For years, researchers have tried to identify the biological basis of memory. This basis might take many forms, such as the model we will discuss this week, but the physical trace of the memory has become known as the engram. While it is likely that there are multiple ways in which memory is stored, the current model for the formation of new memories is Long-Term Potentiation.

QUESTION

Discussion: Biological Basis of Memory

For years, researchers have tried to identify the biological basis of memory. This basis might take many forms, such as the model we will discuss this week, but the physical trace of the memory has become known as the engram. While it is likely that there are multiple ways in which memory is stored, the current model for the formation of new memories is Long-Term Potentiation. This model was described by Donald Hebb, who summarized it in 1949 by saying “Neurons that fire together, wire together.” This model suggests that when neurons are typically activated at the same time, the connection between those cells is strengthened. In the terms we have described earlier in our class, the postsynaptic cell becomes more responsive to the neurotransmitters released by the presynaptic cell. Nearly 20 years after Hebb’s quote, the process of LTP was actually observed in the hippocampus. Today, this model is the basis for our understanding of how new memories are formed. A more recent, and less well-understood process is long-term depression, in which the connections between two cells are actively weakened.

For this Discussion, you will explore this LTP model including the neurotransmitters and receptors involved. You will consider what activates each receptor and what changes within the receptor when it is activated.

Post a response to the following:

• Explain Long-Term Potentiation in your own words.
• Include a description of the receptor involved in LTP and what happens when it is stimulated by its ligand.
• Explain the changes that happen in both the presynaptic and postsynaptic cell as part of the LTP process.
• Briefly summarize the articles you found in the library that support how LTP is beneficial in your daily life. Include full APA references for your articles.

References

Breedlove, S. M., & Watson, N. V. (2019). Behavioral neuroscience (9th ed.). New York, NY: Oxford University Press.

• Chapter 17, “Learning and Memory”

• ANSWER

• The biological basis of memory: Long-Term Potentiation and its impact on daily life.

  Long-Term Potentiation (LTP) is a process in the brain that is believed to be the cellular mechanism underlying the formation and storage of long-term memories. It refers to the long-lasting strengthening of the synapses (connections) between neurons, which enhances the communication between them.

  One of the key receptors involved in LTP is the NMDA receptor (N-methyl-D-aspartate receptor). When the NMDA receptor is stimulated by its ligand, glutamate, several steps occur. Initially, the postsynaptic neuron needs to be depolarized, meaning it becomes more positive inside (Kratzer et al., 2012). This depolarization removes the voltage-dependent magnesium block from the NMDA receptor channel, allowing calcium ions (Ca2+) to enter the postsynaptic neuron.

  The entry of calcium ions into the postsynaptic neuron triggers a series of intracellular events. Calcium activates various enzymes, including protein kinases, which lead to the modification and strengthening of the synapse. This can involve the insertion of additional receptors at the postsynaptic membrane, changes in gene expression, and structural modifications that contribute to the long-term changes in synaptic strength (Takai et al., 1979).

  In the presynaptic cell, LTP leads to an increase in the release of neurotransmitters. This can occur through the recruitment of additional synaptic vesicles containing neurotransmitters or by increasing the probability of release from existing vesicles (Gulisano et al., 2019). As a result, when the presynaptic neuron fires action potentials, it releases a greater amount of neurotransmitters into the synaptic cleft, facilitating stronger synaptic transmission.

  In summary, during LTP, the NMDA receptor is stimulated by glutamate, leading to calcium influx into the postsynaptic neuron. Calcium triggers various intracellular processes that result in the strengthening of the synapse. This includes modifications in the postsynaptic cell to enhance its responsiveness and changes in the presynaptic cell to increase neurotransmitter release.

  References

  Gulisano, W., Melone, M., Ripoli, C., Tropea, M. R., Puma, D. D. L., Giunta, S., Cocco, S., Marcotulli, D., Origlia, N., Palmeri, A., Arancio, O., Conti, F., Grassi, C., & Puzzo, D. (2019). Neuromodulatory Action of Picomolar Extracellular Aβ42 Oligomers on Presynaptic and Postsynaptic Mechanisms Underlying Synaptic Function and Memory. The Journal of Neuroscience, 39(30), 5986–6000. https://doi.org/10.1523/jneurosci.0163-19.2019 

  Kratzer, S., Mattusch, C., Kochs, E., Eder, M., Haseneder, R., & Rammes, G. (2012). Xenon Attenuates Hippocampal Long-term Potentiation by Diminishing Synaptic and Extrasynaptic N -methyl-D-aspartate Receptor Currents. Anesthesiology, 116(3), 673–682. https://doi.org/10.1097/aln.0b013e3182475d66 

  Takai, Y., Kishimoto, A., Kikkawa, U., Mori, T., & Nishizuka, Y. (1979). Unsaturated diacylglycerol as a possible messenger for the activation of calcium-activated, phospholipid-dependent protein kinase system. Biochemical and Biophysical Research Communications, 91(4), 1218–1224. https://doi.org/10.1016/0006-291x(79)91197-5