excitation-contraction coupling

Examples of excitation-contraction coupling in the following topics:

• Peripheral Motor Endings

  • The highly excitable region of muscle fiber plasma membrane is responsible for initiation of action potentials across the muscle's surface, ultimately causing the muscle to contract.
  • This depolarization spreads across the surface of the muscle fiber and continues the excitation–contraction coupling to contract the muscle.
  • The affects of myasthenia gravis illustrate the importance of effective and functioning neuromuscular junctions for communication between neurons and muscles to allow contraction and relaxation of muscle fibers.
  • Skeletal muscle contracts following activation by an action potential.
  • The binding of acetylcholine at the motor end plate leads to intracellular calcium release and interactions between myofibrils to elicit contraction.

• Mechanism and Contraction Events of Cardiac Muscle Fibers

  • The gap junctions spread action potentials to support the synchronized contraction of the myocardium.
  • In cardiac, skeletal, and some smooth muscle tissue, contraction occurs through a phenomenon known as excitation contraction coupling (ECC).
  • The actual mechanical contraction response in cardiac muscle occurs via the sliding filament model of contraction.
  • The pathway of contraction can be described in five steps:
  • This removal of the troponin complex frees the actin to be bound by myosin and initiates contraction.

• Interactions of Skeletal Muscles

  • Skeletal muscle contractions can be grouped based on the length and frequency of contraction.
  • The time between the stimulus and the initiation of contraction is termed the latent period, which is followed by the contraction period.
  • When a weak signal is sent by the central nervous system to contract a muscle, the smaller motor units, being more excitable than the larger ones, are stimulated first.
  • As the strength of the signal increases, more (and larger) motor units are excited.
  • If the frequency of these contractions increases to the point where maximum tension is generated and no relaxation is observed then the contraction is termed a tetanus.

• Adrenergic Neurons and Receptors

  • There are two main groups of adrenergic receptors, α and β, with several subtypes. α receptors have the subtypes α1 (a Gq coupled receptor) and α2 (a Gi coupled receptor).
  • Adrenaline or noradrenaline are receptor ligands to α1, α2 or βadrenergic receptors (the pathway is shown in ). α1 couples to Gq, which results in increased intracellular Ca2+ which results in smooth muscle contraction. α2, on the other hand, couples to Gi, which causes a decrease of cAMP activity, resulting in smooth muscle contraction. β receptors couple to Gs, and increases intracellular cAMP activity, resulting in heart muscle contraction, smooth muscle relaxation and glycogenolysis.
  • Specific actions of the α1 receptor mainly involve smooth muscle contraction.
  • Other areas of smooth muscle contraction are as follows:
  • Adrenaline and noradrenaline are ligands to α1, α2, or β-adrenergic receptors. α1 receptors couple to Gq, resulting in increased intracellular Ca2+ and causing smooth muscle contraction. α2 receptors couple to Gi, causing a decrease in cAMP activity and resulting in smooth muscle contraction. β receptors couple to Gs, increasing intracellular cAMP activity and resulting in heart muscle contraction, smooth muscle relaxation and glycogenolysis.

• Electrical Events

  • Cardiac contraction is initiated in the excitable cells of the sinoatrial node by both spontaneous depolarization and sympathetic activity.
  • The SA and AV nodes initiate the electrical impulses that cause contraction within the atria and ventricles of the heart.
  • The SA node nerve impulses travel through the atria and cause muscle cell depolarization and contraction of the atria directly.
  • The SA node impulses also travel to the AV node, which stimulates ventricular contraction.
  • Without autonomic nervous stimulation, it sets the rate of ventricular contraction at 40-60 bpm.

• Rigor Mortis

  • Physiologically, rigor mortis is caused a release of calcium facilitating crossbridges in the sarcomeres; the coupling between myosin and actin cannot be broken, creating a constant state of muscle contraction until enzymatic decomposition eventually removes the crossbridges.
  • Unlike muscular contractions during life, the body after death is unable to complete the cycle and release the coupling between the myosin and actin, creating a state of muscular contraction until the breakdown of muscle tissue by enzymes (endogenous or bacterial) during decomposition .
  • As part of the process of decomposition, the myosin heads are degraded by the enzymes, allowing the muscle contraction to release and the body to relax.

• Hypotonia and Hypertonia

  • The loss of motor neuron control leads to increased excitability of muscle fibers.
  • Effects of hypertonia include spasticity dystonia (a state of prolonged muscle contractions) and rigidity (a state of muscle stiffness and decreased flexibility).
  • Spastic hypertonia is the general condition of muscle spasms caused by random contractions of the muscles, and is typical in cerebral palsy and spinal cord injuries; it can also occur from stroke.
  • Dystonic hypertonia is the resistance to passive stretching in muscles, and the return of limbs to fixed positions after contraction.
  • Hypotonia is the state of reduced muscle tone and tension, resulting in lessened ability to generate force from muscle contractions.

• Female Sexual Response

  • Sexual arousal (also sexual excitement) is the arousal of sexual desire, during or in anticipation of sexual activity.
  • If sexual stimulation continues, then sexual arousal may peak into orgasm, resulting in rhythmic muscular contractions in the pelvic region characterized by an intense sensation of pleasure.
  • The uterus typically contracts during orgasm, and with advancing age, those contractions may actually become painful.

• Cholinergic Neurons and Receptors

  • Sodium ions then enter the muscle cell, initiating a sequence of steps that finally produce muscle contraction.
  • Although acetylcholine induces contraction of skeletal muscle, it acts via a different type of receptor (muscarinic, see ) to inhibit contraction of cardiac muscle fibers.
  • In the cerebral cortex, tonic ACh inhibits layer 4 neurons, the main targets of thalamocortical inputs while exciting pyramidal cells in layers 2/3 and 5.
  • At the same time, acetylcholine acts through nicotinic receptors to excite certain groups of inhibitory interneurons in the cortex, which further dampen cortical activity.

• Structural Diversity of Neurons

  • Neurons are electrically excitable cells that are the structural unit of the nervous system.
  • Motor neurons receive signals from the brain and spinal cord to initiate muscle contractions and affect glands.