Neuroplasticity and the Functions of Memory Repair

By Lady Sherry Anne Dow Podolchuk

Neurons communicate with each other through the release of chemical messengers called neurotransmitters. These neurotransmitters are released from the axon of one neuron and travel across a tiny space called a synapse to bind with receptors on the dendrite of another neuron. This binding can cause changes in the receiving neuron, such as the generation of an electrical signal known as an action potential.

The process of relearning information involves changes in the strength and number of connections between neurons, known as synaptic plasticity. This can occur through several mechanisms, including the formation of new synapses, the strengthening or weakening of existing synapses, and changes in the number or sensitivity of receptors on the dendrites of neurons. These changes are thought to be driven by experience and can result in the formation of new neural pathways that allow for the storage and retrieval of information.

Synaptic plasticity is the ability of synapses, the junctions between neurons, to change in strength over time, depending on their activity. This change in synaptic strength is one of the important neurochemical foundations of learning and memory.

There are several underlying mechanisms that cooperate to achieve synaptic plasticity, including changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters. For example, two molecular mechanisms for synaptic plasticity involve the NMDA and AMPA glutamate receptors. Opening of NMDA channels leads to a rise in post-synaptic calcium concentration, which has been linked to long-term potentiation (LTP). Strong depolarization of the post-synaptic cell completely displaces the magnesium ions that block NMDA ion channels and allows calcium ions to enter a cell, probably causing LTP. Weaker depolarization only partially displaces the magnesium ions, resulting in less calcium entering the post-synaptic neuron and lower intracellular calcium concentrations, which activate protein phosphatases and induce long-term depression (LTD).

These activated protein kinases serve to phosphorylate post-synaptic excitatory receptors (e.g., AMPA receptors), improving cation conduction and thereby potentiating the synapse. Also, these signals recruit additional receptors into the post-synaptic membrane, stimulating the production of a modified receptor type, thereby facilitating an influx of calcium. This in turn increases post-synaptic excitation by a given pre-synaptic stimulus. This process can be reversed via the activity of protein phosphatases, which act to dephosphorylate these cation channels.

Synaptic plasticity works through changes in the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those neurotransmitters. These changes are mediated by several underlying mechanisms that cooperate to achieve synaptic plasticity.

Changing the strength of connections between neurons is widely assumed to be the mechanism by which memory traces are encoded and stored in the central nervous system. The synaptic plasticity and memory hypothesis asserts that activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the encoding and trace storage of the type of memory mediated by the brain area in which it is observed.

Synaptic plasticity relates to memory through its ability to change the strength of connections between neurons, which is thought to underlie the storage of information in memory.

One example of how neurons can relearn information is through the process of neuroplasticity. Neuroplasticity refers to the brain's ability to change and adapt in response to new experiences, learning, and injury. This can occur through several mechanisms, including the formation of new synapses, the strengthening or weakening of existing synapses, and changes in the number or sensitivity of receptors on the dendrites of neurons.

For instance, when someone learns a new skill, such as playing a musical instrument, the brain undergoes changes to support this new learning. As the person practices and becomes more proficient, the connections between neurons involved in playing the instrument become stronger and more efficient. This can result in changes in the brain's structure and function that support the person's ability to play the instrument.

Another example of how neurons can relearn information is through recovery from injury. When someone suffers a brain injury, such as a stroke, some neurons may be damaged or die. However, through rehabilitation and therapy, the brain can reorganize itself and form new connections between neurons to compensate for the lost function. This process is known as neural reorganization or cortical remapping.

Neuroplastisity can be used as a treatment for memory loss. Neuroplasticity refers to the brain's ability to change and adapt in response to new experiences, learning, and injury. This can occur through several mechanisms, including the formation of new synapses, the strengthening or weakening of existing synapses, and changes in the number or sensitivity of receptors on the dendrites of neurons.

In some cases, improving neuroplasticity can itself be part of mental health treatment. Brains in the early stages of dementia often use neuroplasticity to compensate for cognitive decline. Aerobic exercise and cognitively challenging activities can increase a brain’s overall neuroplasticity. Additionally, research into neuroplasticity can help doctors develop more effective treatments for those who suffer brain injuries through trauma, stroke or from neurodegenerative diseases such as Alzheimer’s.

In summary, neurons relearn information through changes in their connections with other neurons, which are mediated by neurotransmitters and their receptors. These changes can result in the formation of new neural pathways that allow for the storage and retrieval of new information. Synaptic plasticity is the ability of synapses, the junctions between neurons, to change in strength over time, depending on their activity. This change in synaptic strength is one of the important neurochemical foundations of learning and memory.

Neurons can relearn information through changes in their connections with other neurons, which are mediated by neuroplasticity. These changes can result in the formation of new neural pathways that allow for the storage and retrieval of information. Neuroplasticity can be used as a treatment for memory loss by improving the brain's ability to change and adapt in response to new experiences, learning, and injury.