The Experts below are selected from a list of 150 Experts worldwide ranked by ideXlab platform
Linggang Wu - One of the best experts on this subject based on the ideXlab platform.
-
Post Tetanic Potentiation is caused by two signalling mechanisms affecting quantal size and quantal content
The Journal of Physiology, 2010Co-Authors: Linggang WuAbstract:A high-frequency action potential train induces Post-Tetanic Potentiation (PTP) of transmission at many synapses by increasing the intra-terminal calcium concentration, which may increase the quantal content by activation of protein kinase C (PKC). A recent study found that an increase of the mEPSC size, caused by compound vesicle fusion, parallels PTP, suggesting that the quantal size increase also contributes to the PTP generation. However, the strength of this suggestion is somewhat undermined by recent studies suggesting that vesicles responsible for spontaneous and evoked EPSCs may originate from different pools. Furthermore, it is unclear whether the quantal size increase is also mediated by PKC. The present work addressed these issues at a large calyx of Held synapse. We found that PTP was caused by both a PKC-dependent increase of the quantal content and a PKC-independent increase of the quantal size. In addition, we found that mEPSCs and EPSCs were subjected to similar up- and down-regulation, which verifies the basic assumption of quantal analysis – the same mechanism controls the quantal size of spontaneous and evoked release. This verification supports the use of quantal analysis at central synapses. However, unlike the traditional quantal analysis that attributes the quantal size change to a Postsynaptic mechanism, the present work, together with one of our previous studies, suggests that the quantal size increase is caused by a presynaptic mechanism, the compound fusion among vesicles that forms large compound vesicles.
-
calcium synaptotagmin mediated compound fusion increases quantal size and causes Post Tetanic Potentiation at synapses
Biophysical Journal, 2009Co-Authors: Liming He, Jianhua Xu, Benjamin D Mcneil, Ernestina Melicoff, Roberto Adachi, Linggang WuAbstract:Exocytosis at synapses generally refers to fusion between vesicles and the plasma membrane. Although fusion between vesicles, known as compound fusion, occurs in non-neuronal secretory cells and has recently been proposed at ribbon-type synapses, it remains unclear whether it exists, how it is mediated, and what role it plays at the vast majority of synapses, where release occurs at conventional active zones. Here we addressed this issue in rats and mice at a large nerve terminal containing conventional active zones. High potassium application induced giant capacitance up-steps at the release face of nerve terminals, which were larger than the membrane capacitance of regular vesicles. These giant up-steps were not comprised of several smaller steps, nor were they bulk endocytic vesicles that had re-fused. High potassium application also induced giant vesicle-like structures in nerve terminals and giant miniature EPSCs (mEPSCs) that reflected release of a large amount of transmitter. The giant up-steps, giant vesicle-like structures, and giant mEPSCs were abolished by removing the extracellular calcium or by knocking out synaptotagmin II, the calcium sensor mediating fusion at calyces. These results suggest that calcium binding with synaptotagmin II mediates compound fusion and increases quantal size. Compound fusion significantly contributed to the generation of a widely observed synaptic plasticity, Post-Tetanic Potentiation (PTP) of the EPSC, because 1) action potential trains that generated PTP also evoked giant up-steps and increased the mEPSC amplitude, 2) the time course and the degree of the mEPSC amplitude increase paralleled those of PTP, and 3) both the mEPSC amplitude increase and PTP were abolished by the calcium buffer EGTA or synaptotagmin II knockout. Our finding may be of wide application because intense nerve activity, PTP, and giant miniature currents occur in physiological conditions at many synapses.
