Brain & Behavior Week 4 Notes
Brain & Behavior Week 4 Notes Natural Science 2
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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 APCalcium 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 calciumtriggers 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 opensmore 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’