scholarly journals Dynamin-1 deletion enhances post-tetanic potentiation and quantal size after tetanic stimulation at the calyx of Held

2016 ◽  
Vol 595 (1) ◽  
pp. 193-206 ◽  
Author(s):  
Satyajit Mahapatra ◽  
Xuelin Lou
Keyword(s):  
Tetanic Stimulation ◽  
Calyx Of Held ◽  
Quantal Size ◽  
Post Tetanic Potentiation

Evidence That Post-Tetanic Potentiation Is Mediated by Neuropeptide Release in Aplysia

2001 ◽  
Vol 86 (6) ◽  
pp. 2845-2855 ◽  
Author(s):  
Lyle E. Fox ◽  
Philip E. Lloyd
Keyword(s):  
Motor Neurons ◽  
High Frequency ◽  
Tetanic Stimulation ◽  
Neuropeptide Release ◽  
Neuromuscular Synapses ◽  
Excitatory Junction Potentials ◽  
Post Tetanic Potentiation ◽  
Central Synapses ◽  
Activity Dependent ◽  
Frequency Of Stimulation

Many neuromuscular and central synapses exhibit activity-dependent plasticity. The sustained high-frequency firing needed to elicit some forms of plasticity are similar to those often required to release neuropeptides. We wanted to determine if neuropeptide release could contribute to post-tetanic potentiation (PTP) and chose neuromuscular synapses in buccal muscle I3a to explore this issue. This muscle is innervated by two motor neurons (termed B3 and B38) that show PTP in response to tetanic stimulation. B3 and B38 use glutamate as their fast transmitter but express different modulatory neuropeptides. B3 expresses FMRFamide, a neuropeptide that only slightly increases its own excitatory junction potentials (EJPs). B38 expresses the small cardioactive peptide (SCP), a neuropeptide that dramatically increases its own EJPs. It was our hypothesis that SCP released from B38's terminals during tetanic stimulation mediated a component of PTP for B38. Because no antagonist to SCP currently exists, we used several indirect approaches to test this hypothesis. First, we studied the effects of increasing stimulation frequency during the tetanus or lowering temperature on PTP. Both of these changes are known to dramatically increase SCP release. We found that increasing the frequency of stimulation increased PTP for both neurons; however, the effects were larger for B38. Decreasing the temperature tended to reduce PTP for B3, while increasing PTP for B38. These results were consistent with known properties of SCP release from B38. Next we selectively superfused the neuromuscular synapses with exogenous SCP to determine if this would occlude the effects of SCP released from B38 during a tetanus. We found that exogenous SCP dramatically reduced PTP for B38 but had little effect on PTP for B3. Thus our results support the hypothesis that physiological stimulation of B38 elicits PTP that is predominantly dependent on the release of SCP from its own terminals. They also demonstrate that the mechanisms underlying PTP can be very different for two motor neurons innervating the same target muscle.

Effects of tetanic stimulation on monosynaptic and dorsal root reflexes in kittens

1991 ◽  
Vol 69 (10) ◽  
pp. 1428-1435
Author(s):  
Parveen Bawa
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Monosynaptic Reflex ◽  
Cutaneous Afferents ◽  
Tetanic Stimulation ◽  
Dorsal Root Reflex ◽  
Peripheral Afferents ◽  
Post Tetanic Potentiation ◽  
Tetanic Depression ◽  
Stimulation Of

The effects of tetanic stimulation of peripheral afferents were examined on monosynaptic reflexes and dorsal root reflexes in kittens of various ages. Concomitantly recorded monosynaptic and dorsal root reflexes resulting from the stimulation of muscle nerves showed similar post-tetanic changes, namely, predominantly post-tetanic depression in neonates and post-tetanic potentiation in older kittens or adults. However, the changes in post-tetanic responses expressed as a percentage of control in dorsal root reflexes were much smaller than those in monosynaptic reflexes. When dorsal root reflexes originating from muscle and cutaneous afferents were compared, dorsal root reflexes from the latter behaved quite differently. For all ages, post-tetanic effects on dorsal root reflexes arising from cutaneous afferents were either insignificant or very small. The possible mechanisms underlying differences in post-tetanic effects from muscle and cutaneous afferents in adults and neonates are discussed.Key words: cat, kitten, development, dorsal root reflex, monosynaptic reflex, spinal cord, post-tetanic potentiation.

scholarly journals Calcium/synaptotagmin-mediated Compound Fusion Increases Quantal Size And Causes Post-tetanic Potentiation At Synapses

2009 ◽  
Vol 96 (3) ◽  
pp. 100a
Author(s):  
Liming He ◽  
Lei Xue ◽  
Jianhua Xu ◽  
Benjamin D. McNeil ◽  
Ernestina Melicoff ◽  
...  
Keyword(s):  
Quantal Size ◽  
Post Tetanic Potentiation

scholarly journals Munc18-1 is a dynamically regulated PKC target during short-term enhancement of transmitter release