-
Calcium/synaptotagmin-mediated Compound Fusion Increases Quantal Size And Causes Post-Tetanic Potentiation At Synapses
Biophysical Journal, 2009Co-Authors: Liming He, Jianhua Xu, Benjamin D Mcneil, Ernestina Melicoff, Roberto Adachi, Linggang WuAbstract:Exocytosis at synapses generally refers to fusion between vesicles and the plasma membrane. Although fusion between vesicles, known as compound fusion, occurs in non-neuronal secretory cells and has recently been proposed at ribbon-type synapses, it remains unclear whether it exists, how it is mediated, and what role it plays at the vast majority of synapses, where release occurs at conventional active zones. Here we addressed this issue in rats and mice at a large nerve terminal containing conventional active zones. High potassium application induced giant capacitance up-steps at the release face of nerve terminals, which were larger than the membrane capacitance of regular vesicles. These giant up-steps were not comprised of several smaller steps, nor were they bulk endocytic vesicles that had re-fused. High potassium application also induced giant vesicle-like structures in nerve terminals and giant miniature EPSCs (mEPSCs) that reflected release of a large amount of transmitter. The giant up-steps, giant vesicle-like structures, and giant mEPSCs were abolished by removing the extracellular calcium or by knocking out synaptotagmin II, the calcium sensor mediating fusion at calyces. These results suggest that calcium binding with synaptotagmin II mediates compound fusion and increases quantal size. Compound fusion significantly contributed to the generation of a widely observed synaptic plasticity, Post-Tetanic Potentiation (PTP) of the EPSC, because 1) action potential trains that generated PTP also evoked giant up-steps and increased the mEPSC amplitude, 2) the time course and the degree of the mEPSC amplitude increase paralleled those of PTP, and 3) both the mEPSC amplitude increase and PTP were abolished by the calcium buffer EGTA or synaptotagmin II knockout. Our finding may be of wide application because intense nerve activity, PTP, and giant miniature currents occur in physiological conditions at many synapses.
Katsuei Shibuki - One of the best experts on this subject based on the ideXlab platform.
-
sequence dependence of Post Tetanic Potentiation after sequential heterosynaptic stimulation in the rat auditory cortex
The Journal of Physiology, 2001Co-Authors: Kenjiro Seki, Masaharu Kudoh, Katsuei ShibukiAbstract:To investigate the mechanisms for the coding stimulus sequence in the auditory cortex (AC), Post-Tetanic Potentiation (PTP) was recorded after sequentially combined heterosynaptic stimulation was applied in rat AC slices. Brief Tetanic stimulation (TS) was applied at two sites on AC slices at intervals of 0.5–10 s. PTP of field potentials was induced by the earlier TS, rather than the later TS. PTP was followed by sequence-dependent long-term Potentiation (LTP). Using Ca2+ imaging in the slices loaded with rhod-2, a Ca2+ indicator, a sequence-dependent distribution of PTP was found in AC slices. The sequence-dependent PTP in excitatory Postsynaptic potentials (EPSPs) was observed in supragranular pyramidal neurons. The sequence dependence of PTP was not significantly affected by 1 μm bicuculline, an antagonist of GABAA receptors, or 100 μm 2-hydroxysaclofen, an antagonist of GABAB receptors. Depolarization and firing recorded in pyramidal neurons during the later TS were less vigorous than when the slices were incubated in the control medium. However, this suppression of the responses during the later TS was not observed in the presence of 50 μm atropine, an antagonist of muscarinic receptors. PTP was induced by the earlier and later TS in the presence of 50 μm atropine, so that the sequence dependence of PTP was abolished. Pirenzepine (50 μm), an antagonist of muscarinic M1 receptors, but not methoctramine (30 μm), an antagonist of M2 receptors, eliminated the sequence dependence of PTP. These findings suggest that the sequence dependence of PTP in AC might have a role in the temporal processing of auditory information on the scale of seconds.
-
Sequence dependence of Post‐Tetanic Potentiation after sequential heterosynaptic stimulation in the rat auditory cortex
The Journal of Physiology, 2001Co-Authors: Kenjiro Seki, Masaharu Kudoh, Katsuei ShibukiAbstract:To investigate the mechanisms for the coding stimulus sequence in the auditory cortex (AC), Post-Tetanic Potentiation (PTP) was recorded after sequentially combined heterosynaptic stimulation was applied in rat AC slices. Brief Tetanic stimulation (TS) was applied at two sites on AC slices at intervals of 0.5–10 s. PTP of field potentials was induced by the earlier TS, rather than the later TS. PTP was followed by sequence-dependent long-term Potentiation (LTP). Using Ca2+ imaging in the slices loaded with rhod-2, a Ca2+ indicator, a sequence-dependent distribution of PTP was found in AC slices. The sequence-dependent PTP in excitatory Postsynaptic potentials (EPSPs) was observed in supragranular pyramidal neurons. The sequence dependence of PTP was not significantly affected by 1 μm bicuculline, an antagonist of GABAA receptors, or 100 μm 2-hydroxysaclofen, an antagonist of GABAB receptors. Depolarization and firing recorded in pyramidal neurons during the later TS were less vigorous than when the slices were incubated in the control medium. However, this suppression of the responses during the later TS was not observed in the presence of 50 μm atropine, an antagonist of muscarinic receptors. PTP was induced by the earlier and later TS in the presence of 50 μm atropine, so that the sequence dependence of PTP was abolished. Pirenzepine (50 μm), an antagonist of muscarinic M1 receptors, but not methoctramine (30 μm), an antagonist of M2 receptors, eliminated the sequence dependence of PTP. These findings suggest that the sequence dependence of PTP in AC might have a role in the temporal processing of auditory information on the scale of seconds.
