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Long Term Potentiation and Memory Formation, Animation

Role of the hippocampus, synaptic plasticity, the 2 phases of LTP, connection with short-term and long-term memory. Purchase a license to download a non-watermarked version of this video on AlilaMedicalMedia(dot)com Check out our new Alila Academy - AlilaAcademy(dot)com - complete video courses with quizzes, PDFs, and downloadable images. Voice by: Sue Stern ©Alila Medical Media. All rights reserved. The process of learning begins in the cortex. Sensory signals are then transmitted to the hippocampus. If a signal is strong, or repeated, a long-term memory is established and wired back to the cortex for storage. Lesions in the hippocampus impair formation of new memories, but do not affect the older ones. The brain consists of billions of neurons. Neurons communicate with each other through a synapse. Synaptic connections can change over time, a phenomenon known as synaptic plasticity. Synaptic plasticity follows the “use it or lose it” rule: frequently used synapses are strengthened while rarely used connections are eliminated (synaptic pruning). Synaptic plasticity is believed to underlie the process of learning and memory retention. High-frequency signals or repeated stimulations STRENGTHEN synaptic connections over time. This is known as long-term potentiation, or LTP, and is thought to be the cellular basis of memory formation. LTP can occur at most excitatory synapses all over the brain, but is best studied at the glutamate synapse of the hippocampus. When a glutamatergic neuron is stimulated, action potentials travel down its axon and trigger the release of glutamate into the synaptic cleft. Glutamate then binds to its receptors on the post-synaptic neuron. The 2 main glutamate receptors that often co-exist in a synapse are AMPA and NMDA receptors. These are ion channels that activate upon binding to glutamate. When the pre-synaptic neuron is stimulated by a WEAK signal, only a small amount of glutamate is released. Although both receptors are bound by the glutamate, only AMPA is activated by weak stimulation. Sodium influx through the AMPA channel results in a SLIGHT DE-polarization of the post-synaptic membrane. The NMDA channel remains closed because its pore is blocked by magnesium ions. When the pre-synaptic neuron is stimulated by a STRONG or REPEATING signal, a large amount of glutamate is released; the AMPA receptor stays open for a longer time, admitting more sodium into the cell, thus resulting in a GREATER DE-polarization. Increased influx of positive ions EXPELS magnesium from the NMDA channel, which NOW activates, allowing not only sodium but also CALCIUM into the cell. Calcium is the mediator of LTP induction. There are 2 distinct phases of LTP. In the early phase, calcium initiates signaling pathways that activate several protein kinases. These kinases enhance synaptic communication in 2 ways: they phosphorylate the existing AMPA receptors, thereby increasing AMPA conductance to sodium; and help to bring more AMPA receptors from intracellular stores to the post-synaptic membrane. This phase is thought to be the basis of short-term memory, which lasts for several hours. In the late phase, NEW proteins are made and gene expression is activated to further enhance the connection between the 2 neurons. These include newly synthesized AMPA receptors, and expression of other proteins that are involved in the growth of NEW dendritic spines and synaptic connections. The late phase may correlate with formation of long-term memory. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Always seek the advice of a qualified healthcare provider with any questions you may have regarding a medical condition.