16.2 How Neurons Communicate – Concepts Of Biology

Summary

Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired. The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.

Exercises

  1. Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K+ through voltage-gated K+ channels. Which part of the action potential would you expect potassium channels to affect?
  2. For a neuron to fire an action potential, its membrane must reach ________.
    1. hyperpolarization
    2. the threshold of excitation
    3. the refractory period
    4. inhibitory postsynaptic potential
  3. After an action potential, the opening of additional voltage-gated ________ channels and the inactivation of sodium channels, cause the membrane to return to its resting membrane potential.
    1. sodium
    2. potassium
    3. calcium
    4. chloride
  4. What is the term for protein channels that connect two neurons at an electrical synapse?
    1. synaptic vesicles
    2. voltage-gated ion channels
    3. gap junction protein
    4. sodium-potassium exchange pumps
  5. How does myelin aid propagation of an action potential along an axon? How do the nodes of Ranvier help this process?
  6. What are the main steps in chemical neurotransmission?

Answers

  1. Potassium channel blockers slow the repolarization phase, but have no effect on depolarization.
  2. B
  3. B
  4. C
  5. Myelin prevents the leak of current from the axon. Nodes of Ranvier allow the action potential to be regenerated at specific points along the axon. They also save energy for the cell since voltage-gated ion channels and sodium-potassium transporters are not needed along myelinated portions of the axon.
  6. An action potential travels along an axon until it depolarizes the membrane at an axon terminal. Depolarization of the membrane causes voltage-gated Ca2+ channels to open and Ca2+ to enter the cell. The intracellular calcium influx causes synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. Depending on the specific neurotransmitter and postsynaptic receptor, this action can cause positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions to enter the cell.

Glossary

action potential self-propagating momentary change in the electrical potential of a neuron (or muscle) membrane depolarization change in the membrane potential to a less negative value excitatory postsynaptic potential (EPSP) depolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell hyperpolarization change in the membrane potential to a more negative value inhibitory postsynaptic potential (IPSP) hyperpolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell long-term depression (LTD) prolonged decrease in synaptic coupling between a pre- and postsynaptic cell membrane potential difference in electrical potential between the inside and outside of a cell refractory period period after an action potential when it is more difficult or impossible for an action potential to be fired; caused by inactivation of sodium channels and activation of additional potassium channels of the membrane saltatory conduction “jumping” of an action potential along an axon from one node of Ranvier to the next summation process of multiple presynaptic inputs creating EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential synaptic cleft space between the presynaptic and postsynaptic membranes synaptic vesicle spherical structure that contains a neurotransmitter

Tag » When Calcium Ions Enter The Synaptic Terminal