A De Haan - One of the best experts on this subject based on the ideXlab platform.
-
Low-frequency fatigue, Post-Tetanic Potentiation and their interaction at different muscle lengths following eccentric exercise.
The Journal of experimental biology, 2020Co-Authors: J M Rijkelijkhuizen, C J De Ruiter, P A J B M Huijing, A De HaanAbstract:Low-frequency fatigue (LFF) and Post-Tetanic Potentiation (PTP) were quantified at different muscle lengths in rat medial gastrocnemius (GM) muscle. In situ experiments were performed on GM muscle-tendon complexes of anaesthetised (urethane, 1.5 g kg(-1) i.p.) Wistar rats (N=8). Force-length characteristics were determined at maximal (200 Hz) and submaximal (60 Hz) stimulation. Data for submaximally stimulated muscle were obtained in a non-potentiated and in a potentiated condition. LFF was induced by a series of 40 eccentric contractions. Post-exercise (40-80 min), data for the force-length relationships were obtained once more. Whereas force loss at 200 Hz-stimulation was least at optimum muscle length, L(0,200 Hz), (17.0+/-1.4%, mean +/-S.E.M.), force loss at 60 Hz-stimulation was maximal near L(0,200 Hz) (55.1+/-4.3% at L(0,200 Hz)-1 mm). When the muscle was potentiated, force loss at 60 Hz-stimulation was maximal at short muscle length: L(0,200 Hz)-4 mm (53.5+/-3.8%). The extent of LFF, quantified by a decrease in the 60:200 Hz force ratio, varied with muscle length: LFF increased with decreasing muscle lengths when muscles were potentiated. However, in the non-potentiated condition, LFF was maximal at a length just below L(0,200 Hz); the 60:200 Hz force ratio had decreased to 54.6+/-5.9% of the pre-exercise ratio at L(0,200 Hz)-1 mm. Compared with the non-potentiated condition, LFF was less pronounced in the potentiated condition. PTP counteracted LFF particularly at long muscle lengths. However, at short muscle lengths, LFF was still observed in potentiated muscles.
-
low frequency fatigue Post Tetanic Potentiation and their interaction at different muscle lengths following eccentric exercise
The Journal of Experimental Biology, 2005Co-Authors: J M Rijkelijkhuizen, C J De Ruiter, P A J B M Huijing, A De HaanAbstract:SUMMARY Low-frequency fatigue (LFF) and Post-Tetanic Potentiation (PTP) were quantified at different muscle lengths in rat medial gastrocnemius (GM) muscle. In situ experiments were performed on GM muscle-tendon complexes of anaesthetised (urethane, 1.5 g kg -1 i.p.) Wistar rats ( N =8). Force-length characteristics were determined at maximal (200 Hz) and submaximal (60 Hz) stimulation. Data for submaximally stimulated muscle were obtained in a non-potentiated and in a potentiated condition. LFF was induced by a series of 40 eccentric contractions. Post-exercise (40-80 min), data for the force-length relationships were obtained once more. Whereas force loss at 200 Hz-stimulation was least at optimum muscle length, L 0,200Hz , (17.0±1.4%, mean ± s.e.m.), force loss at 60 Hz-stimulation was maximal near L 0,200Hz (55.1±4.3% at L 0,200Hz -1 mm). When the muscle was potentiated, force loss at 60 Hz-stimulation was maximal at short muscle length: L 0,200Hz -4 mm (53.5±3.8%). The extent of LFF, quantified by a decrease in the 60:200 Hz force ratio, varied with muscle length: LFF increased with decreasing muscle lengths when muscles were potentiated. However, in the non-potentiated condition, LFF was maximal at a length just below L 0,200Hz ; the 60:200 Hz force ratio had decreased to 54.6±5.9% of the pre-exercise ratio at L 0,200Hz -1 mm. Compared with the non-potentiated condition, LFF was less pronounced in the potentiated condition. PTP counteracted LFF particularly at long muscle lengths. However, at short muscle lengths, LFF was still observed in potentiated muscles.
