I. Introduction Action potentials are generated as a result of a neuron’s membrane reaching a specific threshold. In order to reach this threshold, a cell must depolarize. Typically, cells depolarize with the opening of voltage-gated sodium channels. During the rising phase of the action potential, these channels allow positive sodium ions to flow into the cell in what is called the depolarization phase. The flow of these ions into the cell is often referred to as the sodium current. Once the cell is depolarized, voltage-gated potassium channels are signaled to open, allowing potassium to flow out of the cell and repolarize it. The flow of potassium ions out of the cell is often referred to as the potassium current [1]. The rapid flow of potassium
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Blocking only Na channels worked more efficiently than blocking Na and K channels because with TTX, the Na current essentially lost to the K current. Since “Na and K currents compete in trying to depolarize and repolarize a membrane,” the duration and amplitude of spikes “reflect the changing contributions of the two currents” [2]. Therefore, when the Na current is decreased, the rate of rise and the amplitude of the spike decrease as well. Since the K conductance is unaffected by TTX, it defeats the Na current faster, which contributes to the slower rate of rise and shorter peak as well. The mismatch in Na and K currents allowed TTX to be more effective in preventing the generation of a spike. Although large doses of TTX can cause significant damage to a human’s nervous system, recently, researchers have proposed using small doses of TTX to alleviate pain. In one experiment, researchers delivered small doses of TTX in “animals under different pain conditions” to evaluate whether TTX could be used “as a potential therapeutic agent for pain” [4]. It was found that TTX could be useful to treat those “in pathological pain conditions” since pain is part of the sensory system, and temporarily blocking these neurons from firing would prevent an individual from feeling pain
Blocking only Na channels worked more efficiently than blocking Na and K channels because with TTX, the Na current essentially lost to the K current. Since “Na and K currents compete in trying to depolarize and repolarize a membrane,” the duration and amplitude of spikes “reflect the changing contributions of the two currents” [2]. Therefore, when the Na current is decreased, the rate of rise and the amplitude of the spike decrease as well. Since the K conductance is unaffected by TTX, it defeats the Na current faster, which contributes to the slower rate of rise and shorter peak as well. The mismatch in Na and K currents allowed TTX to be more effective in preventing the generation of a spike. Although large doses of TTX can cause significant damage to a human’s nervous system, recently, researchers have proposed using small doses of TTX to alleviate pain. In one experiment, researchers delivered small doses of TTX in “animals under different pain conditions” to evaluate whether TTX could be used “as a potential therapeutic agent for pain” [4]. It was found that TTX could be useful to treat those “in pathological pain conditions” since pain is part of the sensory system, and temporarily blocking these neurons from firing would prevent an individual from feeling pain