Membrane Potential
Normal function in a single neuron as it participates in the processing of information is manifested as electrical potentials. These potentials are called membrane potentials. The membrane potential is the difference in electrical potential between the inside and the outside of a cell. All neurons, axons, and muscle fibers have a membrane potential. Membrane potentials include resting potentials, action potentials, and local potentials such as synaptic potentials, generator (or receptor) potentials, and electrotonic potentials. All membrane potentials result from ion flow through channels in the membrane.
Local potentials are localized changes in a number of ion channels that change the membrane potential in response to stimuli. They are graded signals whose size varies in proportion to the size of the stimulus. They remain localized in the area of the cell in which they are generated; that is they do not spread to involve the entire cell. Local potentials can be summated and integrated by single cells and are an integral part of the processing of information by the nervous system. Changes in ion channels underlying local potentials are generated by neurochemical transmitters synaptic and generator potentials or the flow of electrical current, the electrotonic potentials
The concentration of sodium, calcium, and chloride ions is higher extracellularly and that of potassium ions and impermeable anions (A) is higher intracellularly (Table 1). The equilibrium potential of each ion is the voltage difference across the membrane that exactly offsets the tendency of the ion to move down its concentration gradient. Ions can move across the cell membrane passively through ion channels or by adenosine triphosphate (ATP)-dependent binding to carrier molecules. Some ion channels are open at rest, but most open (or close) in response to stimuli, including changes in membrane potential (voltage-gated ion channels), binding receptor (ligand-gated channels), or chemical changes in the cytoplasm (chemical-gated ion channels). The opening of a channel for a particular ion brings the membrane potential toward the equilibrium potential of that ion.
Thus, at a given time, the membrane potential is determined by the concentration gradient of the ions (which determines their respective equilibrium potentials) and by any changes in the permeability to individual ions across the membrane (Fig. 1). The survival and excitability of the cell depend on the membrane potential. Maintaining this potential requires energy metabolism for the ATP- dependent sodium/potassium pump.
As a result of the selective permeability of the membrane and the imbalance in concentration of the potassium (K+), the potassium ions flow outward from the cell interior. The net movement of potassium (K+) out of the cell creates a resting potential across the nerve cell membrane of about -70 mV with an excess of negative charge (-) inside and an excess of positive (+) charge outside the cell. It is the energy of this resting potential that the neuron taps each time an impulse is generated.
Following a stimulus, there is a sudden change in permeability of the membrane to sodium (Na+) (opening of the channels to sodium), which rushes into the cell interior, causing a rapid alteration in the voltage at the membrane from -70 mV to +35 mV. This reversal in the polarity of the charge at the membrane is called depolarization. Note the arrangement of charges at the membrane during this time, they are reversed. After 0.8 millisecond, the sodium (Na+) channels close; at the same time, an increased number of potassium (K+) channels open (potassium permeability) and intracellular potassium (K+) escapes to the outside. This event drives the membrane potential back toward its initial value, -70 mV, a phenomenon called re-polarization. During this stage, there is a brief hyperpolarization or "overshooting" of the membrane potential.
The restorative process is made complete by the sodium (Na+) and potassium (K+)pumps, which move sodium (Na+) and potassium (K+), respectively, out of and into the cell. These ions are moved against their gradients by these metabolic, energy-utilizing, enzyme-operated pumps until a stable, resting membrane potential of about -70mV is once again achieved.
As a result of the selective permeability of the membrane and the imbalance in concentration of the potassium (K+), the potassium (K+) ions flow outward from the cell interior. The net movement of potassium (K+) out of the cell creates a resting potential across the nerve cell membrane of about -70mV with an excess of negative charge (-) inside and an excess of positive (+) charge outside the cell. It is the energy of this resting potential that the neuron taps each time an impulse is generated.
Generator, or receptor potentials occur in receptors in neural structures in the body, such as the touch receptors in the skin or the light receptors in the eye that respond to specific stimuli. Receptor potentials are also local potentials caused by opening of ion channels and are localized and graded. They can generate electrotonic potentials and thereby initiate action potentials.
Synaptic potentials are local potentials arising from postsynaptic ion channels opening in response to the action of a neurotransmitter released by presynaptic cells. Neurotransmitters transmit information from one cell to another by converting the electrical signal (action potential) into a chemical signal (neurotransmitter release) and then back into an electrical signal (synaptic potential or membrane potential change.) In turn, synaptic potentials produce electrotonic potentials, which can then initiate another action potential.