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Özgür Genç ◽  
Olexiy Kochubey ◽  
Ruud F Toonen ◽  
Matthijs Verhage ◽  
Ralf Schneggenburger
Keyword(s):  
Transmitter Release ◽  
Molecular Mechanisms ◽  
Gene Replacement ◽  
Target Protein ◽  
Phosphorylation Sites ◽  
Short Term ◽  
Calyx Of Held ◽  
Replacement Strategy ◽  
Kinase C ◽  
Post Tetanic Potentiation

Transmitter release at synapses is regulated by preceding neuronal activity, which can give rise to short-term enhancement of release like post-tetanic potentiation (PTP). Diacylglycerol (DAG) and Protein-kinase C (PKC) signaling in the nerve terminal have been widely implicated in the short-term modulation of transmitter release, but the target protein of PKC phosphorylation during short-term enhancement has remained unknown. Here, we use a gene-replacement strategy at the calyx of Held, a large CNS model synapse that expresses robust PTP, to study the molecular mechanisms of PTP. We find that two PKC phosphorylation sites of Munc18-1 are critically important for PTP, which identifies the presynaptic target protein for the action of PKC during PTP. Pharmacological experiments show that a phosphatase normally limits the duration of PTP, and that PTP is initiated by the action of a ‘conventional’ PKC isoform. Thus, a dynamic PKC phosphorylation/de-phosphorylation cycle of Munc18-1 drives short-term enhancement of transmitter release during PTP.

scholarly journals Post-tetanic potentiation lowers the energy barrier for synaptic vesicle fusion independently of Synaptotagmin-1

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Vincent Huson ◽  
Marieke Meijer ◽  
Rien Dekker ◽  
Mirelle ter Veer ◽  
Marvin Ruiter ◽  
...  
Keyword(s):  
Synaptic Vesicle ◽  
Energy Barrier ◽  
Phorbol Esters ◽  
Release Kinetics ◽  
Vesicle Fusion ◽  
Tetanic Stimulation ◽  
Release Rates ◽  
Synaptotagmin 1 ◽  
Post Tetanic Potentiation ◽  
Synaptic Vesicle Fusion

Previously, we showed that modulation of the energy barrier for synaptic vesicle fusion boosts release rates supralinearly (Schotten, 2015). Here we show that mouse hippocampal synapses employ this principle to trigger Ca2+-dependent vesicle release and post-tetanic potentiation (PTP). We assess energy barrier changes by fitting release kinetics in response to hypertonic sucrose. Mimicking activation of the C2A domain of the Ca2+-sensor Synaptotagmin-1 (Syt1), by adding a positive charge (Syt1D232N) or increasing its hydrophobicity (Syt14W), lowers the energy barrier. Removing Syt1 or impairing its release inhibitory function (Syt19Pro) increases spontaneous release without affecting the fusion barrier. Both phorbol esters and tetanic stimulation potentiate synaptic strength, and lower the energy barrier equally well in the presence and absence of Syt1. We propose a model where tetanic stimulation activates Syt1-independent mechanisms that lower the energy barrier and act additively with Syt1-dependent mechanisms to produce PTP by exerting multiplicative effects on release rates.

An Increase in Calcium Influx Contributes to Post-Tetanic Potentiation at the Rat Calyx of Held Synapse

2006 ◽  
Vol 96 (6) ◽  
pp. 2868-2876 ◽  
Author(s):  
Ron L. P. Habets ◽  
J. Gerard G. Borst
Keyword(s):  
Action Potential ◽  
Calcium Influx ◽  
Calcium Currents ◽  
Calyx Of Held ◽  
Calcium Buffer ◽  
Whole Cell Patch Clamp ◽  
Auditory Brain Stem ◽  
Post Tetanic Potentiation ◽  
Presynaptic Calcium ◽  
Fluorescence Transients

We studied the contribution of a change in presynaptic calcium influx to posttetanic potentiation (PTP) in the calyx of Held synapse, an axosomatic synapse in the auditory brain stem. We made whole cell patch-clamp recordings of a principal cell after loading of the presynaptic terminal with a calcium dye. After induction of PTP by a high-frequency train of afferent stimuli, the Fluo-4 fluorescence transients evoked by an action potential became on average 15 ± 4% larger ( n = 7). Model predictions did not match the fluorescence transients evoked by trains of brief calcium currents unless the endogenous calcium buffer had low affinity for calcium, making a contribution of saturation of the endogenous buffer to the synaptic potentiation we observed in the present experiments less likely. Our data therefore suggest that the increase of release probability during PTP at the calyx of Held synapse is largely explained by an increase in the calcium influx per action potential.

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