Every year, over 350 million surgeries are performed worldwide, and many of us will have to undergo a procedure requiring general anesthesia at some point in our lives. Despite being a common medical practice, the exact workings of anesthesia drugs in the brain remain largely unknown. However, a new study published in The Journal of Neuroscience sheds light on this process by revealing that general anesthesia only affects specific parts of the brain responsible for alertness and wakefulness.
The study, conducted using fruit flies, discovered a potential mechanism through which anesthesia drugs interact with certain types of neurons in the brain. This interaction is mediated by proteins. The brain contains around 86 billion neurons, and not all of them are the same. These differences allow general anesthesia to be effective.
While we have some understanding of how anesthesia drugs affect consciousness, thanks to a significant discovery made in 1994, understanding the finer details requires examining the minute variations between brain cells.
Broadly speaking, there are two main types of neurons in the brain: excitatory neurons, which keep us alert and awake, and inhibitory neurons, which regulate and control the excitatory neurons. In everyday life, these two types of neurons constantly work together to maintain balance.
When we fall asleep, inhibitory neurons silence the excitatory neurons gradually over time, leading to increasing tiredness throughout the day. General anesthesia speeds up this process by directly silencing the excitatory neurons without any involvement from the inhibitory ones. This is why an anesthetist will tell you they will “put you to sleep” during a procedure.
While we understand why anesthesia puts us to sleep, the question remains as to why we stay asleep during surgery. Researchers have proposed several potential explanations over the years, but they all seem to point to one underlying cause: general anesthesia disrupts communication between neurons.
The recent study found that general anesthesia appears to inhibit communication specifically in excitatory neurons while leaving inhibitory neurons unaffected. This concept is not new, but the study provides compelling evidence as to why only excitatory neurons are impacted.
For neurons to communicate, proteins play a crucial role. One of their tasks is to facilitate the release of neurotransmitters, which are chemical messengers that transmit signals between neurons. The study found that general anesthesia impairs the ability of these proteins to release neurotransmitters but only in excitatory neurons. This was confirmed through experiments using fruit flies and super-resolution microscopy.
The difference between excitatory and inhibitory neurons lies in the types of proteins they express. This is similar to having two cars of the same make and model, but with slight variations. Both cars serve the same purpose, but one has additional features. Similarly, neurotransmitter release is a complex process involving multiple proteins. If any piece of this puzzle is not functioning correctly, general anesthesia will not be effective.
The next step in this research is to identify which specific piece of the puzzle differs between excitatory and inhibitory neurons to understand why general anesthesia only affects excitatory communication.
Ultimately, the study suggests that general anesthesia drugs cause widespread inhibition in the brain by silencing excitability in two ways, leading to sleep and maintaining it during surgery.
