Synaptic Transmission
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What are the five steps in chemical signaling?
• Signaling cell • Signal • Receptor • Target molecule • Response
What are the three types of chemical signals?
• synaptic • paracrine • endocrine
What is the distance between the presynaptic and postsynaptic membranes?
~15nm
What is a “fast” chemical synapse?
a synapse with a delay between presynaptic depolarization and postsynaptic response of < 1 msec
What are two characteristics of fast chemical synapses?
• small molecule releasing synapses 2. tight temporal coupling
What are the two main results of treating a squid axon with agents that block Na and K channels and agents that block calcium channels (fig 5.9)?
• When Na and K channels are blocked, there is still a current through the calcium channels • When calcium channels are blocked, release of nts is inhibited
What are three pieces of evidence that an increase in presynaptic calcium concentration triggers nt release (fig 5.10)?
• Using fluorescence we can see that presynaptic action potentials cause a rise in calcium concentration • Injecting calcium into the presynaptic terminal causes nt release • Injection of BAPTA into the presynaptic terminal prevents nt release
How is nt release measured?
as a depolarization in the postsynaptic terminal
What is BAPTA?
a calcium chelater (binds to calcium in selective way)
What is the graphical relationship of calcium concentration to nt release?
• non-linear • small increases in concentration results in larger changes of release • release = k * [Ca] ^ 4
The relationship between calcium concentration and nt release resulted in what natural occurrence?
release is non-linearly dependent on calcium concentration which is why naturally occurring neurotoxins are designed to block calcium channels
How were early defining experiments conducted to find evidence for transmitter release from vesicles (fig 5.5 A)?
• conducted using neuron-muscle synapses • motor neuron is stimulated with extracellular electrode and intracellular microelectrode inserted into postsynaptic muscle cell to record electrical responses
What is an EPP and what causes it (fig 5.5 B)?
• end plate potential • evoked by stimulation of motor neuron that produces action potential in postsynaptic muscle cell • normally above threshold
What are MEPPs and what causes them (fig 5.5 C)?
• spontaneous miniature EPPs - occur in absence of presynaptic stimulation
What occurs when the neuromuscular junction is bathed in solution of low calcium concentration and the motor neuron is stimulated (fig 5.5 D)?
results in EPPs that are about the same size as MEPPs
How large are MEPPs (fig 5.6)?
• all about the same size of 0.4 mV +/- 1 mV
If calcium concentration is increased inside the terminal, how are the MEPPs affected?
• the frequency of the MEPPs increases - the size/amplitude does not increase
What does the distribution of an EPP amplitude and number of EPPs look like? What does this indicate (fig 5.6)?
• the distribution rises at multiples of 0.4 mV (size of one MEPP) • consistent with an action potential evoked EPSP being composed of multiple independent events with a unit size equal to MEPP
How would the graph of EPP amplitude and number of EPPs change if we doubled the extracellular concentration of calcium (fig 5.6)?
• increases probability that fusion will occur by factor of 100,000? • controls probability of vesicle fusing
What structural evidence is observed in stimulated terminals?
• postulated vesicles fusing with plasma membrane - can also see calcium channels
How are synaptic vesicles released and retrieved?
• exocytosis - endocytosis
What technique was used to observe the structural evidence for synaptic vesicles?
• freeze-fracture electron micrographs at a neuromuscular junction
Why are vesicles practical?
• synchronous • osmotic balance • large amounts can be released at once (5000 nt per vesicle vs 1/s/pump)
Where do vesicles get released as observed in the structural images?
vesicles get released next to rows of calcium channels