chapter 35

• Resting membrane potential


  The difference in total charge between the inside and outside of the cell
• A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts more negative than the outside (-70 mV)
• Resting membrane potential


  • Caused by differences in the concentrations of ions inside and outside the cell
  • Potassium ions (K+) accumulate inside the cell due to a net movement with the concentration gradient
  • Negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement
  • Sodium potassium pumps help to maintain the resting potential
• Action potential


  A brief reversal of the resting membrane potential that allows transmission of a signal within a neuron
• Action potential


  1. Neurotransmitter molecules bind to receptors on neuron's dendrites

  2. Ion channels open, allowing positive ions to enter the neuron and depolarize the membrane

  3. Stimulus depolarizes the neuron to its threshold potential (-55 mV)

  4. Na+ channels in the axon hillock open, allowing positive ions to enter the cell

  5. Neuron completely depolarizes to a membrane potential of about +40 mV

  6. Na+ channels close and the cell resets its membrane voltage back to the resting potential
• Depolarization


  A decrease in the difference in voltage between the inside and outside of the neuron
• Hyperpolarization


  The cell becomes more negatively charged than the resting potential
• Action potentials are considered an "all-or-nothing" event, in that, once the threshold potential is reached, the neuron always completely depolarizes
• Voltage-gated ion channels


  Ion channels that change their structure in response to voltage changes and regulate the relative concentrations of different ions inside and outside the cell
• Voltage-gated ion channels have different configurations: open, closed, and inactive
• Chemical synapse


  Neurotransmitter molecules are released from the presynaptic neuron and bind to receptors on the postsynaptic neuron
• Electrical synapse


  Ions can directly pass between the presynaptic and postsynaptic neurons through gap junctions
• Long-term potentiation


  An increase in the strength of a synapse that can last for hours or days
• Long-term depression


  A decrease in the strength of a synapse that can last for hours or days
• Action potential


  1. Neurotransmitter molecules bind to receptors on neuron's dendrites

  2. Ion channels open

  3. At excitatory synapses, positive ions enter neuron and depolarize membrane

  4. Stimulus depolarizes target neuron to threshold potential

  5. Na+ channels in axon hillock open, allowing positive ions to enter cell

  6. Neuron completely depolarizes to +40 mV

  7. Na+ channels close, K+ channels open, K+ leaves cell

  8. Cell hyperpolarizes

  9. Na+ channels return to resting state
• Action potentials are an "all-or-nothing" event
• Refractory period


  Period in which neuron cannot produce another action potential because sodium channels will not open
• Potassium channel blockers like amiodarone and procainamide

  Impede the movement of K+ through voltage-gated K+ channels
• Potassium channel blockers are used to treat cardiac dysrhythmia
• Propagation of action potential along axon

  Axon membrane depolarizes, then repolarizes
• Myelin


  • Insulates axon, increases speed of action potential conduction
  • In demyelinating diseases like multiple sclerosis, action potential conduction slows
• Nodes of Ranvier


  • Gaps in myelin sheath along axon, contain voltage-gated Na+ and K+ channels
  • Allow action potential to 'jump' from node to node (saltatory conduction)
• Presynaptic neuron


  Neuron transmitting the signal
• Postsynaptic neuron


  Neuron receiving the signal
• Chemical synapse


  1. Action potential depolarizes presynaptic membrane, opens Ca2+ channels

  2. Ca2+ entry causes synaptic vesicles to fuse with membrane and release neurotransmitter

  3. Neurotransmitter diffuses across synaptic cleft and binds to receptors on postsynaptic membrane
• Excitatory postsynaptic potential (EPSP)

  Depolarization of postsynaptic membrane caused by neurotransmitter binding
• Inhibitory postsynaptic potential (IPSP)


  Hyperpolarization of postsynaptic membrane caused by neurotransmitter binding
• Removal of neurotransmitter from synaptic cleft

  Neurotransmitter can diffuse away, be degraded by enzymes, or be recycled by presynaptic neuron
• Types of neurotransmitters


  • Acetylcholine
  • Biogenic amines (dopamine, serotonin, norepinephrine)
  • Amino acids (glycine, glutamate, aspartate, GABA)
  • Neuropeptides (substance P, endorphins)
• Electrical synapse


  Presynaptic and postsynaptic membranes are physically connected by gap junctions, allowing direct flow of current and small molecules
• Signaling in electrical synapses is virtually instantaneous and can be bidirectional
• Synaptic summation


  1. Multiple EPSPs from presynaptic neurons must occur around the same time to depolarize postsynaptic neuron enough to fire action potential

  2. IPSPs can cancel out EPSPs and vice versa

  3. Net change in postsynaptic membrane voltage determines if threshold of excitation is reached
• Synaptic summation and threshold for excitation act as a filter to prevent random "noise" from being transmitted as important information
• Brain-computer interfaces allow "locked-in" ALS patients to communicate by twitching their cheek
• If the EPSPs are strong enough to overcome the IPSPs and reach the threshold of excitation, the neuron will fire
• Brain-computer interface


  Technology that allows paralyzed patients to control a computer using only their thoughts
• Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig's Disease)


  • Neurological disease characterized by the degeneration of the motor neurons that control voluntary movements
  • Begins with muscle weakening and lack of coordination
  • Eventually destroys the neurons that control speech, breathing, and swallowing
  • Can lead to paralysis where patients require assistance from machines to breathe and communicate
• Brain-computer interface (BCI) technology

  Allows paralyzed patients to communicate and retain a degree of self-sufficiency
• Brain-computer interface technology


  1. Neural signals from a paralyzed patient are collected

  2. Decoded

  3. Fed to a tool, such as a computer, a wheelchair, or a robotic arm
• BCI technology can require many hours of training and long periods of intense concentration for the patient, and can also require brain surgery to implant the devices