding & fine tuning c. Pruning & cell survival  i. We’re born w/2x as many neurons & connections as we’ll have as adults ii. Brain volume doubles over the 1  2 years of our lives d. APOPTOSIS (programmed cell­death) i. 3 signals: die, don’t die, die!  ­­regulated by death genes  ii. planned way to get rid of cells we don’t need iii. how is our brain still increasing in size then? 1. Myelination—adds a lot of volume 2. Inhibitory neurons grow & make connections a little later 5. Organize their functions!  ­­defined by intrinsic interactions  a. If you change the gradients, the cortex changes in size b. Experience is key! (mainly for pruning 6. PLAN a. Timing is so important ­­­ ‘critical periods’


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