Quantal release of transmitter at a central synapse.

Miniature end-plate potentials recorded at the neuromuscular junction are caused by a quantal release of acetylcholine and evoked end-plate potentials can be described as integer multiples of the miniature potentials. A variety of factors including the presence of multiple synapses on postsynaptic cells and dendritic filtering, complicate quantal analyses at central synapses. In the present investigation on rat hippocampal slices, transmitter release was blocked except for a localized area on the apical dendrites of CA1 neurons and quantal analysis was performed on miniature excitatory postsynaptic currents (mEPSCs) and evoked EPSCs of low quantum content. The results indicate that under these conditions, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor-mediated mEPSCs exhibit a normal size distribution with S.D. values comparable to those at the neuromuscular junction, and the evoked EPSCs can be described as integer multiples of the miniature currents. The results also support reports in literature that long-term potentiation (LTP) is associated with an increase in mEPSC frequency. Whether the increase is due to (a) the enhancement of quantal release at already functional synapses, or (b) the recruitment of nearby silent synapses where a neglible transmitter release becomes measurable, or clusters of functional receptors are uncovered, cannot yet be distinguished.