IPSP - inhibitory post synaptic potential
The state of a neuron when it is not firing a neural impulse is called the resting potential. This is when the neuron is negatively charged inside compared to outside, waiting for a stimulus to change its electrical charge and initiate an action 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.
The stimuli that can change the resting membrane potential of a cell include changes in ion concentrations inside or outside the cell, neurotransmitter binding to receptors, and mechanical deformation of the cell membrane. These changes can lead to the opening or closing of ion channels, altering the flow of ions across the membrane and affecting the cell's resting membrane potential.
A sudden increase in membrane potential, typically from a resting membrane potential of around -70mV to a threshold potential of around -55mV, triggers the opening of voltage-gated sodium channels leading to depolarization and initiation of an action potential.
In muscle cells the inward current is a sodium + calcium flow through acetycholine activated channels as well as through voltage sensitive calcium channels.
The state of a neuron when it is not firing a neural impulse is called the resting potential. This is when the neuron is negatively charged inside compared to outside, waiting for a stimulus to change its electrical charge and initiate an action 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.
During an action potential, the neuron undergoes a rapid change in membrane potential as sodium ions rush into the cell, leading to depolarization. Subsequently, potassium ions move out of the cell, repolarizing the membrane back to its resting state. This rapid change in membrane potential allows for the transmission of electrical signals along the neuron.
The stimuli that can change the resting membrane potential of a cell include changes in ion concentrations inside or outside the cell, neurotransmitter binding to receptors, and mechanical deformation of the cell membrane. These changes can lead to the opening or closing of ion channels, altering the flow of ions across the membrane and affecting the cell's resting membrane potential.
No, not at all. The axon is the transmitting end of a neuron, and a dendrite is the receiving beginning of another neuron.The axon sends its signal "through" a synapse between the axon terminal and a dendrite via chemicals called neurotransmitters that it releases into the synaptic space, which diffuse to and are taken into structures on dendrites called ligand-gated ion pores, which open to allow sodium ions into the dendrite, which change its electrical charge, which initiates the propagation of a corresponding signal along the dendrite and cell body toward the axon hillock, which, if enough signals from dendrites reach it, will then fire and send the nerve signal onward along the axon, as an action potential.
During the relative refractory period, the threshold for excitation is increased compared to the resting threshold. This is because the membrane potential is closer to its resting state, making it more difficult to depolarize the cell and generate an action potential. It requires a stronger stimulus to overcome this increased threshold and trigger another action potential.
A sudden increase in membrane potential, typically from a resting membrane potential of around -70mV to a threshold potential of around -55mV, triggers the opening of voltage-gated sodium channels leading to depolarization and initiation of an action potential.
When a section of a resting neuron is stimulated, it causes a localized change in membrane potential, typically depolarization. This change occurs because sodium channels open, allowing Na+ ions to flow into the neuron. If the depolarization reaches a certain threshold, it can trigger an action potential, leading to the propagation of the signal along the axon. This process is crucial for neural communication and the transmission of information throughout the nervous system.
In muscle cells the inward current is a sodium + calcium flow through acetycholine activated channels as well as through voltage sensitive calcium channels.
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.
The rate of change of potential with respect to distance is called potential gradient. its unit is volt per meter or newton/coulomb.
Action potential