Memory and learning are based on changes in the functioning of the brain’s neural networks—above all, in how neurons transmit signals to one another. Until recently, it was believed that such changes occurred mainly at the level of synapses, the contact points between neurons. However, a new study has shown that another part of the nerve cell also plays an important role in these processes.

Scientists from the German Center for Neurodegenerative Diseases have, for the first time, observed in the living brain a mechanism of neuroplasticity that had previously been known only from experiments on cell cultures and postmortem tissue samples.

The results of the study were published in Nature Neuroscience.

The focus is on the axon initial segment—a specialized part of the neuron where the electrical impulse is generated.

Neurons form a complex network through which electrical signals are continuously transmitted. This network is not static: under the influence of experience and learning, its properties can change. This ability of the brain to reorganize itself is known as neuroplasticity and underlies memory formation and behavioral adaptation.

The axon initial segment plays a key role in neuronal function. It is here that the decision is made whether a nerve impulse will be generated and how strong it will be. This region is characterized by a high density of ion channels and acts as a kind of “trigger mechanism” for neuronal activity.

In experiments on mice, the researchers observed individual neurons in the cerebral cortex, a brain region associated with learning processes. Using advanced microscopy techniques, they were able to track the same cells over several days before and after learning tasks. This made it possible to record changes in the axon initial segments in real time.

The results showed that during learning, the length of the axon initial segment can change: in some neurons it became longer, while in others it shortened. These changes are functionally significant, as the length of the segment directly affects the excitability of the cell. Neurons with a longer initial segment generate stronger signals, whereas shortening of the segment reduces their activity. In this way, the brain can finely regulate the level of neuronal activity depending on tasks and conditions.

The researchers emphasize that the axon initial segment can be viewed as the neuron’s “main switch.” While synapses determine which signals enter the cell, this region decides whether the neuron will respond and with what strength. The discovery shows that neuroplasticity affects not only the connections between neurons, but also the mechanisms that generate the signals themselves.

Although the study was conducted in a limited area of the brain, the scientists suggest that such changes represent a general principle of learning. In future work, they plan to investigate this mechanism in other brain regions, as well as in the context of neurodegenerative diseases.

Of particular interest is a possible link to Alzheimer’s disease, in which signal transmission between neurons is disrupted. The researchers intend to explore how the protein deposits characteristic of this disease affect axon initial segments. Such data could deepen understanding of the disease mechanisms and, in the long term, point to new directions for therapy.