Long-term potentiation is the basis for neuronal plasticity and thus the remodeling of neuronal structures or circuitry in the nervous system. Without the process, neither the formation of memory nor learning experiences would be possible. Disturbances in longevity potentiation are present, for example, in diseases such as Alzheimer’s disease.
What is long-term potentiation?
Long-term potentiation is the basis for neuronal plasticity and thus the remodeling of neuronal structures or circuitry in the nervous system. Neurons operate with bioelectrical and biochemical action potentials. Action potentials are the language of the central nervous system and are used to transmit excitation. This transmission is also known as synaptic transmission. Neurons respond to increased generation of action potentials with what is known as long-term potentiation. Neuronal plasticity is one of the most important consequences of long-term potentiation. The term neuronal plasticity is used to describe a remodeling within the neuronal structure that adapts it to its current use. Both individual neurons and brain areas can undergo neuronal remodeling. By means of the remodeling processes, the functions of the central and peripheral nervous system are maintained, expanded and adapted to the current situation of use. As the basis of neuronal remodeling, long-term potentiation helps tremendously in ensuring the nervous system functions as effectively and smoothly as possible. Long-term potentiation is also associated with memory formation. In addition, neuronal remodeling is also an inevitable process for learning processes.
Function and task
From the brain‘s point of view, a learned skill is each associated with a morphological correlate corresponding to a network of synaptic connections. Such networks allow for the formation of ideas in the association cortex. When a particular word is pronounced, for example, a special network must already come to activation, which in turn results in a special pattern of action potentials. Whenever a person learns new skills or improves old ones, new circuitry is created in the brain. Unused circuitry is analogously cancelled again. This remodeling corresponds to synaptic plasticity. On the neuronal level, learning is thus an activity-dependent remodeling of patterns of neuronal circuitry and of functional processes of the brain. In addition to presynaptic enhancement, posttetanic potentiation, and synaptic depression, long-term potentiation is also relevant to learning processes. This potentiation corresponds to a long-lasting amplification of synaptic transmissions. This process consists of several subprocesses. Activation of AMPA receptors is the first step of long-term potentiation. Myriad receptors for glutamate are located in postsynaptic membranes. A subset of these glutamate receptors are those of the AMPA type. As soon as an action potential is generated, glutamate is released. The endogenous substance is one of the most important neurotransmitters and, after release, binds to AMPA receptors, which are made to open by the binding. After the receptors open, sodium ions flow in. In this way, an excitatory postsynaptic potential is created. This potential is generated within the postsynaptic membrane during each depolarization. Excitatory postsynaptic potentials are summed and processed by the respective receiving neuron. When a threshold is exceeded, the receiving neurons again form an action potential and transmit it through their axons. In long-term potentiation, the generation of an excitatory postsynaptic potential is followed by activation of NMDA receptors. Once additional action potentials occur, there is increased depolarization of the postsynaptic membrane. Magnesium ions leave the NMDA receptor and the receptor can open. The opening of the NMDA receptors results in the influx of calcium ions and leads to phosphorylation of the AMPA receptors. Phosphorylation in turn increases the conductance of the receptors and also increases protein biosynthesis in the cell. In addition, retrograde messenger substances are secreted during the processes described. These messenger substances correspond, for example, to derivatives of arachidonic acid or gases such as nitric oxide.These second messengers cause the increased release of neurotransmitters at the presynaptic membrane.
Diseases and disorders
Neurological diseases affecting long-term potentiation are a current subject of medical research. For example, one such disease is Alzheimer’s disease. Crohn’s disease also affects the processes described earlier. The fact that these diseases disrupt long-term potentiation is mainly due to the degeneration of neurons. As soon as the neuronal synapses break down, long-term potentiation is no longer possible. This is also how affected people experience the dark areas in their memory, for example. In degenerative diseases of the central nervous system, the brain degrades itself bit by bit. Measures to preserve neuronal structures have now become a major research focus in relation to diseases such as Alzheimer’s. So far, no major successes have been achieved in the preservation of synapses. Only in animals with comparable diseases have breakthrough successes been recorded so far. Scientists have not yet succeeded in transferring these successes to humans. Since long-term differentiation no longer functions in affected individuals, synaptic remodeling can no longer take place. Learning processes are impossible and the general functionality of the brain decreases progressively. New neurons or connections between neurons can no longer form. Old synapses are no longer used and are degraded in the course of remodeling processes. To counteract these processes, medicine now promotes the maintenance of synapses by means of special exercises. The more frequently synapses are used, the sooner the brain recognizes them as necessary. Diseases such as Alzheimer’s or Crohn’s disease can therefore be delayed in their progression by exercises. However, it has so far been impossible to stop these diseases by means of exercise. Most of those affected therefore require 24-hour care from a certain stage of the diseases.
