scholarly journals Modification of transmitter release by ions which prolong the presynaptic action potential

1970 ◽  
Vol 210 (3) ◽  
pp. 681-695 ◽  
Author(s):  
P. R. Benoit ◽  
J. Mambrini
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Presynaptic Action

Isoflurane Inhibits Transmitter Release and the Presynaptic Action Potential

2004 ◽  
Vol 100 (3) ◽  
pp. 663-670 ◽  
Author(s):  
Xin-Sheng Wu ◽  
Jian-Yuan Sun ◽  
Alex S. Evers ◽  
Michael Crowder ◽  
Ling-Gang Wu
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Glutamate Release ◽  
Inhibitory Effect ◽  
Similar Degree ◽  
Action Potential Amplitude ◽  
Potential Amplitude ◽  
Presynaptic Action ◽  
Quantal Size ◽  
Rat Brainstem

Background Isoflurane inhibits the excitatory postsynaptic current (EPSC) at many synapses. Accumulated evidence suggests the involvement of a presynaptic mechanism. However, the extent of the presynaptic contribution has not been quantitatively studied. Furthermore, the mechanism underlying the presynaptic contribution remains unclear. Methods To estimate the presynaptic contribution, the authors compared the effects of isoflurane on the presynaptic capacitance jump, which is proportional to vesicle release, and the postsynaptic glutamate receptor-mediated EPSC at a calyx-type synapse in rat brainstem. The authors determined whether isoflurane affects the waveform of the action potential recorded from nerve terminals. By studying the relation between the EPSC and the presynaptic action potential at the same synapse, the authors determined whether isoflurane inhibits the EPSC by decreasing the presynaptic action potential. Results Isoflurane at 0.35-1.05 mM reduced the EPSC and the presynaptic capacitance jump to a similar degree without affecting the miniature EPSC (an indicator of quantal size), suggesting that isoflurane inhibits the EPSC predominantly by reducing glutamate release. Isoflurane reduced the presynaptic action potential by approximately 3-8%. The EPSC was proportional to the presynaptic action potential amplitude raised to a power of 10.2. Based on this relation, inhibition of the presynaptic action potential contributed to 62-78% of isoflurane-induced inhibition of the EPSC. Conclusions Isoflurane inhibits the EPSC predominantly by inhibition of transmitter release. Isoflurane reduces the presynaptic action potential amplitude, which may contribute significantly to its inhibitory effect on the EPSC.

scholarly journals Kv1.3 channels regulate synaptic transmission in the nucleus of solitary tract

2011 ◽  
Vol 105 (6) ◽  
pp. 2772-2780 ◽  
Author(s):  
Angelina Ramirez-Navarro ◽  
Patricia A. Glazebrook ◽  
Michelle Kane-Sutton ◽  
Caroline Padro ◽  
David D. Kline ◽  
...  
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Brain Slices ◽  
Presynaptic Terminal ◽  
Solitary Tract ◽  
Sensory Afferents ◽  
Peripheral Neurons ◽  
C Fibers ◽  
Nodose Ganglia ◽  
Nucleus Of Solitary Tract

The voltage-gated K+ channel Kv1.3 has been reported to regulate transmitter release in select central and peripheral neurons. In this study, we evaluated its role at the synapse between visceral sensory afferents and secondary neurons in the nucleus of the solitary tract (NTS). We identified mRNA and protein for Kv1.3 in rat nodose ganglia using RT-PCR and Western blot analysis. In immunohistochemical experiments, anti-Kv1.3 immunoreactivity was very strong in internal organelles in the soma of nodose neurons with a weaker distribution near the plasma membrane. Anti-Kv1.3 was also identified in the axonal branches that project centrally, including their presynaptic terminals in the medial and commissural NTS. In current-clamp experiments, margatoxin (MgTx), a high-affinity blocker of Kv1.3, produced an increase in action potential duration in C-type but not A- or Ah-type neurons. To evaluate the role of Kv1.3 at the presynaptic terminal, we examined the effect of MgTx on tract evoked monosynaptic excitatory postsynaptic currents (EPSCs) in brain slices of the NTS. MgTx increased the amplitude of evoked EPSCs in a subset of neurons, with the major increase occurring during the first stimuli in a 20-Hz train. These data, together with the results from somal recordings, support the hypothesis that Kv1.3 regulates the duration of the action potential in the presynaptic terminal of C fibers, limiting transmitter release to the postsynaptic cell.

Presynaptic Ca2+ Influx at the Inhibitor of the Crayfish Neuromuscular Junction: A Photometric Study at a High Time Resolution

2000 ◽  
Vol 83 (1) ◽  
pp. 552-562 ◽  
Author(s):  
Andrey Vyshedskiy ◽  
Jen-Wei Lin
Keyword(s):  
Action Potential ◽  
Time Resolution ◽  
Transmitter Release ◽  
Calcium Influx ◽  
Calcium Transient ◽  
High Time ◽  
High Time Resolution ◽  
Presynaptic Calcium ◽  
Crayfish Neuromuscular Junction ◽  
Fluorescence Transients

