No, hyperpolarization graded potentials do not lead to action potentials. Hyperpolarization makes the membrane potential more negative, which inhibits the generation of an action potential by increasing the distance from the threshold potential needed to trigger an action potential.
More sodium ions pile up (accumulate) at the axon hillock from the combination of the two (or more) graded potentials, which may be then be sufficient to initiate the action potential.
If the axolemma becomes more permeable to potassium ions, it can lead to an increase in the efflux of potassium ions from the axon. This efflux of potassium ions could potentially cause hyperpolarization of the axon, making it more difficult to generate an action potential and conduct electrical signals.
Graded potentials can form on receptor endings in response to stimuli such as pressure, temperature, or chemicals. These graded potentials can lead to the generation of action potentials that transmit the sensory information to the central nervous system for processing.
When a stimulus is applied to a sensory ending, it can lead to the generation of a receptor potential. This receptor potential is a graded potential that can trigger an action potential along the sensory neuron, leading to the transmission of the sensory input to the central nervous system for processing and interpretation.
Temporal
More sodium ions pile up (accumulate) at the axon hillock from the combination of the two (or more) graded potentials, which may be then be sufficient to initiate the action potential.
More sodium ions pile up (accumulate) at the axon hillock from the combination of the two (or more) graded potentials, which may be then be sufficient to initiate the action potential.
If ion pumps open to hyperpolarize the neuron (chloride ions flowing into the neuron) elsewhere, leading to a net polarization/hyperpolarization, then the action potential will not be created.In order for the AP to be induced, a NET depolarization (influx of cations) must be created above the membrane threshold.
If the axolemma becomes more permeable to potassium ions, it can lead to an increase in the efflux of potassium ions from the axon. This efflux of potassium ions could potentially cause hyperpolarization of the axon, making it more difficult to generate an action potential and conduct electrical signals.
Graded potentials can form on receptor endings in response to stimuli such as pressure, temperature, or chemicals. These graded potentials can lead to the generation of action potentials that transmit the sensory information to the central nervous system for processing.
When a stimulus is applied to a sensory ending, it can lead to the generation of a receptor potential. This receptor potential is a graded potential that can trigger an action potential along the sensory neuron, leading to the transmission of the sensory input to the central nervous system for processing and interpretation.
Temporal
No, neurotransmitters do not create new action potentials. They transmit signals between neurons by binding to receptors on the receiving neuron, causing a change in the membrane potential of the receiving neuron which may lead to the generation of a new action potential.
Hypocalcemia can lead to a prolongation of the cardiac action potential due to reduced calcium influx. This can result in an increased risk of arrhythmias, as well as potential impairment of cardiac muscle contractility.
Sub threshold depolarisation of nerves, would be the influx of sodium (and maybe efflux of potassium depending) that doesn't cause enough depolarisation for an action potential to be fired. The summation of sub threshold depolarisations may cause an AP to be released. if they 'tip the balance' far enough. Hope this helps Edit: Above answer is vague. Sub threshold depolarizations do not occur as a result of efflux of potassium, which hyperpolarizes a neuron. They can be generated as EPSPs at the post synaptic membrane or result from persistant sodium channels, which do not completely inactivate (contributing to pacemaking activity). In both cases, gradual depolarization can lead to action potential generation.
The stage that immediately follows depolarization in an action potential is repolarization. During repolarization, potassium ions move out of the cell, causing the membrane potential to return to its resting state.
Under normal circumstances action potential will proceed unilaterally. An action potential cannot proceed down an axon and depolarize in the reverse direction on the same axon. It must carry information on one axon in one direction and then on another axon in a separate direction. In a lab you can depolarize neurons in the middle of an axon and it will depolarize bilaterally.