Facilitation at the Lobster Neuromuscular Junction: A Stimulus-Dependent Mobilization Model

Abstract

Frequency facilitation is a process whereby neurosecretion increases as a function of stimulation frequency during repetitive synaptic activity. To examine the physiological basis underlying facilitation, we have estimated the frequency dependence of the synaptic parameters n (number of units capable of responding to a nerve impulse) and P (average probability of responding) at the lobster neuromuscular junction. Both n and P increase as a function of frequency, suggesting that the efficiency of quantal docking and quantal fusion is regulated by repetitive synaptic activity. In experiments in which facilitation is strong and quantal content does not saturate over the frequency range tested, the value of P saturates at low frequencies of stimulation, and increases in quantal content at higher frequencies of stimulation are due to an increase in n. Therefore the value of P does not limit facilitation. We propose that transmitter release is limited by the rates of quantal mobilization and demobilization, and that each excitatory stimulus causes additional mobilization of quanta to dock at the presynaptic release sites. In such a model the binomial parameter n will correspond to the number of quanta docked at the release sites and available for release. We have developed and solved kinetic equations that describe how the number of docked quanta changes as a function of time and of stimulation frequency. The stimulus-dependent mobilization model of facilitation predicts that the reciprocal value of the quantal content depends linearly on the reciprocal product of the stimulation frequency and the probability of release. Fits of the experimental data confirm the accuracy of this prediction, showing that the model proposed here quantitatively describes frequency facilitation. The model predicts that high rates of quantal demobilization will produce strong frequency facilitation.

Temperature dependent modulation of lobster neuromuscular properties by serotonin

“…Here we describe the temperaturedependent physiology of the lobster dactyl opener muscle and its modulation by the circulating neurohormone serotonin (5-HT). The lobster dactyl opener is a popular model system for studies of synaptic plasticity Bykhovskaia et al, 2001;Bykhovskaia et al, 2004;Glusman and Kravitz, 1982;Goy and Kravitz, 1989;Hamilton et al, 2006;Kravitz et al, 1980;Vorob'eva et al, 1999;Worden et al, 1997), as is the homologous crayfish dactyl opener muscle (Beaumont and Zucker, 2000;Delaney et al, 1991;Dixon and Atwood, 1989a;Dixon and Atwood, 1989b;Qian and Delaney, 1997;Vyshedskiy et al, 1998;Vyshedskiy and Lin, 1997;Wang and Zucker, 1998). We demonstrate that (1) thermal change within a biologically relevant range of temperatures profoundly affects the neurophysiological properties of the lobster dactyl opener neuromuscular system, and (2) the modulatory effects of serotonin on neuromuscular function have distinctly different temperature dependencies and extend the thermal range over which motor movements are effective.…”

“…Another factor is that the time course for neurally evoked synaptic vesicle release depends on temperature. Quantal neurotransmission at dactyl opener muscle synapses is asynchronous at cold (<5°C) temperatures Worden et al, 1997) and becomes more synchronous at warmer temperatures. Finally, it is also possible that temperature regulates the relative amount of neurotransmitter released from synaptic terminals, as demonstrated in crayfish (Dunn and Mercier, 2003).…”

Quantitative Analysis of Calcium-Dependent Vesicle Recruitment and Its Functional Role at the Calyx of Held Synapse

“…However, it has been recognized that depressed steady-state release during high-frequency stimulation is much higher than expected on the basis of the relatively slow recovery from depression after spike trains (Kusano and Landau, 1975;Glavinovic and Narahashi, 1988;Neher, 1998;Zucker and Regehr, 2002). To account for the discrepancy between the observed and the expected steady-state release, an acceleration of the recruitment was postulated as either a consequence of the preceding release (Worden et al, 1997) or, more specifically, a consequence of elevated intraterminal Ca 2ϩ concentration ([Ca 2ϩ ] i ) (Gingrich and Byrne, 1985;Dittman and Regehr, 1998;Stevens and Wesseling, 1998;Wang and Kaczmarek, 1998). Such mechanisms are able to describe many features of short-term plasticity (Dittman and Regehr, 1998;Saviane and Silver, 2006).…”

, Frequency-Dependent Modulation of Short-Term Plasticity of Gabaergic Synaptic Transmission

“…Вважають, що в їх основі лежать процеси, які відбуваються у пресинаптично-му закінченні [1][2][3][4][5][6]. Тобто підвищення ефек-тивності синаптичної передачі при коротко-часній пластичності відображає збільшення ймовірності вивільнення доступних квантів, хоча при цьому не виключається й збіль-шення кількості місць їхнього екзоцитозу [7]. Зменшення амплітуди другої відповіді у парі відбувається через тимчасове зменшення квантового вмісту везикул [8][9][10].…”