In: Anatomy and Physiology
For each of these 3 channels, describe where they are found, how they work, and the role they play in physiology: 1) the cardiac ryanodine channel, 2) the voltage gated calcium channel on neurons, and 3) the dihydropyridine ryanodine channel
1) Cardiac ryanodine channel:
Location: This is a calcium ion channels found on the sarcoplasmic reticulum of the cardiac muscle. This ryanodine channel or RyR helps in the cardiac muscle contraction through calcium ion release. This channels are mainly located in the terminal cistern of the sarcoplasmic reticulum of cardiac muscle.
Mechanism of action: The terminal cistern of the sarcoplasmic reticulum is the store house of the calcium ions. In relax condition this this ryanodine channels are closed. When action potential arrives at the T tubule, the L type calcium channels in the T tubule is opened and calcium influx occure. This calcium ions triggers the opening of ryanodine channels in the sarcoplasmic reticulum. This opening of ryanodine cahnnels causes the release of stored calcium in the sarcoplasm. This calcium induced calcium release is the sole mechanism of ryanodine channels.
Physiological role of this channels: The opening of ryanodine channels results in release of store calcium from the sarcoplasmic reticulum to sarcoplasm. This calcium ion will then binds with troponin C complex of the troponin. This troponin-tropomyosin complex causes the cross bridge formation and results inthe muscle contraction. This contraction of cardiac muscle helps to maintain proper heart beat and contractility power of the heart muscle.
2) Voltage gated calcium channels on the neuron:
Location: This voltage gated calcium channels on neuron is located in the presynaptic membrane of neuromuscular junction.
Mechanism of action: in neuromuscular junction, the presynaptic neuron is excited by a threshold excitation. When a threshold potential is reached the action potential is generated in the presynaptic neurons. This action potential when reach the terminal button of the presynaptic neuron then it opens the voltage gated calcium channels. This opening of voltage gated calcium channels causes rapid influx of calcium ions from the extracellular fluid of the synaptic cleft into the terminal button of presynaptic neuron.
Physiological role of this channels: The calcium influx through this voltage gated calcium channels cause the vesicular docking of neurotransmitter containing vesicles in the docking site of the presynaptic neuron. The calcium ions at first binds with synaptotagmin protein of the vesicle. This calcium binding with synaptotagmin protein causes others vesicular protein to dock in the docking region for exocytosis of neurotransmitter into the synaptic cleft. This released neurotransmitter then binds with the receptor in the postsynaptic membrane of the neuron and causes the transmission of action potential to the postsynaptic neuron. So vesicular docking and exocytosis of neurotransmitter is the main physiological role played by the opening of voltage gated calcium channels in the presynaptic neuron.
3) The dihydropyridine-ryanodine channels:
Location: This calcium channels are located in the skeletal muscle. The dihydropyridine receptor is located in the transverse tubule of the skeletal muscle and ryanodine receptor is located in the sarcoplasmic reticulum of the skeletal muscle.
Mechanism of action: The dihydropyridine channel or receptor is coupled with the ryanodine channels of sarcoplasmic reticulum. In relax condition this two channels are coupled together tightly and block the calcium release by sarcoplasmic reticulum. When excitation is arrived in the T tubule of skeletal muscle the dihydropyridine receptor sense the voltage change in the T tubule and opens up the ryanodine channels. This opening of ryanodine channels by dihydropyridine receptor causes the release of store calcium in the sarcoplasm.
Physiological role of this channels: This opening of ryanodine channels by dihydropyridine channels causes the calcium release from thd sarcoplasmic reticulum. This calcium then bind with the troponin C complex and initiates the cross-bridge formation for muscle contraction. So skeletal muscle contraction is the main physiological role of this dihydropyridine-ryanodine channels.