Activity-Dependent Increase of the AHP Amplitude in T Sensory Neurons of the Leech

2002 ◽  
Vol 88 (5) ◽  
pp. 2490-2500 ◽  
Author(s):  
Rossana Scuri ◽  
Riccardo Mozzachiodi ◽  
Marcello Brunelli
Keyword(s):  
Sensory Neurons ◽  
Time Window ◽  
Training Session ◽  
Repetitive Stimulation ◽  
Short Term ◽  
Pharmacological Agents ◽  
Stimulus Interval ◽  
Short Term Plasticity ◽  
Intracellular Stimulation ◽  
Activity Dependent

We identified a new form of activity-dependent modulation of the afterhyperpolarization (AHP) in tactile (T) sensory neurons of the leech Hirudo medicinalis. Repetitive intracellular stimulation with 30 trains of depolarizing impulses at 15-s inter-stimulus interval (ISI) led to an increase of the AHP amplitude (∼60% of the control). The enhancement of AHP lasted for ≥15 min. The AHP increase was also elicited when a T neuron was activated by repetitive stimulation of its receptive field. The ISI was a critical parameter for the induction and maintenance of AHP enhancement. ISI duration had to fit within a time window with the upper limit of 20 s to make the training effective to induce an enhancement of the AHP amplitude. After recovery from potentiation, AHP amplitude could be enhanced once again by delivering another training session. The increase of AHP amplitude persisted in high Mg2+ saline, suggesting an intrinsic cellular mechanism for its induction. Previous investigations reported that AHP of leech T neurons was mainly due to the activity of the Na+/K+ ATPase and to a Ca2+-dependent K+ current ( I K/Ca). In addition, it has been demonstrated that serotonin (5HT) reduces AHP amplitude through the inhibition of the Na+/K+ATPase. By blocking the I K/Ca with pharmacological agents, such as cadmium and apamin, we still observed an increase of the AHP amplitude after repetitive stimulation, whereas 5HT application completely inhibited the AHP increment. These data indicate that the Na+/K+ATPase is involved in the induction and maintenance of the AHP increase after repetitive stimulation. Moreover, the AHP increase was affected by the level of serotonin in the CNS. Finally, the increase of the AHP amplitude produced a lasting depression of the synaptic connection between two T neurons, suggesting that this activity-dependent phenomenon might be involved in short-term plasticity associated with learning processes.

scholarly journals Ca2+/Calmodulin and Presynaptic Short-Term Plasticity

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Sumiko Mochida
Keyword(s):  
Transmitter Release ◽  
Presynaptic Terminal ◽  
Neuronal Firing ◽  
Firing Activity ◽  
Short Term ◽  
Short Term Plasticity ◽  
Readily Releasable Pool ◽  
Ef Hand ◽  
Sensor Protein ◽  
Activity Dependent

Synaptic efficacy is remodeled by neuronal firing activity at the presynaptic terminal. Presynaptic activity-dependent changes in transmitter release induce postsynaptic plasticity, including morphological change in spine, gene transcription, and protein synthesis and trafficking. The presynaptic transmitter release is triggered and regulated by Ca2+, which enters through voltage-gated Ca2+ (CaV) channels and diffuses into the presynaptic terminal accompanying action potential firings. Residual Ca2+ is sensed by Ca2+-binding proteins, among other potential actions, it mediates time- and space-dependent synaptic facilitation and depression via effects on CaV2 channel gating and vesicle replenishment in the readily releasable pool (RRP). Calmodulin, a Ca2+-sensor protein with an EF-hand motif that binds Ca2+, interacts with CaV2 channels and autoreceptors in modulation of SNARE-mediated exocytosis.

scholarly journals Rapid regulation of vesicle priming explains synaptic facilitation despite heterogeneous vesicle:Ca2+ channel distances

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Janus RL Kobbersmed ◽  
Andreas T Grasskamp ◽  
Meida Jusyte ◽  
Mathias A Böhme ◽  
Susanne Ditlevsen ◽  
...  
Keyword(s):  
Super Resolution ◽  
Release Site ◽  
Stochastic Simulations ◽  
Short Term ◽  
Short Term Plasticity ◽  
Release Probability ◽  
Vesicular Release ◽  
Dependent Inhibition ◽  
Super Resolution Microscopy ◽  
Activity Dependent