-
Post Tetanic Potentiation increases energy cost to a higher extent than work in rat fast skeletal muscle
Journal of Muscle Research and Cell Motility, 2001Co-Authors: F Abbate, J Van Der Velden, Ger J M Stienen, A De HaanAbstract:We studied the effects of (Post-Tetanic) Potentiation on myosin light chain (MLC-2) phosphorylation, work and energy cost in skeletal muscle. Experiments were performed using in situ medial gastrocnemius muscles of male Wistar rats, which were electrically stimulated through the severed sciatic nerve. One group of muscles was first potentiated with an isometric tetanus before a series of 10 concentric contractions (PRC). A second group performed the same series of contractions without previous Potentiation (RC). Following the last contraction the muscles were rapidly frozen and excised after which the high-energy phosphate content, lactate concentration and the level of MLC-2 phosphorylation were measured. The results indicate that PRC muscles had a higher (P < 0.05) total work output 144.5 ± 17.0 (SD) (n = 6) vs. 121.6 ± 11.4 (SD) (n = 6) mJ and level of MLC-2 phosphorylation (49.2 ± 7.3 vs. 40.8 ± 3.6%) than RC muscles. The energy cost of the series of concentric contractions in the PRC muscles (9.8 ± 1.9 μmol∼P/muscle) was significantly higher (P < 0.05) than the energy cost in the RC muscles (6.2 ± 0.97 μmol∼P/muscle). It was shown that the relative increase in energy cost of PRC muscles was higher (P < 0.05) than in total work output. It is proposed that the relative high increase in energy cost is the direct result of the increase in muscle performance rather than a property of Potentiation.
Liming He - One of the best experts on this subject based on the ideXlab platform.
-
calcium synaptotagmin mediated compound fusion increases quantal size and causes Post Tetanic Potentiation at synapses
Biophysical Journal, 2009Co-Authors: Liming He, Jianhua Xu, Benjamin D Mcneil, Ernestina Melicoff, Roberto Adachi, Linggang WuAbstract:Exocytosis at synapses generally refers to fusion between vesicles and the plasma membrane. Although fusion between vesicles, known as compound fusion, occurs in non-neuronal secretory cells and has recently been proposed at ribbon-type synapses, it remains unclear whether it exists, how it is mediated, and what role it plays at the vast majority of synapses, where release occurs at conventional active zones. Here we addressed this issue in rats and mice at a large nerve terminal containing conventional active zones. High potassium application induced giant capacitance up-steps at the release face of nerve terminals, which were larger than the membrane capacitance of regular vesicles. These giant up-steps were not comprised of several smaller steps, nor were they bulk endocytic vesicles that had re-fused. High potassium application also induced giant vesicle-like structures in nerve terminals and giant miniature EPSCs (mEPSCs) that reflected release of a large amount of transmitter. The giant up-steps, giant vesicle-like structures, and giant mEPSCs were abolished by removing the extracellular calcium or by knocking out synaptotagmin II, the calcium sensor mediating fusion at calyces. These results suggest that calcium binding with synaptotagmin II mediates compound fusion and increases quantal size. Compound fusion significantly contributed to the generation of a widely observed synaptic plasticity, Post-Tetanic Potentiation (PTP) of the EPSC, because 1) action potential trains that generated PTP also evoked giant up-steps and increased the mEPSC amplitude, 2) the time course and the degree of the mEPSC amplitude increase paralleled those of PTP, and 3) both the mEPSC amplitude increase and PTP were abolished by the calcium buffer EGTA or synaptotagmin II knockout. Our finding may be of wide application because intense nerve activity, PTP, and giant miniature currents occur in physiological conditions at many synapses.
-
Calcium/synaptotagmin-mediated Compound Fusion Increases Quantal Size And Causes Post-Tetanic Potentiation At Synapses
Biophysical Journal, 2009Co-Authors: Liming He, Jianhua Xu, Benjamin D Mcneil, Ernestina Melicoff, Roberto Adachi, Linggang WuAbstract:Exocytosis at synapses generally refers to fusion between vesicles and the plasma membrane. Although fusion between vesicles, known as compound fusion, occurs in non-neuronal secretory cells and has recently been proposed at ribbon-type synapses, it remains unclear whether it exists, how it is mediated, and what role it plays at the vast majority of synapses, where release occurs at conventional active zones. Here we addressed this issue in rats and mice at a large nerve terminal containing conventional active zones. High potassium application induced giant capacitance up-steps at the release face of nerve terminals, which were larger than the membrane capacitance of regular vesicles. These giant up-steps were not comprised of several smaller steps, nor were they bulk endocytic vesicles that had re-fused. High potassium application also induced giant vesicle-like structures in nerve terminals and giant miniature EPSCs (mEPSCs) that reflected release of a large amount of transmitter. The giant up-steps, giant vesicle-like structures, and giant mEPSCs were abolished by removing the extracellular calcium or by knocking out synaptotagmin II, the calcium sensor mediating fusion at calyces. These results suggest that calcium binding with synaptotagmin II mediates compound fusion and increases quantal size. Compound fusion significantly contributed to the generation of a widely observed synaptic plasticity, Post-Tetanic Potentiation (PTP) of the EPSC, because 1) action potential trains that generated PTP also evoked giant up-steps and increased the mEPSC amplitude, 2) the time course and the degree of the mEPSC amplitude increase paralleled those of PTP, and 3) both the mEPSC amplitude increase and PTP were abolished by the calcium buffer EGTA or synaptotagmin II knockout. Our finding may be of wide application because intense nerve activity, PTP, and giant miniature currents occur in physiological conditions at many synapses.
