| First Author | Kokaia M | Year | 1998 |
| Journal | J Neurosci | Volume | 18 |
| Issue | 21 | Pages | 8730-9 |
| PubMed ID | 9786980 | Mgi Jnum | J:50620 |
| Mgi Id | MGI:1307012 | Doi | 10.1523/JNEUROSCI.18-21-08730.1998 |
| Citation | Kokaia M, et al. (1998) Endogenous neurotrophin-3 regulates short-term plasticity at lateral perforant path-granule cell synapses. J Neurosci 18(21):8730-9 |
| abstractText | In the adult brain, neurotrophin-3 (NT-3) is mainly localized in dentate granule cells, and its expression is decreased by various stimuli, e.g., seizure activity. We have examined the role of endogenous NT-3 for excitatory synaptic transmission at lateral perforant path-dentate granule cell synapses using hippocampal slices from NT-3 knock-out (+/-) and wild-type (+/+) mice. Paired-pulse facilitation (PPF) and also short-term synaptic plasticity induced by a brief, high-frequency train of afferent stimulation were reduced, but the expression of long-term potentiation was not affected in the NT-3+/- mice. Incubation of the slices with recombinant NT-3 reversed the deficit in PPF through a mechanism requiring de novo protein synthesis, implying that the impaired short-term plasticity does not result from a developmental alteration. No changes of overall presynaptic release probability, measured by the progressive block of NMDA receptor-mediated synaptic currents by MK-801, or desensitization of AMPA receptors were detected. Because NT-3 expression is reduced after focal seizures, impaired short-term facilitation may represent a protective response that limits the propagation of epileptiform activity from the entorhinal cortex to the hippocampus. |
