post tetanic potentiation
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Author(s):  
Manuel Dote-Montero ◽  
Ignacio Pelayo-Tejo ◽  
Pablo Molina-Garcia ◽  
Abraham Carle-Calo ◽  
Amador García-Ramos ◽  
...  

Author(s):  
Alexander M. Zero ◽  
Eric A. Kirk ◽  
Charles L. Rice

During activity-dependent potentiation (ADP) motor unit firing rates (MUFRs) are lower, however, the mechanism for this response is not known. During increasing torque isometric contractions at low contraction intensities, MUFR trajectories initially accelerate and saturate demonstrating a non-linear response due to the activation of persistent inward currents (PICs) at the motoneuron. The purpose was to assess whether PICs are a factor in the reduction of MUFRs during ADP. To assess this, MUFR trajectories were fit with competing functions of linear regression and a rising exponential (i.e., acceleration and saturation). Using fine-wire electrodes, discrete MU potential trains were recorded in the tibialis anterior during slowly increasing dorsiflexion contractions to 10% of maximal voluntary contraction following both voluntary (post-activation potentiation; PAP) and evoked (post-tetanic potentiation; PTP) contractions. In 8 participants, 25 MUs were recorded across both ADP conditions and compared to the control with no ADP effect. During PAP and PTP, the average MUFRs were 16.4% and 9.2% lower (both P≤ 0.001), respectively. More MUFR trajectories were better fit to the rising exponential during control (16/25) compared to PAP (4/25, P<0.001) and PTP (8/25, P=0.03). The MU samples that had a rising exponential MUFR trajectory during PAP and PTP displayed an ~11% lower initial acceleration compared to control (P<0.05). Thus, synaptic amplification and MUFR saturation due to PIC properties are attenuated during ADP regardless of the type of conditioning contraction. This response may contribute to lower MUFRs and likely occurred because synaptic input is reduced when contractile function is enhanced.


2021 ◽  
Vol 154 (9) ◽  
Author(s):  
Mina P. Peyton ◽  
Dawn A. Lowe

Twitch force potentiation of fast-twitch skeletal muscle is produced by repetitive stimulation that can be achieved from either (1) the staircase effect (continual low frequency stimulation) or (2) post-tetanic potentiation (a 1–2 s high-frequency tetanic stimulation). Previous studies examining twitch force potentiation have been conducted in vitro and shown that it is related to phosphorylation of myosin regulatory light chain (pRLC). We previously found, in vitro, reduced potentiation of twitch force and decreased pRLC in ovariectomized (Ovx, estrogen-deficient) compared with sham-operated (estrogen-replete) mice. Thus, we questioned whether this phenomenon occurred in vivo and whether age and sex would affect the potentiation of twitch force. Using an in vivo post-tetanic potentiation method (one twitch contraction followed by a tetanic contraction—100 Hz for 1,000 ms with 0.01 ms pulses, and two post-tetanic twitch contractions), we investigated twitch torque potentiation in C57BL/6 young and old, male and female mice. There were significant main effects of sex (P &lt; 0.001) and age (P &lt; 0.001) on body mass and significant main effects of sex (P &lt; 0.001) on tibialis anterior and extensor digitorum longus muscle masses, with males and aged being relatively greater. Analysis of twitch torque using a three-way ANOVA across time, age, and sex showed a significant main effect of time (pre &lt; post; P &lt; 0.001), time × age (P = 0.038), and time × sex (P = 0.028), indicating potentiation occurred in young and old, males and females. Analysis of twitch torque potentiation (percent increase) using a two-way ANOVA revealed a significant main effect of age (young = 45.16 ± 2.04 versus old = 27.88 ± 9.96; P &lt; 0.001) with no effect of sex (P = 0.215). In summary, enhanced generation of twitch force of skeletal muscle using a post-tetanic potentiation method does occur in vivo and is affected by age but not sex, as there is greater twitch torque potentiation in young than old mice.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
David Vandael ◽  
Yuji Okamoto ◽  
Peter Jonas

AbstractThe hippocampal mossy fiber synapse is a key synapse of the trisynaptic circuit. Post-tetanic potentiation (PTP) is the most powerful form of plasticity at this synaptic connection. It is widely believed that mossy fiber PTP is an entirely presynaptic phenomenon, implying that PTP induction is input-specific, and requires neither activity of multiple inputs nor stimulation of postsynaptic neurons. To directly test cooperativity and associativity, we made paired recordings between single mossy fiber terminals and postsynaptic CA3 pyramidal neurons in rat brain slices. By stimulating non-overlapping mossy fiber inputs converging onto single CA3 neurons, we confirm that PTP is input-specific and non-cooperative. Unexpectedly, mossy fiber PTP exhibits anti-associative induction properties. EPSCs show only minimal PTP after combined pre- and postsynaptic high-frequency stimulation with intact postsynaptic Ca2+ signaling, but marked PTP in the absence of postsynaptic spiking and after suppression of postsynaptic Ca2+ signaling (10 mM EGTA). PTP is largely recovered by inhibitors of voltage-gated R- and L-type Ca2+ channels, group II mGluRs, and vacuolar-type H+-ATPase, suggesting the involvement of retrograde vesicular glutamate signaling. Transsynaptic regulation of PTP extends the repertoire of synaptic computations, implementing a brake on mossy fiber detonation and a “smart teacher” function of hippocampal mossy fiber synapses.


