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UGA PSYC 4130 - LTP and the Physiology of Learning
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Psyc4130 1nd Edition Lecture 27 Outline of Last Lecture I. Proposed (Normal) circuitry for Personal Moral Decision MakingII. “But, Your Honor, I Have PFC Damage”a. hypofrontalityb. Serotoninc. SolutionsOutline of Current Lecture I. LTP and the Physiology of Learninga. HCFb. LTPc. What is the physiological basis of learning and memory?d. Hebbs Original Principal e. NMDAf. Ketamineg. Alcoholh. Early LTPi. Late LTPj. Nootropic DrugsCurrent Lecture LTP and the Physiology of Learning (section from chapter 13 on learning and memory)- The whole brain/cortex is connected, project throughout entire brain, networks of interconnected neurons- HCF o CA Fields (CA1)- Entorhinal cortex  HCF  Amygdala- can activate hippocampus and vice versa  Hypothalamus (mammillary bodies) = “papez circuit”- LTPo NMDA glutamate receptor “coincidence detector”o Ketamine, PCP, Dextromethorphan, MK- 801 Alcohol These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.- What is the physiological basis of learning and memory?o New neurons? NO (you don’t grow new neurons aka neurogenesis in brain, new neuronsaren’t the answer)o New connections?No severing’s of brain affect in systematic way Areas of brain damage don't matter, what matters is how much cortex is damaged overallNOT THE ANSWERo Stronger connections?Certain pathways become strengthened, facilitated communication between different synapses-Hebb’s Original Principle: “Hebbian” Synapaseso If neuron A is stimulating neuron B, and at the same time neuron B is also firing, then the strength of the connection between A and B will be enhanced. (hypothesis of what is happening in synaptic strengthening) o “Neurons that fire together, wire together”-Figure 13.8 (look at this in text)o Be able to explain what is going on in situationo Synaptic strengthening occurs when synapses are active while membrane of postsynaptic cell is depolarized o Glutamateo NA is excitatory (epsp’s) - NMDAo Allows sodium in, enhances post synaptic effecto Allows in calcium (calcium is really important for regulating processes) Kick starts cascade within post synaptic membrane, second messenger, initiates LTP process- Ketamineo Attaches itself to NMDA receptors and blocks them- Alcoholo IPSP, neurons don't fire as mucho NMDA receptor blockade effect o Temporary amnesia effect - Early LTPo Doesn't require protein synthesis- Late LTP/During LTPo Stuff you tend to remember in childhood is stuff that was really good or really bado Very robust LTP event, hard to stamp out even with timeo You can get LTP effects that last for several decadeso You want to learn and remember better (learn ochem and remember it)- Nootropic Drugso Aka “smart drugs”o NMDA receptors as agonists, more robusto These drugs can enhance ability to learn, encode, and retrieve info- Big pic questions to noteo Calcium coming in (CaM-KII) Initiating cascade of events that can lead to changes (even in gene expression) AMRA receptors- more powerfully depolarization each time glutamate is released  Sensitisation of AMPA Increased expression AMPA Expainsion on post synaptic membraneo NO = nitric oxide (gas working as neurotransmitter)o Cramming aka MASSED Practice vs


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UGA PSYC 4130 - LTP and the Physiology of Learning

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