voltage-dependent calcium channels

Examples of voltage-dependent calcium channels in the following topics:

• Peripheral Motor Endings

  • Upon the arrival of an action potential at the presynaptic neuron terminal, voltage-dependent calcium channels open and Ca2+ ions flow from the extracellular fluid into the presynaptic neuron's cytosol.
  • The depolarization activates L-type, voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.
  • As intracellular calcium levels rise, the motor proteins responsible for the contractile response are able to interact, as shown in Figure 3, to form cross-bridges and undergo shortening.
  • The binding of acetylcholine at the motor end plate leads to intracellular calcium release and interactions between myofibrils to elicit contraction.

• Ion Channels

  • Voltage-gated sodium ion channels contribute to the "spike" of a neuron's action potential.
  • For example, ion channels can be voltage-sensitive in that they open and close in response to the voltage across the membrane.
  • Voltage-gated ion channels, also known as voltage-dependent ion channels, are channels whose permeability is influenced by the membrane potential.
  • They form another very large group, with each member having a particular ion selectivity and a particular voltage dependence.
  • Many are also time-dependent—in other words, they do not respond immediately to a voltage change, but only after a delay.

• Regulatory Proteins

  • A change in the receptor conformation causes an action potential, activating voltage-gated L-type calcium channels, which are present in the plasma membrane.
  • The inward flow of calcium from the L-type calcium channels activates ryanodine receptors to release calcium ions from the sarcoplasmic reticulum.
  • This mechanism is called calcium-induced calcium release (CICR).
  • It is not understood whether the physical opening of the L-type calcium channels or the presence of calcium causes the ryanodine receptors to open.
  • Calcium remains in the sarcoplasmic reticulum until released by a stimulus.

• Synaptic Transmission

  • When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated Na+ channels.
  • This depolarization causes voltage-gated Ca2+ channels to open.
  • A calcium sensing protein binds calcium and interacts with SNARE proteins.
  • Calcium is quickly removed from the terminal.
  • When the presynaptic membrane is depolarized, voltage-gated Ca2+ channels open and allow Ca2+ to enter the cell.

• Mechanism and Contraction Events of Cardiac Muscle Fibers

  • Cardiac muscle fibers undergo coordinated contraction via calcium-induced calcium release conducted through the intercalated discs.
  • In cardiac muscle, ECC is dependent on a phenomenon called calcium-induced calcium release (CICR), which involves the influx of calcium ions into the cell, triggering further release of ions into the cytoplasm.
  • The mechanism for CIRC is receptors within the cardiomyocyte that bind to calcium ions when calcium ion channels open during depolarization, releasing more calcium ions into the cell.
  • As the action potential travels between sarcomeres, it activates the calcium channels in the T-tubules, resulting in an influx of calcium ions into the cardiomyocyte.
  • Calcium in the cytoplasm then binds to cardiac troponin-C, which moves the troponin complex away from the actin binding site.

• The Action Potential and Propagation

  • The depolarization, also called the rising phase, is caused when positively charged sodium ions (Na+) suddenly rush through open voltage-gated sodium channels into a neuron.
  • The repolarization or falling phase is caused by the slow closing of sodium channels and the opening of voltage-gated potassium channels.
  • As the sodium ion entry declines, the slow voltage-gated potassium channels open and potassium ions rush out of the cell.
  • Hyperpolarization is a phase where some potassium channels remain open and sodium channels reset.
  • The propagation of action potential is independent of stimulus strength but dependent on refractory periods.

• Membrane Potentials as Signals

  • Membrane potential (also transmembrane potential or membrane voltage) is the difference in electrical potential between the interior and the exterior of a biological cell.
  • The opening and closing of ion channels can induce a departure from the resting potential.
  • This is called a depolarization if the interior voltage becomes more positive (say from –70 mV to –60 mV), or a hyperpolarization if the interior voltage becomes more negative (say from –70 mV to –80 mV).
  • The changes in membrane potential can be small or larger (graded potentials) depending on how many ion channels are activated and what type they are.
  • Action potentials are generated by the activation of certain voltage-gated ion channels.

• Gap Junctions

  • Each gap junction channel is made up of two half channels (hemichannels), one in each cell’s membrane. 
  • Each of these half channels is called a connexon. 
  • Examples of this includes calcium ions and cAMP (cyclic adenosine monophosphate).  
  • Depending on the type of gap junction in question, molecules can pass evenly in both directions, or asymmetrically, so in some gap junctions the molecules will move in one direction faster than in the other direction. 
  • The ability of the channel to open or close is made possible in part to calcium ions, which induce a reversible conformational change in the connexin molecules, which leads to the closure of a channel at its extracellular surface. 

• Facilitated transport

  • Channels are specific for the substance that is being transported.
  • Channel proteins are either open at all times or they are "gated," which controls the opening of the channel.
  • Cells involved in the transmission of electrical impulses, such as nerve and muscle cells, have gated channels for sodium, potassium, and calcium in their membranes.
  • This protein binds a substance and, in doing so, triggers a change of its own shape, moving the bound molecule from the outside of the cell to its interior; depending on the gradient, the material may move in the opposite direction .
  • Channel and carrier proteins transport material at different rates.

• Excitation–Contraction Coupling

  • A neural signal is the electrical trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm.
  • The receptors are sodium channels that open to allow the passage of Na+ into the cell when they receive neurotransmitter signal.
  • Neurotransmitter release occurs when an action potential travels down the motor neuron's axon, resulting in altered permeability of the synaptic terminal membrane and an influx of calcium.
  • As a neurotransmitter binds, these ion channels open, and Na+ ions cross the membrane into the muscle cell.
  • This reduces the voltage difference between the inside and outside of the cell, which is called depolarization.