Steven Crane Compiled Section Handouts. Human Behavioral Biology 2012

Advanced Neuroscience

What complexities do we have at the level of the action potential?

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  Dale 1: all axon terminals receive AP. Wrong!
  
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  Differential spread/shunting of APs
  

^o By regulating density of channels at branch points

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  Dendrites regulate the input power: not all dendrites equally influential on a downstream AP
  
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  Shifting axon hillock to regulate propensity to fire an AP
  
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  Vesicle release enzyme complexities: synaptotagmin on vescicle surface, receives Ca++ and triggers many cascades
  
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  Exocytotic pores, not just fusion of vesicle with axon terminal membrane
  

What complexities do we have at the level of NTs?

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  Dale 2: one NT per neuron. Wrong!
  
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  Multiplicity of NTs
  

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  Different speeds of action: fast excitation followed by slow inhibition
  
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  Therefore multiplicity of receptors for different NTs
  

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  Autoreceptors doing bookkeeping
  

^o Sometimes using the second NT as a marker of how much first NT released

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  Retrograde NTs
  

^o ATP, adenosine

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  Lateral NTs
  

^o Gasses like NO

What NT receptor complexities do we have?

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  Not just excitatory, but also inhibitory receptors
  
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  Outward ion flow
  
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  Multiple receptors for the same NT: non-NMDA and NMDA receptors for glutamate giving us non-linearity in excitation.
  

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  NMDA is threshold-dependent. Non-NMDA is non-threshold dependent (like most normal, well-behaved receptors)
  
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  The more non-NMDA providing a graded response, the more likely to reach the threshold and trigger the NMDA receptor to let Ca++ rush in.
  

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