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Updated: Aug 23, 2026

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
Published on: August 11, 2019
Developmental changes in release properties of the CA3-CA1 glutamate synapse in rat hippocampus
P Wasling1, E Hanse, B Gustafsson
1Institute of Physiology and Pharmacology, Department of Physiology, Göteborg University, Box 432, 405 30 Göteborg, Sweden. pontus.wasling@physiol.gu.se
Insights
Paired-pulse facilitation (PPF) increases in rat hippocampus during development, linked to decreased release probability (Pr) at CA3-CA1 synapses. This change is synapse-specific and not dependent on neural activity.
Area of Science:
- Neuroscience
- Developmental Biology
- Synaptic Plasticity
Background:
- Understanding synaptic development is crucial for comprehending brain maturation.
- CA3-CA1 synapses in the hippocampus play a key role in learning and memory.
- Developmental changes in neurotransmitter release influence synaptic function.
Purpose of the Study:
- To investigate developmental changes in release probability (Pr) and paired-pulse plasticity (PPF) at CA3-CA1 synapses in neonatal rats.
- To determine the relationship between PPF and Pr during early postnatal development.
- To explore the role of neural activity in these developmental changes.
Main Methods:
- Field excitatory postsynaptic potential (EPSP) recordings in hippocampal slices from neonatal rats.
- Pharmacological manipulation using MK-801 (an N-methyl-D-aspartate receptor antagonist) to assess Pr.
- In vivo tetanus toxin injection to block neural activity.
Main Results:
- Paired-pulse facilitation (PPF) was absent in the first postnatal week and increased during the second postnatal week.
- The developmental increase in PPF correlated with a decrease in release probability (Pr).
- Pr heterogeneity was observed early and the developmental decrease in Pr was selective for high-Pr synapses.
Conclusions:
- Developmental increase in PPF at CA3-CA1 synapses is associated with a selective reduction in Pr, particularly at high-Pr synapses.
- This developmental shift in release probability may involve a reduction in the release probability of individual vesicles (Pves), potentially due to altered Ca2+ influx.
- The observed developmental changes in release are not critically dependent on normal neural activity during the second postnatal week.
Abstract:
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 excitatory postsynaptic potential (EPSP) recordings. Paired-pulse facilitation (PPF) at these synapses was, on average, absent in the first postnatal week but emerged and became successively larger during the second postnatal week. This developmental increase in PPF was associated with a reduction in Pr, as indicated by the slower progressive block of the N-methyl-D-aspartate (NMDA) EPSP by the noncompetitive 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 first 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, seems to explain the reduction in Pr. In vivo injection of tetanus toxin at the end of the first 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 second postnatal week.
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