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1 Physiology, Physiology and Pharmacology, Goteborg, Sweden
* To whom correspondence should be addressed. E-mail: pontus.wasling{at}physiol.gu.se.
Developmental changes in release probability (Pr) and paired-pulse plasticity at CA3 - CA1 glutamate synapses in hippocampal slices of neonatal rats were examined using field EPSP recordings. Paired-pulse facilitation (PPF) at these synapses was, on average, absent in the 1st postnatal week but emerged and became successively larger during the 2nd postnatal week. This developmental increase in PPF was associated with a reduction in Pr, as indicated by the slower progressive block of the NMDA EPSP by the non-competitive NMDA receptor antagonist MK-801. This developmental reduction in Pr was not homogenous among the synapses. As shown by the MK-801 analysis, the Pr heterogeneity observed among adult CA3-CA1 synapses is present already during the 1st postnatal week, and the developmental Pr reduction was found to be largely selective for synapses with higher Pr values, leaving Pr of the vast majority of the synapses essentially unaffected. A reduction in Pves, the release probability of the individual vesicle, possibly caused by reduction in Ca2+ influx, appears to explain the reduction in Pr. In vivo injection of tetanus toxin at the end of the 1st postnatal week did not prevent the increase in PPF indicating that this developmental change in release is not critically dependent on normal neural activity during the 2nd postnatal week.
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