Low calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ions, causing a progressive depolarization, which increases the possibility of action potentials. These action potentials may be spontaneously generated, causing contraction of skeletal muscles (tetany).
Calcium
In smooth muscle, the calcium needed for contraction primarily comes from the extracellular space. When smooth muscle cells are stimulated, calcium channels in the cell membrane open, allowing calcium ions to flow into the cell. Additionally, some calcium can also be released from the sarcoplasmic reticulum, but the extracellular influx is the main source for initiating contraction. This influx of calcium activates the contraction process by interacting with calmodulin and subsequently activating myosin light chain kinase.
Yes, hypercalcemia causes nervous system depression - the opposite of (see below) According to the Human Anatomy and Physiology Textbook by Marieb, hypocalcemia causes neuron excitation and if severe enough, leads to tetany and then paralysis. this is because both serum calcium and intracellular calcium are increased. The reason hypocalcemia causes neuron excitation (contrary to the above logic) is because a decrease in extracellular calcium concentration increases the neuron membrane's permeability to sodium and allows sodium to easily depolarize the neuron's membrane and cause an action potential. Additionally The membrane threshold becomes refractory to depolarization thus many of the symptoms are related to the loss of cell membrane excitability. How extracellular calcium controls sodium membrane permeability is another question.
When an action potential arrives at the presynaptic terminal, voltage-gated calcium channels open, allowing calcium ions to enter the cell. The influx of calcium triggers the release of neurotransmitter vesicles from the presynaptic terminal into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, leading to changes in the postsynaptic cell's membrane potential.
depolarization of the presynaptic membrane due to an arriving action potential
There is no neurotransmitter release from the axon terminal when there are no calcium ions in the extracellular solution. This is because the exocytosis of the synaptic vesicles is calcium dependent.
Calcium
The principal elements in the extracellular fluid are sodium, potassium and calcium.
False. The most abundant negative ion in extracellular fluid is chloride, not calcium. Calcium is usually found as a positively charged ion in extracellular fluid.
In smooth muscle, the calcium needed for contraction primarily comes from the extracellular space. When smooth muscle cells are stimulated, calcium channels in the cell membrane open, allowing calcium ions to flow into the cell. Additionally, some calcium can also be released from the sarcoplasmic reticulum, but the extracellular influx is the main source for initiating contraction. This influx of calcium activates the contraction process by interacting with calmodulin and subsequently activating myosin light chain kinase.
calcium ; sodium
This electrical charge is called the resting membrane potential. It is generated by the unequal distribution of ions such as sodium, potassium, chloride, and calcium inside and outside the cell. The resting membrane potential plays a crucial role in cell communication and proper functioning of the nervous system.
Yes, hypercalcemia causes nervous system depression - the opposite of (see below) According to the Human Anatomy and Physiology Textbook by Marieb, hypocalcemia causes neuron excitation and if severe enough, leads to tetany and then paralysis. this is because both serum calcium and intracellular calcium are increased. The reason hypocalcemia causes neuron excitation (contrary to the above logic) is because a decrease in extracellular calcium concentration increases the neuron membrane's permeability to sodium and allows sodium to easily depolarize the neuron's membrane and cause an action potential. Additionally The membrane threshold becomes refractory to depolarization thus many of the symptoms are related to the loss of cell membrane excitability. How extracellular calcium controls sodium membrane permeability is another question.
When an action potential arrives at the presynaptic terminal, voltage-gated calcium channels open, allowing calcium ions to enter the cell. The influx of calcium triggers the release of neurotransmitter vesicles from the presynaptic terminal into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, leading to changes in the postsynaptic cell's membrane potential.
Calcium
depolarization of the presynaptic membrane due to an arriving action potential
The membrane action potential triggers the release of calcium ions from the sarcoplasmic reticulum through a process called excitation-contraction coupling. This is mediated by the protein complex known as the ryanodine receptor, which allows calcium to flow out of the sarcoplasmic reticulum and into the cytoplasm upon stimulation by the action potential.