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
  polarity (-80mv inside)

Overshoot period is called the relative refractory period
(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
myelinated axons.

• The action potential appears to jump from
  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