Chemical synaptic transmission relies on the Ca2+-induced fusion of transmitter-laden vesicles whose coupling distance to Ca2+ channels determines synaptic release probability and short-term plasticity, the facilitation or depression of repetitive responses. Here, using electron- and super-resolution microscopy at the Drosophila neuromuscular junction we quantitatively map vesicle:Ca2+ channel coupling distances. These are very heterogeneous, resulting in a broad spectrum of vesicular release probabilities within synapses. Stochastic simulations of transmitter release from vesicles placed according to this distribution revealed strong constraints on short-term plasticity; particularly facilitation was difficult to achieve. We show that postulated facilitation mechanisms operating via activity-dependent changes of vesicular release probability (e.g. by a facilitation fusion sensor) generate too little facilitation and too much variance. In contrast, Ca2+-dependent mechanisms rapidly increasing the number of releasable vesicles reliably reproduce short-term plasticity and variance of synaptic responses. We propose activity-dependent inhibition of vesicle un-priming or release site activation as novel facilitation mechanisms.

scholarly journals Synaptotagmin 7 switches short-term synaptic plasticity from depression to facilitation by suppressing synaptic transmission

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takaaki Fujii ◽  
Akira Sakurai ◽  
J. Troy Littleton ◽  
Motojiro Yoshihara
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Synaptic Vesicle ◽  
Neuromuscular Junctions ◽  
Binding Protein ◽  
Repetitive Stimulation ◽  
Evoked Response ◽  
Short Term ◽  
Short Term Plasticity ◽  
Null Mutants

AbstractShort-term synaptic plasticity is a fast and robust modification in neuronal presynaptic output that can enhance release strength to drive facilitation or diminish it to promote depression. The mechanisms that determine whether neurons display short-term facilitation or depression are still unclear. Here we show that the Ca2+-binding protein Synaptotagmin 7 (Syt7) determines the sign of short-term synaptic plasticity by controlling the initial probability of synaptic vesicle (SV) fusion. Electrophysiological analysis of Syt7 null mutants at Drosophila embryonic neuromuscular junctions demonstrate loss of the protein converts the normally observed synaptic facilitation response during repetitive stimulation into synaptic depression. In contrast, overexpression of Syt7 dramatically enhanced the magnitude of short-term facilitation. These changes in short-term plasticity were mirrored by corresponding alterations in the initial evoked response, with SV release probability enhanced in Syt7 mutants and suppressed following Syt7 overexpression. Indeed, Syt7 mutants were able to display facilitation in lower [Ca2+] where release was reduced. These data suggest Syt7 does not act by directly sensing residual Ca2+ and argues for the existence of a distinct Ca2+ sensor beyond Syt7 that mediates facilitation. Instead, Syt7 normally suppresses synaptic transmission to maintain an output range where facilitation is available to the neuron.

Time Window from Visual Images to Visual Short-Term Memory: Consolidation or Integration?

2004 ◽  
Vol 51 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Yuhong Jiang
Keyword(s):  
Short Term Memory ◽  
Time Window ◽  
Short Interval ◽  
Visual Images ◽  
Short Term ◽  
Temporal Window ◽  
Term Memory ◽  
Visual Short Term Memory ◽  
Probe Task ◽  
Long Time

Abstract. When two dot arrays are briefly presented, separated by a short interval of time, visual short-term memory of the first array is disrupted if the interval between arrays is shorter than 1300-1500 ms ( Brockmole, Wang, & Irwin, 2002 ). Here we investigated whether such a time window was triggered by the necessity to integrate arrays. Using a probe task we removed the need for integration but retained the requirement to represent the images. We found that a long time window was needed for performance to reach asymptote even when integration across images was not required. Furthermore, such window was lengthened if subjects had to remember the locations of the second array, but not if they only conducted a visual search among it. We suggest that a temporal window is required for consolidation of the first array, which is vulnerable to disruption by subsequent images that also need to be memorized.

scholarly journals Subcortical short‐term plasticity elicited by deep brain stimulation

2021 ◽  
Author(s):  
Mohammad Z. Awad ◽  
Ryan J. Vaden ◽  
Zachary T. Irwin ◽  
Christopher L. Gonzalez ◽  
Sarah Black ◽  
...  
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Deep Brain
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