Immunoelectron microscopic localization of the neural recognition molecules L1, NCAM, and its isoform NCAM180, the NCAM-associated polysialic acid, Beta1 integrin and the extracellular matrix molecule tenascin-R in synapses of the adult rat hippocampus

We have investigated the possibility that morphologically different excitat ory glutamatergic synapses of the "trisynaptic circuit" in the adult rodent hippocampus, which display different. types of long-term potentiation (LTP ), may express the immunoglobulin superfamily recognition molecules L1 and NCAM, the extracellular matrix molecule tenascin-R, and the extracellular m atrix receptor constituent beta1 integrin in a differential manner. The neu ral cell adhesion molecules L1, NCAM (all three major isoforms), NCAM180 (t he largest major isoform with the longest cytoplasmic domain), betal integr in, polysialic acid (PSA) associated with NCAM, and tenascin-R were localiz ed by pre-embedding immunostaining procedures in the CA3/CA4 region (mossy fiber synapses) and in the dentate gyrus (spine synapses) of the adult rat hippocampus. Synaptic membranes of,mossy fiber synapses where LTP is expres sed presynaptically did not show detectable levels of immunoreactivity for any of the molecules/epitopes studied. L1, NCAM, and PSA, but not NCALNZ180 or betal integrin, were detectable on axonal membranes of fasciculating mo ssy fibers. In contrast to mossy fiber synapses, spine synapses in the oute r third of the molecular layer of the dentate gyrus, which display postsyna ptic expression mechanisms of LTP, were both immunopositive and immunonegat ive for NCAM, NCAM180, betal integrin; and PSA. Those spine synapses postsy napticalIy immunoreactive for NCAM or PSA also showed immunoreactivity on t heir presynaptic membranes. NCAM180 was not detectable presynaptically in s pine synapses. L1 could not be found in spine synapses either pre- or posts ynaptically. Also, the extracellular matrix molecule tenascin-R was not det ectable in synaptic clefts of all synapses tested, but was amply present be tween fasciculating axons, axon-astrocyte contact areas, and astrocytic gap junctions. Differences in expression of the membrane-bound adhesion molecu les at both types of synapses may reflect the different mechanisms for indu ction and/or maintenance of synaptic plasticity. (C) 2001 John whey & Sons, Inc.