Perforated axospinous synapses with multiple, completely partitioned transmission zones: probable structural intermediates in synaptic plasticity.

Analysis of axospinous synapses in the rat dentate gyrus, using three-dimensional reconstructions from electron micrographs of serial sections, revealed a novel synaptic subtype. Synapses of this subtype exhibit partitions that emanate from the postsynaptic spine head and invaginate the presynaptic axon terminal, dividing its portion contracted by the spine into distinct protrusions. Such complete spine partitions provide barriers between two to four discrete transmission zones, each one being formed by a separate axon terminal protrusion and delineated by a separate segment of the postsynaptic density (PSD). Spine partitions that differ from the complete ones were found in two other synaptic subtypes. One of these is characterized by a sectional partition the base of which is placed between the arms of a horseshoe-shaped PSD. Synapses of another subtype exhibit a focal partition the base of which is restricted to a perforation in a fenestrated PSD. Although both sectional and focal partitions invaginate a presynaptic axon terminal, they do not divide into separate protrusions and do not split a single transmission zone into disjointed entities. All three subtypes of partitioned synapses have nonpartitioned counterparts exhibiting segmented, horseshoe-shaped, or fenestrated PSDs. These observations suggest a model of structural modifications underlying synaptic plasticity. According to this model, synapses with multiple, completely partitioned transmission zones that appear to be designed as elements of an unusually high strength, represent pivotal structural intermediates in synaptic plasticity. The formation of such synapses from those that belong to other subtypes is postulated to result in a sustained increase in the efficacy of synaptic transmission. Conversely, a disassembly of complete partitions with the transformation of multiple transmission zones into a single one is proposed to lead to a persistent depression of synaptic responses.