the conduction of neural information to the muscle fiber
False
Potassium plays a crucial role in maintaining the resting membrane potential of cardiac cells. It helps establish the negative charge inside the cell by moving out of the cell through potassium channels. This outward movement of potassium ions contributes to the polarization of the cell membrane, creating a negative resting membrane potential.
Not much. Changing the extracellular chloride changes the level inside the cell so they will be in equilibrium again. The chloride ion plays little role in resting potential.
A change in extracellular sodium concentration would not alter the resting membrane potential of a neuron because the resting potential is primarily determined by the relative concentrations of sodium and potassium ions inside and outside the cell, as mediated by the sodium-potassium pump and leak channels. Changes in extracellular sodium concentration would not directly affect this equilibrium.
An increase in Na⁺ conductance would lead to an influx of sodium ions into the cell, causing the membrane potential to become more positive and move closer to the sodium equilibrium potential, which is typically around +60 mV. This depolarization could make the resting membrane potential less negative or even shift it above the threshold for action potential generation. Conversely, a decrease in Na⁺ conductance would reduce sodium influx, potentially stabilizing the resting membrane potential at a more negative value. Overall, changes in Na⁺ conductance directly influence the excitability of the neuron or muscle cell.
Hypokalemia, characterized by low potassium levels in the blood, leads to a more negative resting membrane potential due to a decreased concentration of extracellular potassium ions. This hyperpolarization makes it more difficult for neurons and muscle cells to reach the threshold for action potentials, resulting in decreased excitability. Consequently, the generation of action potentials becomes impaired, potentially leading to symptoms such as muscle weakness and arrhythmias.
depressants affect the heart rate by its heart rate
Depressants slow (or depress) the functioning of the entire body.
Hyperkalemia causes depolarization of the resting membrane potential, leading to reduced excitability of cells. This shift makes it harder for action potentials to fire, as the threshold for depolarization is increased. Additionally, hyperkalemia can alter the function of voltage-gated sodium channels, further impairing action potential generation.
stimulants increase activity and depressants decrease activity.
Drinking alcohol temporarily slows the rate of respiration.
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