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What affect does lowering extracellular calcium have on the resting membrane potential of a neuron?
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).
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What restores and puts the cell membrane to resting conditions after an action potential?
Calcium
What sequence of events occurs when an action potential arrives at the presynaptic terminal?
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.
Does hypercalcemia cause depression 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.
What causes calcium channels in the synaptic knob to open?
depolarization of the presynaptic membrane due to an arriving action potential
How does the membrane action potential get to the sarcoplasmic reticulum?
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.
What happened to the neurotransmitter release when switched from the control extracellular fluid to the extracellular fluid with no calcium?
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.
What restores and puts the cell membrane to resting conditions after an action potential?
Calcium
What is found in extracellular fluid?
The principal elements in the extracellular fluid are sodium, potassium and calcium.
True or False The most abundant negative ion in extracellular fluid is 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.
Electrical charge resulting from the difference between positive and negative ions outside and inside the brain cell membrane is called?
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.
What is the most cation extracellular fluid?
calcium ; sodium
What sequence of events occurs when an action potential arrives at the presynaptic terminal?
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.
Does hypercalcemia cause depression 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.
What causes calcium channels in the synaptic knob to open?
depolarization of the presynaptic membrane due to an arriving action potential
What is an extracellular cation that contributes to the hardness of bones and teeth?
Calcium
How does the membrane action potential get to the sarcoplasmic reticulum?
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.
What causes the vesicles inside a neuron to fuse with the plasma membrane?
When an action potential reaches the axon terminal, it triggers the opening of voltage-gated calcium channels. The influx of calcium causes the synaptic vesicles to move towards the cell membrane and fuse with it, releasing neurotransmitters into the synaptic cleft.
