The sensitivity of nerve cells to incoming signals can be adjusted on their own. A mechanism that does this has recently been found, according to a recent study led by the University of Bonn. The Max Planck Institute for Neurobiology of Behavior and the German Center for Neurodegenerative Diseases contributed to the project. The outcomes were just released in the journal Cell Reports.
Anyone who has ever used a cell phone to send a voice message is aware of how important loudness is. A recording that is distorted and hazy is the effect of shouting into the microphone. However, whispering is also a bad option because the outcome is too quiet and makes it hard to understand. Because they adjust each microphone’s gain to correspond with the incoming signal, sound experts make sure every performance and talk show has the ideal sound.
Additionally, the brain’s neurons have the ability to adjust their sensitivity—even on their own. How they do this is demonstrated in a recent study conducted by the University of Bonn and the University Hospital Bonn. For this purpose, the participants looked into the nerve cell networks that are involved in touch, vision, and hearingdemonstrated in a recent study conducted by the University of Bonn and the University Hospital Bonn. For this purpose, the participants looked into the nerve cell networks that are involved in touch, vision, and hearing. The so-called thalamus, a region buried deep in the core of the brain, receives the signal first. It is subsequently carried to the cerebral cortex for additional processing there.
Each neuron adjusts itself
Prof. Dr. Heinz Beck of the University Hospital Bonn’s Institute of Experimental Epileptology and Cognition Research says that the signals from the thalamus activate the neurons in the cerebral cortex to produce action potentials. “These are brief voltage pulses that are then sent to different brain regions.” “The neurons must adjust to the strength of the excitatory signals for that to function properly.”
If the incoming stimuli were particularly potent, for instance, they would need to lower their sensitivity. The spokesperson for the University of Bonn’s transdisciplinary research area “life and health,” Beck, explains, “We have now found that a particular enzyme named SLK plays a role in this process.” The ability to individually calibrate their own excitability is provided to neurons. The microphones would automatically change their sensitivity to ensure that the recording is neither too quiet nor overamplified, which is analogous to not having a sound engineer.
Dr. Pedro Royero from Beck’s study team says that specific nerve cells known as interneurons are crucial to this mechanism. The majority of the trials were carried out by him, who also received his doctorate with this research at the Max Planck International Graduate School. Interneurons send inhibitory action potentials to activate neurons. They essentially adjust the knob that lessens their sensitivity. The strength of the interneurons’ inhibitory action, as measured by the SLK, now dictates how much this regulator can be changed by them.
Interneurons come in two main varieties: Some are immediately stimulated by incoming thalamic signals. They already block the neurons, while the thalamus is also causing them to fire. One type, however, is exclusively activated by the activity of the cerebral cortex’s neurons, i.e., the neurons they are later intended to suppress. Therefore, they are part of a feedback loop. Royero observes that, “interestingly, the SLK is not active in this feedback inhibition, but only in the first scenario.”
New insights into the development of diseases
Additionally, the researchers were able to demonstrate that certain genes are turned on during sensitivity adjustment. They now want to learn more about how they contributed to the process. This is also intriguing because proper brain function is heavily reliant on the balance of excitement and inhibition. This is evident in epilepsy, for instance: large regions of nerve cells are overexcited during seizures, which causes the typical seizures. In fact, research indicates that SLK levels in some epilepsy patients are lower than average. So maybe the research will also help us understand the disease mechanisms better.
Institutions taking part and financial support:
In addition to the University of Bonn and the University Hospital Bonn, the German Center for Neurodegenerative Diseases (DZNE), the Max Planck Institute for Behavioral Neurobiology — caesar and the University of Sidney were involved in the work. The study was funded by the German Research Foundation (DFG), the European Research Council (ERC) and the Bonfor Fellowship Program of the University Hospital Bonn.
