Much of what we know about the mechanisms underlying Homosynaptic Depression (HSD) and heterosynaptic facilitation is based on intracellular recordings of integrated postsynaptic potentials (PSPs). This methodological approach views the presynaptic apparatus as a single compartment rather than taking a more realistic representation reflecting the fact that it is made up of tens to hundreds of individual and independent Presynaptic Release Boutons (PRBs). Using cultured Aplysia sensorimotor synapses, we reexamined HSD and its dishabituation by imaging the release properties of individual PRBs. We find that the PRB population is heterogeneous and can be clustered into three groups: ~25% of the PRBs consistently release neurotransmitter throughout the entire habituation paradigm (35 stimuli, 0.05 Hz) and have a relatively high quantal content, 36% of the PRBs display intermittent failures only after the tenth stimulation, and 39% are low quantal-content PRBs that exhibit intermittent release failures from the onset of the habituation paradigm. 5HT-induced synaptic dishabituation by a single 5HT application was generated by the enhanced recovery of the quantal content of the habituated PRBs and did not involve the recruitment of new release boutons. The characterization of the PRB population as heterogeneous in terms of its temporal pattern of release-probability and quantal content provides new insights into the mechanisms underlying HSD and its dishabituation.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3781340 | PMC |
http://dx.doi.org/10.3389/fncel.2013.00165 | DOI Listing |
J Physiol
December 2024
Université Paris Cité, CNRS, ENS Paris Saclay, Centre Borelli UMR 9010, Paris, France.
Terminal Schwann cells (TSCs) are capable of regulating acetylcholine (ACh) release at the neuromuscular junction (NMJ). We have identified GABA as a gliotransmitter at mouse NMJs. When ACh activates α7 nicotinic ACh receptor (nAChRs) on TSCs, GABA is released and activates GABA receptors on the nerve terminal that subsequently reduce ACh release.
View Article and Find Full Text PDFNeuropharmacology
January 2025
(")Rita Levi-Montalcini" Department of Neuroscience, University of Turin, Turin, Italy. Electronic address:
Glyphosate (Gly) is a broad-spectrum herbicide responsible for the inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate synthase known to be expressed exclusively in plants and not in animals. For decades Gly has been thought to be ineffective in mammals, including humans, until it was demonstrated that rodents treated with the Gly-based herbicide Roundup showed reduced content of neurotransmitters (e.g.
View Article and Find Full Text PDFNeuron
November 2024
Department of Bioengineering, Stanford University, Stanford, CA 94305, USA; Department of Neurobiology, Stanford University, Stanford, CA 94305, USA. Electronic address:
J Physiol
August 2024
Department of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Repetitive synaptic stimulation can induce different forms of synaptic plasticity but may also limit the robustness of synaptic transmission by exhausting key resources. Little is known about how synaptic transmission is stabilized after high-frequency stimulation. In the present study, we observed that tetanic stimulation of the Drosophila neuromuscular junction (NMJ) decreases quantal content, release-ready vesicle pool size and synaptic vesicle density for minutes after stimulation.
View Article and Find Full Text PDFCell Rep
July 2024
Department of Cellular Biophysics, Institute of Medical Physics and Biophysics, University of Münster, Robert-Koch-Str. 31, 48149 Münster, Germany; Center for Soft Nanoscience SoN, University of Münster, Busso-Peus-Str.10, 48149 Münster, Germany; Cells in Motion Interfaculty Center, University of Münster, 48149 Münster, Germany. Electronic address:
The quantal content of an evoked postsynaptic response is typically determined by dividing it by the average spontaneous miniature response. However, this approach is challenged by the notion that different synaptic vesicle pools might drive spontaneous and evoked release. Here, we "silence" synaptic vesicles through pharmacological alkalinization and subsequently rescue them by optogenetic acidification.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!