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  1.  Ion Channels    





    In a Word document, describe in detail the “sequence of events” from the stimulation of a neuronal dendrite to the relaxation of a skeletal muscle. Some events overlap, so you may want to create a separate list for neuron and for muscle. Be sure to note where the lists link together. Include a reference list and at least the following items and concepts:

    Action potentials
    Active transport
    Contractile proteins
    Graded potentials (IPSP and/or EPSP)
    Ligand-gated channels
    Refractory period
    Regulatory proteins
    Resting potentials
    Sarcoplasmic reticulum
    Voltage-gated channels


Subject Nursing Pages 6 Style APA


Ion Channels: Neuron and Muscle Stimulation

            Muscle contraction occurs when a muscle receive a signal or an impulse from the nervous system. A motor neuron uses a neurotransmitter to signal contraction of the muscle fibers; this is point where there is point of intersection between or link between neuronal stimulation and muscle contraction (Khurana, 2018). Sequence of events that occur in a typical neuron to contraction and relaxation of a skeletal muscle is as described below. Step (xi.) of neuron stimulation and impulse transmission overlaps or intersects with step (i.) of muscular contraction.

Neuron Stimulation and Impulse Transmission

  1. A sensory impulse is first received on the receptors on the sensory nerve dendrites and converted into an electrical signal in the form a graded potential. The graded potential is initiated by a stimulus and transmitted to the axon hillock where it is converted into an action potential. The neuronal membrane on the dendritic end is depolarized from a resting membrane potential (-70mV) to stimulation of an action potential when the depolarization goes beyond the threshold (-55mV) (Khurana, 2018).
  2. In a resting membrane potential there are more Na+ ions outside the neuron than inside; whereas, there are more K+ ions inside a neuron than on the outside. However, a slightly small proportion of K+ and Na2+ ions continue to flow freely out or into a neuron through leakage channels (Khurana, 2018).
  • When a neuronal dendrite is stimulated the Na+ voltage gated channels open thus, allowing Na+ ions move into a neuronal cytoplasm leading to depolarization of a neuron. During this instance, K+ voltage-gated channels remain closed (Khurana, 2018).
  1. When depolarization goes beyond the threshold an action potential is initiated. It results in closure of Na+ voltage-gated channels and subsequent opening of the K+ voltage-gated channels as neuronal membrane depolarizes to +30mV. K+ ions then escape the neuronal cytoplasm and flows outside as a result of difference in ion gradient. This leads to repolarization (Khurana, 2018).
  2. Opening of the Na2+/ K+ ATPase pumps also facilitates fast repolarization of the neuronal membrane since depends on active transport of 2 K+ ions into the neuronal cytoplasm and 3 Na2+ ions out into the neuron (Khurana, 2018).
  3. Closure of Na+ channels and opening of K+ channels and Na2+/ K+ ATPase pumps leads to hyperpolarization of the neuronal membrane. This is repolarization of the membrane beyond -70mV before closure of these channels. Na2+ and K+ leaky channels are responsible for adjusting the membrane resting potential to -70mV (Khurana, 2018).
  • The entire period between one stimulus that causes an action potential in a neuron to another is called refractory period (Song, Zhou, & Juusola, 2017).
  • At this step, action potential is transmitted from one section of neuron to the next in a wavelike motion to the respective sensory centers in the brain, where a nerve impulse is integrated and redirected to a respective motor center. Nerve transmission from one neuron to another is transmitted by release and diffusion of neurotransmitters such as dopamine from one neuron to another through a synaptic cleft. Motor neurons then transmit an impulse to the neuromuscular junction (Drukarch et al., 2018).
  1. At the neuromuscular junction, an action potential stimulates opening of voltage-gated Ca2+ ion channels, which leads to inflow of Ca2+ ions into a motor neuronal ending at near the synaptic cleft (Khurana, 2018).
  2. In the motor neuron, Ca2+ ions activate regulatory proteins, which in turn lead to phosphorylation of synapsin proteins. This leads to docking of the synaptic vesicles on the membrane neuronal membrane at the synaptic cleft (Khurana, 2018).
  3. Synaptic vesicles then fuse with the neuronal membrane leading to release of acetylcholine into the synaptic cleft. Acetylcholine then diffuses through the synaptic cleft to the bind to receptors on the postsynaptic membrane. Release of acetylcholine and its binding on the post-synaptic receptors is the point of intersection or overlap at which neuron transmission begins to stimulate muscle cells contraction (Khurana, 2018). Thus, (xi.) step of neuron stimulation and impulse transmission overlaps or intersects with step (i.) of muscular contraction.


Muscular Contraction

  1. Binding of acetylcholine on receptors at the post-synaptic membrane results in opening of ligand-gated channels (Slater, 2017).
  2. Ligand-gated channels aids inflow of Na+ ions into the muscle cell and outflow of K+ ions. In addition, voltage gated Na+ ions open that increasing inflow of Na+ ions into the muscle cell (Slater, 2017).
  • Activation of the muscle leads to propagation of an action potential in a muscle fiber, which in turn results in release of Ca2+ ions from sarcoplasmic reticulum into myofibrils (Slater, 2017).
  1. Ca2+ ions bind to and lead to displacement of tropomyosin from the myosin-binding-site on the actin fiber. Myosin and action are both muscular contractile proteins (Slater, 2017).
  2. Binding of the myosin on the actin filaments leads to formation of cross-bridges (Slater, 2017).
  3. Consumption of ATP leads to contraction of the myosin against actin filaments at the cross-bridge (Slater, 2017).
  • Binding to and release of myosin from the myosin-binding site on the actin filament is a cycle that leads to expenditure of energy in the form of ATP and results in muscle contraction (Slater, 2017).
  • When there is no more neural stimulation of the muscle cell, acetylcholinesterase that degrades acetylcholine at the synaptic cleft leading to cessation of muscle stimulation (Slater, 2017).
  1. This leads to active pumping of Ca2+ ions from the myofibrils to the sarcoplasmic reticulum (Slater, 2017).
  2. Besides, Na2+/ K+ ATPase pumps are activated thus leading to active pumping of 3 Na2+ ions out and 2 K+ ions out of the muscle cell, thus, stopping continuous muscle stimulation (Slater, 2017).
  3. Tropomyosin then binds on the myosin-bind site on actin thus blocking myosin from binding on it. This results in muscle relaxation (Slater, 2017).






Drukarch, B., Holland, H.A., Velichkov, M., Geurts, J.J., Glas, G., & Regt, H.W. (2018). Thinking about nerve impulse: A critical analysis of the electricity-centered conception of nerve excitability. Progress in Neurobiology, 169, 172-185. https://doi.org/10.1016/j.pneurobio.2018.06.009  

Khurana, I. (2018). Concise textbook of human physiology (3rd ed.). Philadelphia: Elsevier Health Sciences.

Slater C. R. (2017). The Structure of Human Neuromuscular Junctions: Some Unanswered Molecular Questions. International journal of molecular sciences18(10), 2183. doi:10.3390/ijms18102183.

Song, Z., Zhou, Y., & Juusola, M. (2017). Modelling elucidates how refractory period can provide profound nonlinear gain control to graded potential neurons. Psychological Reports, 5(11), e13306.






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