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The most popular medication for causing general anesthesia is propofol. Propofol is frequently used in clinical settings, but it is unclear exactly how it produces anesthesia. A group of researchers from the Rensselaer Polytechnic Institute discovered a propofol effect in neurons that was previously unknown in a recent study that was published in Molecular Biology of the Cell. The study discovered that exposure to propofol affected how neurons move proteins, which are biomolecules that carry out the majority of cellular functions, to the cell surface.

The efficient movement of protein material between compartments is essential for the functioning of nearly all animal cells, including human cells. In tiny carriers known as “vesicles,” proteins are transported from their site of synthesis to the location where they carry out their function. To preserve cellular organization and function, this transport must be effective and very specialized. Dr. Marvin Bentley, an assistant professor in the Department of Biological Sciences whose lab studies vesicle transport in neurons, served as the team leader. Because axons, which are frequently organized in nerve bundles, can span distances of up to 1 meter in humans, neurons are especially dependent on vesicle transport. Neurodevelopmental and neurodegenerative diseases like Parkinson’s and Alzheimer’s have been linked to vesicle transport errors.

According to this recent study, propofol has an impact on the kinesin protein family. Kinesins are tiny “motor proteins” that propel vesicles along microtubules, which are minuscule filaments. The research team led by Dr. Bentley found that cells exposed to propofol had significantly less Kinesin-1 and Kinesin-3 vesicle movement. The researchers then demonstrated that protein delivery to axons was significantly reduced as a result of transport delays brought on by propofol. Propofol’s mechanism of action is not fully understood, according to Bentley. What we found was unexpected: propofol changed the way vesicles moved through living neurons.

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Overall, the study significantly advances our knowledge of propofol’s mechanism of action. The majority of research on the anesthetic action of propofol has concentrated on how it interacts with the GABAA receptor, an ion channel that, when activated, blocks neurotransmission. According to this new study, vesicle transport is another mechanism that might be crucial for propofol’s anesthetic effect. The identification of this novel propofol effect has important implications for human health and could result in the creation of more effective anesthetics. According to Curt M. Breneman, dean of the School of Science, “Dr. Bentley’s team has advanced our understanding of the mechanism of action of a widely used drug that is already having a daily impact on human health.” “Dr. Bentley’s research may open the door for the development of related drugs that target crippling neurodegenerative diseases using the same mechanisms.” The study’s co-authors included Dr. Susan P. Gilbert, head of Rensselaer’s department of biological sciences, doctoral candidates Madeline Frank and Alec T. Nabb, and Dr. Bentley.

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