ArticleThe Journal of physiology2002
Presynaptic and postsynaptic mechanisms underlie paired pulse depression at single GABAergic boutons in rat collicular cultures.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 88 citations in OpenAlex.
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- Postnatal development of vasoactive intestinal polypeptide-expressing GABAergic interneurons in mouse somatosensory cortex.Acta physiologica (Oxford, England) · 2025Article
- Glutamate Spillover Dynamically Strengthens Gabaergic Synaptic Inhibition of the Hypothalamic Paraventricular Nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Age and sex effects on paired-pulse suppression and prepulse inhibition of auditory evoked potentials.Frontiers in neuroscience · 2024Article
- Keeping Excitation-Inhibition Ratio in Balance.International journal of molecular sciences · 2022Review
- Synaptic vesicle release during ribbon synapse formation of cone photoreceptors.Frontiers in cellular neuroscience · 2022Article
- Developmental GABA polarity switch and neuronal plasticity in Bioengineered Neuronal Organoids.Nature communications · 2020Article
- Corticostriatal plasticity in the nucleus accumbens core.Journal of neuroscience research · 2019Article
- Single Synapse Indicators of Impaired Glutamate Clearance Derived from Fast iGluThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Presynaptic Inhibition of Primary Nociceptive Signals to Dorsal Horn Lamina I Neurons by Dopamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Developmental Changes in Serotonergic Modulation of GABAergic Synaptic Transmission and Postsynaptic GABACerebellum (London, England) · 2018Article
- Regulation of Nociceptive Glutamatergic Signaling by Presynaptic Kv3.4 Channels in the Rat Spinal Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Plasticity-Related Gene 1 Affects Mouse Barrel Cortex Function via Strengthening of Glutamatergic Thalamocortical Transmission.Cerebral cortex (New York, N.Y. : 1991) · 2016Article
- Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.Frontiers in cellular neuroscience · 2016Review
- Cocaine-seeking is associated with PKC-dependent reduction of excitatory signaling in accumbens shell D2 dopamine receptor-expressing neurons.Neuropharmacology · 2015Article
- The effect of sevoflurane on the cognitive function of rats and its association with the inhibition of synaptic transmission.International journal of clinical and experimental medicine · 2015Article
- Soluble pathological tau in the entorhinal cortex leads to presynaptic deficits in an early Alzheimer's disease model.Acta neuropathologica · 2014Article
- Inhibitory glycinergic neurotransmission in the mammalian auditory brainstem upon prolonged stimulation: short-term plasticity and synaptic reliability.Frontiers in neural circuits · 2014Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paired pulse depression (PPD) is a common form of short-term synaptic plasticity. The aim of this study was to characterise PPD at the level of a single inhibitory bouton. Low-density collicular cultures were loaded with the Ca2+ indicator Oregon Green-1, active boutons were stained with RH414, and action potentials were blocked with TTX. Evoked IPSCs (eIPSCs) and presynaptic Ca2+ transients were recorded in response to direct presynaptic depolarisation of an individual bouton. The single bouton eIPSCs had a low failure rate (< 0.1), large average quantal content (3-6) and slow decay (tau(1) = 15 ms, tau(2) = 81 ms). The PPD of eIPSCs had two distinct components: PPD(fast) and PPD(slow) (tau = 86 ms and 2 s). PPD(slow) showed no dependence on extracellular Ca2+ concentration, or on the first eIPSC's failure rate or amplitude. Most probably, it reflects a release-independent inhibition of exocytosis. PPD(fast) was only observed in normal or elevated Ca2+. It decreased with the failure rate and increased with the amplitude of the first eIPSC. It coincided with paired pulse depression of the presynaptic Ca2+ transients (tau = 120 ms). The decay of the latter was accelerated by EGTA, which also reduced PPD(fast). Therefore, a suppressive effect of residual presynaptic Ca2+ on subsequent Ca2+ influx is considered the most likely cause of PPD(fast). PPD(fast) may also have a postsynaptic component, because exposure to a low-affinity GABA(A) receptor antagonist (TPMPA; 300 microM) counteracted PPD(fast), and asynchronous IPSC amplitudes were depressed for a short interval following an eIPSC. Thus, at these synapses, PPD is produced by at least two release-independent presynaptic mechanisms and one release-dependent postsynaptic mechanism.
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