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Flashcards in Action Potentials Deck (16):

Resting Membrane Potential and Concentration Gradients

-Resting membrane potential of -40 - -90mV

 - [Na] is higher outside the cell, [K] is higher inside the cell

 - cell membrane is super permeable to [K] due to potassium leakage channels

 - maintains gradients through K/Na pumps, ATP-ase pumps 3 Na out, 2 K in


Sodium Voltage-Gated Channels: Gates and States

-Gate-m (activation gate) is normally closed, but opens when the cell becomes positive

-Gate-h (deactivation gate) is normally open, but closes when the cell becomes very positive


1) Deactivated: closed, @resting potential

2) Activated: open when threshold is reached

3) Inactivated: closed as neuron depolarizes and h-gate swings shut


Potassium Voltage-Gated Channels: Gate and Function

-The n-gate is normally closed, but opens when the cell is depolarized


Stages of an Action Potential

0) A triggering depolarizes the cell body

 - usually the result of neurotransmitter-gated ion channels

1) Depolarization: cell becomes less polar

 - threshold is reached, and V-gated Na channels open

2) Repolarization: brings cells back to resting potential

 - inactivation of sodium channels via closing of h-gate

 - K channels open, K flows outside cell

3) Hyperpolarization

 - K channels lag, staying open a bit past resting potential

 - fixed by Na/K pumps


Graded Potentials vs Action Potentials


Cation and Anion Gradients

  • Cations
    • Potassium, K (inside)
    • Sodium, Na (outside)
    • Calcium, Ca (outside)
  • Anions
    • Chloride, Cl (outside)
    • Organic Anions, OA (inside)
      • the membrane is impermeable to OA's


Potassium Leakage/Gradient/Equilibrium

  • Equilibrium occurs at around -70mV, with the chemical gradient pushing it outside and the electrical gradient retaining it inside


Chloride Gradient and Maintenence

  • Resting membrane potential is the dominant force for the movement of chloride, so at resting potential (-60mV) there is a low intracellular concentration of Cl
  • Chloride-Potassium Symporter uses the gradient-based diffusion of potassium to move chloride out of the cell


Maintenence of Intracellular Calcium Conentrations

  • Sodium/Calcium Exchanger uses the gradient-driven diffusion of sodium into the cell to expell calcium
  • The equilibrium potential of calcium is ~+120mV, but permeability of calcium is VERY low


Types of Action Potential Firing Patterns

  1. Activity-dependent: excitatory input leads to action potentials. Large, sustained input leads to a train of action potentials
  2. Steady-firing neurons: differences in leakage channels leads to rythmic firing of action potentials, excitatory input --> increased frequency, inhibitory input --> decreased frequency
  3. Steady-firing burst neurons: fire bursts of action potentials at steady frequency, input changes both frequency and number of action potentials per burst
  • Steady firing neurons can relay both excitatory and inhibitory information


Pre-Synaptic Neurotransmitter Release Mechanism

  1. AP travels down axon and depolarizes the axon terminal, opening V-gated calcium channels
  2. Calcium activates Synaptotagmin (vesicle protein)
  3. Synaptotagmin binds and activates Complexin (vesicle protein that prevents vesicle fusion in deactivated state)
  4. Activated Complexin promotes SNARE-formation, leading to vesicle fusion and neurotransmitter release


Post-Synaptic Response: Direct and Plasticity

  • Direct: mainly ligand-gated ion channels, which can be either excitatory or inhibitory depending on which ion they are permeable to.
  • Plasticity: indirect, the activated receptor sets off a cascade that can lead to the insertion or removal of receptors into the membrane (up and down-regulation, respectively)


Two Types of Synapses

  1. Chemical Synapse: has a gap in between the terminals, and uses receptors to pass signal.
  2. Electrical Synapse: uses gap junctions to directly pass ions into the post-synaptic neuron


Two Categories of Neurotransmitter Receptors

  1. Ionotropic: ligand-gated ion channels
  2. Metabotropic: NT binding leads to activation of secondary messengers
  • the effects are slower than ionotropic receptors, but can be bigger, more widespread, and last longer


Neurotransmitter Removal

  1. Diffusion (passive)
  2. Enzymatic: enzymes break down NT in synapse
  3. Pre-Synaptic Reuptake Pumps
  4. Astrocyte Endfeet: pump NT out of synapse and into astrocyte



Synaptic: changes in synapses or in response to input

  • Presynaptic: changes in the amount of NT released (more=potentiation, less=depression)
  • Postsynaptic: change in receptors

Structural: occurs on the level of entire cells

  • Changes in the number of either presynaptic terminals or postsynaptic dendrites