This Is Not A REPLACEMENT FOR YOUR OWN NOTES etc etc INFO may or may not on exam ETC ETC DISCLAIMER junk The review is available https docs google com document d 1G22u2qf 2bssgNiXwcfmOfodB T56DFuZcPbic0IIY edit usp sharing Notes for Exam 2 3 4 14 2 11 13 Neurobiological Mechanisms Learning from an invertebrate STIMULUS PREEXPOSURE EFFECTS Continued Kandel Aplysia Sea slug Advantages 1 simple nervous system only have 20 000 neurons 2 large neurons 3 invariant neuralanatomy not quite clones but they re nearly identical in terms of neural architecture engram a a physical biological memory essentially the data that your brain stores to keep a memory present b many believe it is somewhere in the hippocampus or cerebellum Nonassociative learning The reflex gill withdrawal Habituation tactile stimulus to siphon no effect on the magnitude of the reflex elicited by tactile stimulus the degree to which a receptor is engaged depends on proximity to For example touch mechanical receptors engage dendrites of SN cell body to mantle shelf and vice versa Sensitization shock to tail locus of stimulation axon motor neuron muscles reflex SN sensory neuron is presynaptic MN motor neuron is postsynaptic SEE FLOW CHART IN FB GROUP 1 This Is Not A REPLACEMENT FOR YOUR OWN NOTES etc etc INFO may or may not on exam ETC ETC DISCLAIMER junk The review is available https docs google com document d 1G22u2qf 2bssgNiXwcfmOfodB T56DFuZcPbic0IIY edit usp sharing Neural circuit simple S R Sensory Neuron SN activated by touch or sense Motor Neuron MN activated by sensory neuron in this circuit we see habituation there is less neurotransmitter release from SN and less uptake by MN Facilitatory interneuron shock sits at the end of the SN on presynaptic side presynaptically innervates the sensory neuron here we see sensitization increases transmitter release and augments amplifies uptake by MN Changes in amount of transmitter released from SN with habituation observe a decrease with sensitization observe an increase Review Basic neural function resting potential Na K neural membranes are semipermeable at rest the membrane is impermeable to the ion Na 70 mV end up with excess of positive charge outside of the cell sets up electrical potential 1 sets up electrical charge across membranes 2 keeps other positively charged ions from flowing out Unstable state of affairs the Na would really like to get into the cell b c attracted to Particles like to flow down concentration gradients AKA diffusion Na wants to go in K wants to flow out Action Potential Initiated by depolarizing the cell move from 70 mV towards zero Rising phase Na flowing into the cell Electrically sensitive channels that swing open when a cell get less negative 60 mV Re establishing the resting potential K flows out electrical potential goes back to 70 mV suppose we slowed the flow of K out of the cell it would take longer to re establish resting potential or in other words make actional potential longer Synaptic transmission 2 This Is Not A REPLACEMENT FOR YOUR OWN NOTES etc etc INFO may or may not on exam ETC ETC DISCLAIMER junk The review is available https docs google com document d 1G22u2qf 2bssgNiXwcfmOfodB T56DFuZcPbic0IIY edit usp sharing there are channels on the side of the presynaptic side that allow Ca into cell these channels open when actional potential arises how long the Ca channels stay open depends on duration of action potential Ca channel Vesicles Ca causes vesicles to move towards the presynaptic cleft neurotransmitter is inside of vesicles Neurotransmitter travels across synapse to MN Less K longer action potential more Ca more neurotransmitter bigger response In the case of habituation and sensitization actional potential is normal Quantum analysis shows that with habituation decreases number of vesicles released Why Due to a change in the Ca channels How inactivates Ca channels and causes a chain reaction less Ca less transmitter etc This describes short term habituation Spontaneous recovery only applies to short term habituation Long term habituation engages proteins that facilitates a structural modification and the axon essentially ceases to exist STIMULUS PREEXPOSURE EFFECTS Continued 2 13 14 Biochemical mechanisms Habituation Inactivation of Ca Channels Short term Sensitization Shock Biochemical cascade Serotonin comes from facilitatory interneuron Serotonin receptor on sensory neuron engaged by serotonin G protein adenylate cyclase enzyme that converts ATP into cAMP ATP cAMP protein kinase closes K channels 3 This Is Not A REPLACEMENT FOR YOUR OWN NOTES etc etc INFO may or may not on exam ETC ETC DISCLAIMER junk The review is available https docs google com document d 1G22u2qf 2bssgNiXwcfmOfodB T56DFuZcPbic0IIY edit usp sharing K channel Ca channel Long term sensitization Increases the duration of the action potential because it slows the flow of K out cell what preserves the pathway over time Protein kinase stays active for a few hours MAP PKA engage gene expression via CREB1 CREB2 The genes come back down and modification protein kinase Creates new regulatory subunit changes the PKA so that it only closes K channels There are also other genes that are engaged that produce structural change They create more synapses Nociceptive Plasticity Nociceptive pain transmission sensitization pain is a psychological phenomena a large part of sensitization is in the brain In Aplysia and vertebrates nociception neural activity in the pathway Studying central sensitization within the vertebrate spinal cord Why spinal cord because Electrophysiological observations Similarity to long term potentiation LTP Neurochemical mechanisms AMPA and NMDA receptors AMPA works just like a normal channel when it is activated with glutimate it allows sodium to flow into the cell which kick off the process of causing action potential NMDA receptor acts like a gated channel under normal circumstances magnesium is clogging this channel to allow this channel to work magnesium has to be displaced by strong depolarization when its turned on really strongly the magnesium flows away strong input produces strong polarization once magnesium is displaced when gludimate comes along calcium can now enter the cell the NMDA receptor causes two conditions to work Allows Ca entry Activates Ca calmodulin dependent protein kinase CaMK II this goes around modifing exsisting AMPA receptors Awakens silent AMPA receptors Modifies AMPA receptors increases Na conductance 4 This