Kenjiro Seki - One of the best experts on this subject based on the ideXlab platform.
-
sequence dependence of Post Tetanic Potentiation after sequential heterosynaptic stimulation in the rat auditory cortex
The Journal of Physiology, 2001Co-Authors: Kenjiro Seki, Masaharu Kudoh, Katsuei ShibukiAbstract:To investigate the mechanisms for the coding stimulus sequence in the auditory cortex (AC), Post-Tetanic Potentiation (PTP) was recorded after sequentially combined heterosynaptic stimulation was applied in rat AC slices. Brief Tetanic stimulation (TS) was applied at two sites on AC slices at intervals of 0.5–10 s. PTP of field potentials was induced by the earlier TS, rather than the later TS. PTP was followed by sequence-dependent long-term Potentiation (LTP). Using Ca2+ imaging in the slices loaded with rhod-2, a Ca2+ indicator, a sequence-dependent distribution of PTP was found in AC slices. The sequence-dependent PTP in excitatory Postsynaptic potentials (EPSPs) was observed in supragranular pyramidal neurons. The sequence dependence of PTP was not significantly affected by 1 μm bicuculline, an antagonist of GABAA receptors, or 100 μm 2-hydroxysaclofen, an antagonist of GABAB receptors. Depolarization and firing recorded in pyramidal neurons during the later TS were less vigorous than when the slices were incubated in the control medium. However, this suppression of the responses during the later TS was not observed in the presence of 50 μm atropine, an antagonist of muscarinic receptors. PTP was induced by the earlier and later TS in the presence of 50 μm atropine, so that the sequence dependence of PTP was abolished. Pirenzepine (50 μm), an antagonist of muscarinic M1 receptors, but not methoctramine (30 μm), an antagonist of M2 receptors, eliminated the sequence dependence of PTP. These findings suggest that the sequence dependence of PTP in AC might have a role in the temporal processing of auditory information on the scale of seconds.
-
Sequence dependence of Post‐Tetanic Potentiation after sequential heterosynaptic stimulation in the rat auditory cortex
The Journal of Physiology, 2001Co-Authors: Kenjiro Seki, Masaharu Kudoh, Katsuei ShibukiAbstract:To investigate the mechanisms for the coding stimulus sequence in the auditory cortex (AC), Post-Tetanic Potentiation (PTP) was recorded after sequentially combined heterosynaptic stimulation was applied in rat AC slices. Brief Tetanic stimulation (TS) was applied at two sites on AC slices at intervals of 0.5–10 s. PTP of field potentials was induced by the earlier TS, rather than the later TS. PTP was followed by sequence-dependent long-term Potentiation (LTP). Using Ca2+ imaging in the slices loaded with rhod-2, a Ca2+ indicator, a sequence-dependent distribution of PTP was found in AC slices. The sequence-dependent PTP in excitatory Postsynaptic potentials (EPSPs) was observed in supragranular pyramidal neurons. The sequence dependence of PTP was not significantly affected by 1 μm bicuculline, an antagonist of GABAA receptors, or 100 μm 2-hydroxysaclofen, an antagonist of GABAB receptors. Depolarization and firing recorded in pyramidal neurons during the later TS were less vigorous than when the slices were incubated in the control medium. However, this suppression of the responses during the later TS was not observed in the presence of 50 μm atropine, an antagonist of muscarinic receptors. PTP was induced by the earlier and later TS in the presence of 50 μm atropine, so that the sequence dependence of PTP was abolished. Pirenzepine (50 μm), an antagonist of muscarinic M1 receptors, but not methoctramine (30 μm), an antagonist of M2 receptors, eliminated the sequence dependence of PTP. These findings suggest that the sequence dependence of PTP in AC might have a role in the temporal processing of auditory information on the scale of seconds.