A delayed response enhancement during hippocampal presynaptic plasticity in mice
Open accessAbstract
High frequency afferent stimulation of chemical synapses often induces short‐term increases in synaptic efficacy, due to increased release probability and/or increased supply of readily releasable synaptic vesicles. This may be followed by synaptic depression, often caused by vesicle depletion. We here describe an additional, novel type of delayed and transient response enhancement phase which occurred during prolonged stimulation at 5–20 Hz frequency of excitatory glutamatergic synapses in slices from the adult mouse CA1 hippocampal region. This second enhancement phase, which was most clearly defined at physiological temperatures and essentially absent at 24°C, was dependent on the presence of F‐actin filaments and synapsins I and/or II, and could not be ascribed to changes in presynaptic action potentials, inhibitory neurotransmission or glutamate receptor desensitization. Time course studies showed that the delayed response phase interrupted the synaptic decay 3–4 s after stimulus train initiation and continued, when examined at 5–10 Hz frequencies, for approximately 75 stimuli before decay. The novel response enhancement, probably deriving from a restricted pool of synaptic vesicles, may allow maintenance of synaptic efficacy during prolonged periods of excitatory synaptic activity.
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The failure of ultrafast endocytosis at room temperature is attributable to slowed actin turnover at room temperature.
“Based on the reliance of ultrafast endocytosis on F-actin7 and the high sensitivity of actin polymerization to temperature change74–76, we attribute this result to a slowed actin turnover at the room temperature7.”
From Membrane compression by synaptic vesicle exocytosis triggers ultrafast endocytosis (2023) · cites this paper as [76]
The Discussion (page not available in our copy) reports that room temperature essentially abolished delayed response enhancement (DRE) and that actin cycling may be essential for DRE. The paper does not establish that ultrafast endocytosis fails at room temperature or that slowed actin turnover causes such a failure; it studies a different presynaptic response. (LLM, conf=0.85)
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References 73 · Cited by 33
- Authors
- Jensen, V., Walaas, S. I., Hilfiker, S., Ruiz, A., & Hvalby, Ø.
- Affiliations
- University of Oslo (NO)
- Consejo Superior de Investigaciones Científicas (ES)
- UCL Queen Square Institute of Neurology (GB)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2007-08
- Volume
- 583
- Issue
- 1
- Pages
- 129-143
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC2277251
- OpenAlex
- W1532309947
- Cited by
- 33
- References
- 73
- Citations by year
- 2026: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2017: 1 · 2015: 3 · 2014: 2 · 2013: 2 · 2012: 2
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Universitetet i Oslo
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- presynaptic plasticity, hippocampal CA1, glutamatergic synapses, synaptic vesicle depletion, F-actin, synapsin I, synapsin II, synaptic efficacy, high-frequency stimulation, synaptic depression, temperature dependence
- MeSH terms
- Actins, Action Potentials, Animals, Calcium, Electric Stimulation, Hippocampus, Synaptic Transmission, Neuronal Plasticity, Synapses, Synaptic Vesicles, Temperature, Synapsins, Presynaptic Terminals, Receptors, GABA, Mice, Knockout, Patch-Clamp Techniques, Mice
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