Pain can be an uncomfortable sensation that surges through our body that can range from mild to very painful. Although we don’t like to feel pain, it is a necessary occurrence in order to signal to the brain that we need to get away from the thing that is causing us the pain. In the previous paper, the journey from the nerves, to the spinal cord, and lastly to the brain was discussed. Information was sent through a multitude of action potentials from the afferent neuron to the 2nd-order neuron to the thalamus. Once it got to the thalamus, the information was transmitted through the cortexes of the brain, leading to pain perception. The tricky part can be when the signal does not go through, we don’t feel any pain at all. This is possible for
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The alpha subunit has four different sections I - IV that have functions of different levels in voltage sensors, allowing the sodium to be able to pass through once they are in place. Sodium channels assist in forming the excitability of each distinct neuron. The gene of SCN9A has the specifications of forming a single section of the alpha subunit from the sodium channel named NaV1.7, which are precisely located in nociceptors. NaV1.7 creates and transmits action potentials and is essential for determining the electrical signaling for the majority of excitable cells. This sodium channel is located in the nociceptors. A large portion of these nociceptors will be found in the dorsal root ganglia. These nociceptors are the nerve cells that are involved in the transmission of pain signals in the peripheral nervous system. Since the alpha subunit is not able to continue on with its instructions to become functional, it is not able to be integrated into the channel, losing all functionality of the NaV1.7 sodium channel. As many as 13 different alterations of the SCN9A gene are the root of not being able to recognize pain, which is why finding a cure is extremely difficult. Once functionality of the sodium channels is lost, transferring pain signals from damage to pain perception is
The alpha subunit has four different sections I - IV that have functions of different levels in voltage sensors, allowing the sodium to be able to pass through once they are in place. Sodium channels assist in forming the excitability of each distinct neuron. The gene of SCN9A has the specifications of forming a single section of the alpha subunit from the sodium channel named NaV1.7, which are precisely located in nociceptors. NaV1.7 creates and transmits action potentials and is essential for determining the electrical signaling for the majority of excitable cells. This sodium channel is located in the nociceptors. A large portion of these nociceptors will be found in the dorsal root ganglia. These nociceptors are the nerve cells that are involved in the transmission of pain signals in the peripheral nervous system. Since the alpha subunit is not able to continue on with its instructions to become functional, it is not able to be integrated into the channel, losing all functionality of the NaV1.7 sodium channel. As many as 13 different alterations of the SCN9A gene are the root of not being able to recognize pain, which is why finding a cure is extremely difficult. Once functionality of the sodium channels is lost, transferring pain signals from damage to pain perception is