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Chemical transmission – EPP recordings

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Chemical transmission – EPP recordings. Fluctuation in EPP amplitude. Quantal fluctuations of EPP amplitude. Statistical estimation of EPP amplitude distribution. Correlating vesicle fusion with quantal content. Quantum Hypothesis (del Castillo and Katz, 1954).

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Chemical transmission – EPP recordings

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  1. Chemical transmission – EPP recordings

  2. Fluctuation in EPP amplitude

  3. Quantal fluctuations of EPP amplitude

  4. Statistical estimation of EPP amplitude distribution

  5. Correlating vesicle fusion with quantal content

  6. Quantum Hypothesis (del Castillo and Katz, 1954) • units of release are quanta (contents of single vesicle) • evoked response in multiples of quanta m = np m, quantal content (# of units released) n, total # of available units p, probability of release

  7. Quantal analysis Characterizing the quantal properties gives insight into the function of a given synapse: NMJ: m=~200, p=high  stimulus = contraction CNS: m=1, p=variable  synaptic integration

  8. Ca2+ and releasePostsynaptic potentials (PSPs) • Ca2+ requirement for synaptic transmission • Fast (ionotropic) EPSPs • ionotropic IPSPs

  9. The role of calcium

  10. Evidence for the Ca2+ hypothesis Ca2+ injection induces release Ca2+ buffer (BAPTA) injection eliminates release Ca2+ in the presynaptic terminal More Ca2+ = more release

  11. Short-term dynamics of synaptic release 2.5mM Ca2+ outside 0.28mM Ca2+ outside Short term facilitation: “Residual Calcium Hypothesis” (Katz and Miledi): Increased transmitter release is due to residual Ca2+ within the axon terminal, still bound to the vesicle release mechanisms (helps trigger the next release cycle) Short term depression: frequent (or strong) stimulation depletes the pool of releasable vesicles (“readily releasable pool”) Usually: high probability of release leads to depression, low probability of release leads to facilitation

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