1QQ# 13 for 10:30. Why is action potential conduction velocity slower in a non-myelinated axon compared to a myelinated axon? In what ways do voltage-gated Na+ channels differ from voltage-gated K+ channels?. 1QQ# 13 for 11:30.
Most neurotransmitters are synthesized in the axon terminal.
Exceptions: Peptide NTs originate in cell body, move in vesicles by fast orthograde axonal transport to axon terminal.
Vesicle release proportional to Ca++ influx (High f AP leads to residual Ca++ in terminal)
Tetanus toxin & Botulinum toxin disrupt SNARE function.
Size of PSP is Variable!
Mechanism: vary Ca++ entry in presynaptic terminal B.
Release, diffusion, binding,
Post-synaptic Receptor Types: Inotropic or Metabotropic
Excitatory (closer to threshold for AP)
Inhibitory (stabilizes or hyperpolarizes)
Types of Ligand-Gated Receptors
= ACH = Acetylcholine
Agonist = Nicotine
Agonist = Muscarine
Antagonist = Curare
Antagonist = Atropine
Types of Acetylcholine Receptors so named for agonist:
Nicotinic AChR and Muscarinic AChR
Priority by proximity
To axon hillock!
Some ion Channels that allow flux of Na+ and K+ simultaneously
e.g. nicotinic Acetylcholine Receptor (nAChR)
EPSPs :which ion moving in which direction?
Duration of PSP vs AP
IPSPs :which ion moving in which direction?
Some IPSPs result in no change in membrane potential by opening Chloride channels that stabilize membrane potential at resting value (Nernst Potential for Cl- = -70mV) or in cells that actively transport Cl- out.
Summation and Synaptic Integration
Challenge question: Suppose each IPSP hyperpolarizes by 5 mV and each EPSP depolarizes by 5 mV.
If 4 inhibitory synapses are active at the same time, how many excitatory synapses must be active simultaneously to exceed threshold (-55 mV) if the resting membrane potential is -70mV?
Synapses named for NT used: -ergic