Behavioral Neuroscience - Action Potential

• Action potential

  • All mental activity
  • nervous sys consists of neurons which carry info
  • neuro info is carried as electrical currents
  • between neurons info is carried as NTs

• To start action potential

  • when threshold is reached at axon hillock voltage dependent gates Na+ gates (ion channels) open at massive amounts
  • voltage dependent: ion channel that opens or closes according to the value of the membrane potential
  • strong influx (inward flow) of Na+
  • electrostatic and concentration gradient drive Na+ inside of neuron
  • influx is so strong that a reversal in polarity occurs
  • inside becomes +40, outside becomes negative (different from postsynaptic potential)

• Peak of action potential

  • electrical gradients are reversed; now both gradients are now in the same direction
  • K pushed out by electrical gradient b/c outside is more negative than inside and concentration gradient b/c actual concentration grad doesn’t change much
  • At this point – NA+ channels are closed
  • Rapid efflux (outward flow of K+ )
  • So much rushes out, that there is an overshoot of the original \n polarity (-80mv inside)

• Overshoot period is called the relative refractory period \n (Afterpotentials )

  • Hard to get cell to re-fire at this time

• Resting potential restored by natural diffusion and NA+/K+ pump (transporter)

• Pumps NA+ out, and K+ into the neuron

• Protein found in the membrane that extrudes sodium ions from and transports potassium ions into the cell

• for myelinated neurons process re-occurs at each node of Ranvier (saltatory conduction)

• Saltatory conduction: conduction of action potential by \n myelinated axons.

  • The action potential appears to jump from \n one node of Ranvier to the next

    

• Exocytosis

  • When AP reaches axon terminal/terminal buttons, Ca 2+ channels open (voltage-dependent)
  • AP activates heteroreceptors (found in axon terminals) which open Ca 2+ channels
  • b/c of gradients, Ca2+ enters the cell
  • activates enzymes that propel vesicles along microtubules running down TB (even removes blocking proteins!)
  • Vesicles merge with presynaptic membrane , drop NT into synapse, and diffuse across to activate receptors on next locations
  • if neuron = produces IPSP/EPSP, if muscle/gland = inhibit/excite
  • this process = exocytosis

• several specialized long-chain proteins called SNARES mediate exocytosis

  • serve as tethers: those attached to vesicles are called v-SNARES, while those attached to the presynaptic membrane = t-SNARES (t for target)

• when v-SNARES on the vesicle attach to t-SNARES the vesicle is said to be docked ready to be released

• another protein attached to the vesicle called synaptotagmin, serves as Ca 2+ sensors

• when the AP arrives at axon terminal, incoming Ca ion binds and activates synaptotagmin which then triggers the final fusion (t and v connect.

• Final stage --- clearing out synapse

  • Reuptake: the entry of NTs just liberated by a terminal button back through its membrane, thus terminating the postsynaptic potential
  • NT is packaged and brought back into th pre-synaptic neuron
  • Enzymatic breakdown: the destruction of a neurotransmitter by an enzyme after its release
  • ex. the destruction of acetylcholine by acetylcholinesterase
  • NTs reduced to inactive molecules; they diffuse away
  • Autoreceptors: receptors on the axon terminal that become active when large number of NT present
  • inhibits release of additional neurotransmitters
  • nothing to do w/ AP

• Synapse

• Most drugs (medical/recreational) influence what happens in the synapse

• Drugs can have 2 effects

• agonist - increases activity of an NT

• antagonist - decrease the lvl of a NT

• many most substances can both act as an agonist for one neurotransmitter and an antagonist for another

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