eNeuro ◽  
2021 ◽  
pp. ENEURO.0450-20.2021
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo

2021 ◽  
Author(s):  
Chih-Chieh Wang ◽  
Christopher Weyrer ◽  
Diasynou Fioravante ◽  
Pascal S. Kaeser ◽  
Wade G. Regehr

AbstractPost tetanic potentiation (PTP) is a form of short-term plasticity that lasts for tens of seconds following a burst of presynaptic activity. It has been proposed that PTP arises from protein kinase C (PKC) phosphorylation of Munc18-1, an SM (Sec1/Munc-18 like) family protein that is essential for release. To test this model, we made a knockin mouse in which all Munc18-1 PKC phosphorylation sites were eliminated through serine-to-alanine point mutations (Munc18-1 SA mice). Expression of Munc18-1 was not altered in Munc18-1SA mice, and there were no obvious behavioral phenotypes. At the hippocampal CA3 to CA1 synapse, and the granule cell parallel fiber to Purkinje cell (PF to PC) synapse, basal transmission was largely normal except for small decreases in paired-pulse facilitation that are consistent with a slight elevation in release probability. Phorbol esters that mimic activation of PKC by diacylglycerol still increased synaptic transmission in Munc18-1 SA mice. In Munc18-1 SA mice, 70% of PTP remained at CA3 to CA1 synapses, and the amplitude of PTP was not reduced at PF to PC synapses. These findings indicate that at both CA3 to CA1 and PF to PC synapses, phorbol esters and PTP enhance synaptic transmission primarily by mechanisms that are independent of PKC phosphorylation of Munc18-1.Significance StatementA leading mechanism for a prevalent form of short-term plasticity, post-tetanic potentiation (PTP), involves protein kinase C phosphorylation of Munc18-1. This study tests this mechanism by creating a knock in mouse in which Munc18-1 is replaced by a mutated form of Munc18-1 that cannot be phosphorylated. The main finding is that most PTP at hippocampal CA3 to CA1 synapses, or at cerebellar granule cell to Purkinje cell synapses does not rely on PKC phosphorylation of Munc18-1. Thus, mechanisms independent of PKC phosphorylation of Munc18-1 are important mediators of PTP.


2020 ◽  
Author(s):  
Sachin Makani ◽  
Stefano Lutzu ◽  
Pablo J. Lituma ◽  
David L. Hunt ◽  
Pablo E. Castillo

ABSTRACTIn the hippocampus, the excitatory synapse between dentate granule cell axons – or mossy fibers (MF) – and CA3 pyramidal cells (MF-CA3) expresses robust forms of short-term plasticity, such as frequency facilitation and post-tetanic potentiation (PTP). These forms of plasticity are due to increases in neurotransmitter release, and can be engaged when dentate granule cells fire in bursts (e.g. during exploratory behaviors) and bring CA3 pyramidal neurons above threshold. While frequency facilitation at this synapse is limited by endogenous activation of presynaptic metabotropic glutamate receptors, whether MF-PTP can be regulated in an activity-dependent manner is unknown. Here, using physiologically relevant patterns of mossy fiber stimulation in acute mouse hippocampal slices, we found that disrupting postsynaptic Ca2+ dynamics increases MF-PTP, strongly suggesting a form of Ca2+-dependent retrograde suppression of this form of plasticity. PTP suppression requires a few seconds of MF bursting activity and Ca2+ release from internal stores. Our findings raise the possibility that the powerful MF-CA3 synapse can negatively regulate its own strength not only during PTP-inducing activity typical of normal exploratory behaviors, but also during epileptic activity.SIGNIFICANCE STATEMENTThe powerful mossy fiber-CA3 synapse exhibits strong forms of plasticity that are engaged during location-specific exploration, when dentate granule cells fire in bursts. While this synapse is well-known for its presynaptically-expressed LTP and LTD, much less is known about the robust changes that occur on a shorter time scale. How such short-term plasticity is regulated, in particular, remains poorly understood. Unexpectedly, an in vivo-like pattern of presynaptic activity induced robust post-tetanic potentiation (PTP) only when the postsynaptic cell was loaded with a high concentration of Ca2+ buffer, indicating a form of Ca2+–dependent retrograde suppression of PTP. Such suppression may have profound implications for how environmental cues are encoded into neural assemblies, and for limiting network hyperexcitability during seizures.


eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Vincent Huson ◽  
Marieke Meijer ◽  
Rien Dekker ◽  
Mirelle ter Veer ◽  
Marvin Ruiter ◽  
...  

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.


2020 ◽  
Author(s):  
Vincent Huson ◽  
Marieke Meijer ◽  
Rien Dekker ◽  
Mirelle ter Veer ◽  
Marvin Ruiter ◽  
...  

AbstractPreviously, 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 dependent and independent mechanisms that lower the energy barrier independently in an additive manner to produce PTP by multiplication of release rates.


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