Transient alterations in function are the result of reversible disturbances in neuronal excitability., the reversible disturbances in neuronal excitability, the ability to propagate action potentials, or communication via chemical synapses. Transient disorders reflect abnormalities in resting, local, or action potentials due to the failure of ion pumps to maintain electrochemical gradients, impaired function of the ion channels or alterations in the ionic composition of the extracellular fluid. Transient disorders may be generalized or focal and be manifested by excessive activity, decreased activity or both.
Local potentials are localized changes in a number of ion channels that change the membrane potential in response to stimuli. They are graded signals whose size varies in proportion to the size of the stimulus. They remain localized in the area of the cell in which they are generated; that is they do not spread to involve the entire cell. Local potentials can be summated and integrated by single cells and are an integral part of the processing of information by the nervous system. Changes in ion channels underlying local potentials are generated by neurochemical transmitters synaptic and generator potentials or the flow of electrical current, the electrotonic potentials
The concentration of sodium, calcium, and chloride ions is higher extracellularly and that of potassium ions and impermeable anions (A) is higher intracellularly (Table 1). The equilibrium potential of each ion is the voltage difference across the membrane that exactly offsets the tendency of the ion to move down its concentration gradient. Ions can move across the cell membrane passively through ion channels or by adenosine triphosphate (ATP)-dependent binding to carrier molecules. Some ion channels are open at rest, but most open (or close) in response to stimuli, including changes in membrane potential (voltage-gated ion channels), binding receptor (ligand-gated channels), or chemical changes in the cytoplasm (chemical-gated ion channels). The opening of a channel for a particular ion brings the membrane potential toward the equilibrium potential of that ion.
Thus, at a given time, the membrane potential is determined by the concentration gradient of the ions (which determines their respective equilibrium potentials) and by any changes in the permeability to individual ions across the membrane (Fig. 1). The survival and excitability of the cell depend on the membrane potential. Maintaining this potential requires energy metabolism for the ATP- dependent sodium/potassium pump.
As a result of the selective permeability of the membrane and the imbalance in concentration of the potassium (K+), the potassium ions flow outward from the cell interior. The net movement of potassium (K+) out of the cell creates a resting potential across the nerve cell membrane of about -70 mV with an excess of negative charge (-) inside and an excess of positive (+) charge outside the cell. It is the energy of this resting potential that the neuron taps each time an impulse is generated.
Following a stimulus, there is a sudden change in permeability of the membrane to sodium (Na+) (opening of the channels to sodium), which rushes into the cell interior, causing a rapid alteration in the voltage at the membrane from -70 mV to +35 mV. This reversal in the polarity of the charge at the membrane is called depolarization. Note the arrangement of charges at the membrane during this time, they are reversed. After 0.8 millisecond, the sodium (Na+) channels close; at the same time, an increased number of potassium (K+) channels open (potassium permeability) and intracellular potassium (K+) escapes to the outside. This event drives the membrane potential back toward its initial value, -70 mV, a phenomenon called re-polarization. During this stage, there is a brief hyperpolarization or "overshooting" of the membrane potential.
The restorative process is made complete by the sodium (Na+) and potassium (K+)pumps, which move sodium (Na+) and potassium (K+), respectively, out of and into the cell. These ions are moved against their gradients by these metabolic, energy-utilizing, enzyme-operated pumps until a stable, resting membrane potential of about -70mV is once again achieved.
As a result of the selective permeability of the membrane and the imbalance in concentration of the potassium (K+), the potassium (K+) ions flow outward from the cell interior. The net movement of potassium (K+) out of the cell creates a resting potential across the nerve cell membrane of about -70mV with an excess of negative charge (-) inside and an excess of positive (+) charge outside the cell. It is the energy of this resting potential that the neuron taps each time an impulse is generated.
Generator, or receptor potentials occur in receptors in neural structures in the body, such as the touch receptors in the skin or the light receptors in the eye that respond to specific stimuli. Receptor potentials are also local potentials caused by opening of ion channels and are localized and graded. They can generate electrotonic potentials and thereby initiate action potentials.
Synaptic potentials are local potentials arising from postsynaptic ion channels opening in response to the action of a neurotransmitter released by presynaptic cells. Neurotransmitters transmit information from one cell to another by converting the electrical signal (action potential) into a chemical signal (neurotransmitter release) and then back into an electrical signal (synaptic potential or membrane potential change.) In turn, synaptic potentials produce electrotonic potentials, which can then initiate another action potential.
Transient alterations in function are the result of reversible disturbances in neuronal excitability., the reversible disturbances in neuronal excitability, the ability to propagate action potentials, or communication via chemical synapses. Transient disorders reflect abnormalities in resting, local, or action potentials due to the failure of ion pumps to maintain electrochemical gradients, impaired function of the ion channels or alterations in the ionic composition of the extracellular fluid. Transient disorders may be generalized or focal and be manifested by excessive activity, decreased activity or both.