In the fast response action potential of cardiac muscle, the sarcolemma rapidly depolarizes and reaches a plateau. In the plateau phase, Ca2+ released by the glycocalyx comes into the muscle cell from the extracellular fluid. This Ca2+ is called "trigger Ca2+" because it induces the release of Ca2+ from the sarcoplasmic reticulum.
Calcium....
The structure responsible for storing calcium in skeletal muscle fibers at rest is the sarcoplasmic reticulum. This organelle regulates the release of calcium ions during muscle contraction to trigger the muscle fiber to contract.
When calcium is needed, the parathyroid gland sends the parathyroid hormone to the kidneys to trigger the production of vitamin D (which is actually classified as a hormone). The vitamin D hormone, in turn, prompts the intestines to transfer calcium from food to the blood. When calcium intake is too small to support normal functions, both vitamin D and the parathyroid hormone trigger a process in which stored calcium is mobilized from the bones.
Factors such as cellular stress, hormone fluctuations, or disruption of ion channels or pumps can raise the concentration of calcium ions in a cell. Additionally, certain intracellular signaling pathways can trigger the release of calcium from internal stores.
The calcium ion is responsible for causing the presynaptic vesicle to fuse to the axon membrane in a process called exocytosis. When an action potential reaches the presynaptic terminal, calcium ions enter the terminal and trigger the fusion of the vesicle with the axon membrane, releasing neurotransmitters into the synaptic cleft.
Calcium....
Calcium ions
Only calcium ion channels to pass through it.
sodium-potassium ions
The structure responsible for storing calcium in skeletal muscle fibers at rest is the sarcoplasmic reticulum. This organelle regulates the release of calcium ions during muscle contraction to trigger the muscle fiber to contract.
The ion needed to initiate the release of acetylcholine into the synaptic cleft is calcium (Ca2+). When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium to enter and trigger the release of acetylcholine-containing vesicles.
When calcium is needed, the parathyroid gland sends the parathyroid hormone to the kidneys to trigger the production of vitamin D (which is actually classified as a hormone). The vitamin D hormone, in turn, prompts the intestines to transfer calcium from food to the blood. When calcium intake is too small to support normal functions, both vitamin D and the parathyroid hormone trigger a process in which stored calcium is mobilized from the bones.
The structure that allows calcium ions to enter cardiac muscle cells is the voltage-gated L-type calcium channels, also known as dihydropyridine receptors. These channels open in response to depolarization of the cell membrane, allowing calcium to flow into the cell and trigger muscle contraction.
The ion that enters the axon nerve terminal to trigger neurotransmitter release is calcium (Ca2+). When an action potential reaches the nerve terminal, voltage-gated calcium channels open, allowing calcium ions to flow into the cell and initiate the process of exocytosis of neurotransmitter-containing vesicles.
Calcium ions trigger the release of neurotransmitter at the presynaptic membrane. When an action potential reaches the presynaptic terminal, it causes voltage-gated calcium channels to open, allowing calcium ions to enter the cell. The influx of calcium ions triggers the fusion of synaptic vesicles with the presynaptic membrane, leading to the release of neurotransmitter into the synaptic cleft.
The stimulus for acetylcholine release is the action potential traveling down the axon of the presynaptic neuron. This depolarization causes calcium channels to open, allowing calcium ions to enter the axon terminal and trigger the release of acetylcholine into the synaptic cleft.
The organelle that stores calcium in resting muscle cells is the sarcoplasmic reticulum. Calcium ions are released from the sarcoplasmic reticulum during muscle contraction to trigger muscle activity.