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Telencephalin (TLCN) is a cell adhesion molecule belonging to the immunoglobulin superfamily whose expression is restricted to neurons within the most highly developed brain segment, telencephalon. Immunoelectronmicroscopic study revealed that in the hippocampal CA1 region, TLCN was localized at the surface membrane of postsynaptic spines of pyramidal cell dendrites but not at that of axonal terminals. Blocking of TLCN function using anti-TLCN antibody or recombinant soluble TLCN protein caused a striking suppression of the long-term potentiation (LTP) at the Schaffer collateral-CA1 synapses. The suppression was observed even when the blocking was initiated immediately after the tetanic stimuli. These observations suggest a role for TLCN-mediated cell-cell interactions as a key step in the development of LTP.

We examined the effects of [Arg8]-vasopressin (AVP) on long term potentiation (LTP) of the field excitatory postsynaptic potentials at CA1 and CA3 synapses in adult guinea pig hippocampal slices. AVP (10 nM) depressed the magnitude of LTP without any effects on basal responses at both synaptic pathways. The depressive effect by AVP at CA1 synapses appears to be receptor-mediated since it was inhibited by an AVP V1-receptor antagonist, [Pmp1,Tyr(Me)2]-AVP. From these results, AVP may play an inhibitory role on the induction of LTP via V1 receptors in the guinea pig hippocampus.

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