Presynaptic calcium influx at the inhibitor of the crayfish neuromuscular junction was investigated by measuring fluorescence transients generated by calcium-sensitive dyes. This approach allowed us to correlate presynaptic calcium influx with transmitter release at a high time resolution. Systematic testing of the calcium indicators showed that only low-affinity dyes, with affinities in the range of micromolar, should be used to avoid saturation of dye binding and interference with transmitter release. Presynaptic calcium influx was regulated by slowly increasing the duration of the action potential through progressive block of potassium channels. The amplitude of the calcium transient, measured from a cluster of varicosities, was linearly related to the duration of the action potential with a slope of 1.2. Gradual changes in potassium channel block allowed us to estimate the calcium cooperativity of transmitter release over a 10-fold range in presynaptic calcium influx. Calcium cooperativity measured here exhibited one component with an average value of 3.1. Inspection of simultaneously recorded presynaptic calcium transients and inhibitory postsynaptic currents (IPSCs) showed that prolonged action potentials were associated with a slow rising phase of presynaptic calcium transients, which were matched by a slow rate of rise of IPSCs. The close correlation suggests that fluorescence transients provide information on the rate of calcium influx. Because there is an anatomic mismatch between the presynaptic calcium transient, measured from a cluster of varicosities, and IPSC, measured with two-electrode voltage clamp, macropatch recording was used to monitor inhibitory postsynaptic responses from the same cluster of varicosities from which the calcium transient was measured. Inhibitory postsynaptic responses recorded with the macropatch method exhibited a faster rising phase than that recorded with two-electrode voltage clamp. This difference could be attributed to slight asynchrony of transmitter release due to action potential conduction along fine branches. In conclusion, this report shows that fluorescence transients generated by calcium-sensitive dyes can provide insights to the properties of presynaptic calcium influx, and its correlation with transmitter release, at a high time resolution.

Platelet-activating factor: lack of direct action on guinea pig myocardium and possible transmitter release from cardiac sympathetic nerve endings at high concentrations

1989 ◽  
Vol 67 (6) ◽  
pp. 669-674 ◽  
Author(s):  
Koki Shigenobu ◽  
Tatsuya Mori ◽  
Katsuo Kamata ◽  
Yutaka Kasuya
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Sympathetic Nerve ◽  
Transmitter Release ◽  
Platelet Activating Factor ◽  
Nerve Endings ◽  
Slow Response ◽  
Ca Current ◽  
Cardiac Action ◽  
High Concentrations

Microelectrode and mechanical studies were performed with isolated guinea pig myocardium (right ventricular free walls and papillary muscles) to examine the effects of platelet-activating factor (PAF) and lysophosphatidylcholine (LPC). Low concentrations of PAF (10−8 to 10−6 M, a range equivalent to the blood concentrations that produce marked hypotension in vivo) had no effects on action potential configuration and contractile force. High concentrations (10−5 to 10−4 M) of PAF and LPC per se elicited slow response action potentials with concomitant contraction (restored contraction) in the myocardium depolarized with elevated K+ (25 mM); they also augmented slow responses and restored contractions produced by a low concentration of isoproterenol (10−8 M). Although these results suggested there was an increase in slow Ca current, the slow responses and restored contractions thus produced were greatly suppressed or abolished by the addition of a β-adrenoceptor blocking agent, sotalol (10−5 M), and by pretreatment with reserpine (5 mg/kg i.p., 24 h prior). In accordance with our previous conclusions, the present results suggest that direct cardiac action is not involved in the mechanisms of hypotension produced by PAF. It was also shown that high concentrations of PAF and LPC may act nonspecifically as amphiphilic compounds to induce transmitter release from sympathetic nerve endings, which may in turn augment the Ca current channels in the myocardial cell membrane.Key words: platelet-activating factor, cardiac action potential, slow response, Ca2+ channel, sympathetic nerve ending.

Tetraethylammonium facilitation of single-pulse mediated action potential, [Ca2+]i and transmitter release in sympathetic neurons

1993 ◽  
Vol 247 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Dennis A. Przywara ◽  
Vishwas Mashalkar ◽  
Sanjiv V. Bhave ◽  
Taruna D. Wakade ◽  
Arun R. Wakade
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Sympathetic Neurons ◽  
Single Pulse ◽  
Mediated Action

scholarly journals Effect of changes in action potential shape on calcium currents and transmitter release in a calyx–type synapse of the rat auditory brainstem

1999 ◽  
Vol 354 (1381) ◽  
pp. 347-355 ◽  
Author(s):  
J. G. G. Borst ◽  
B. Sakmann
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Time Course ◽  
Calcium Influx ◽  
Auditory Brainstem ◽  
Calcium Currents ◽  
Medial Nucleus ◽  
Potential Shape ◽  
Presynaptic Calcium ◽  
Rat Brainstem

We studied the relation between the size of presynaptic calcium influx and transmitter release by making simultaneous voltage clamp recordings from presynaptic terminals, the calyces of Held and postsynaptic cells, the principal cells of the medial nucleus of the trapezoid body, in slices of the rat brainstem. Calyces were voltage clamped with different action potential waveforms. The amplitude of the excitatory postsynaptic currents depended supralinearly on the size of the calcium influx, in the absence of changes in the time–course of the calcium influx. This result is in agreement with the view thact at this synapse most vesicles are released by the combined action of multiple calcium channels.

scholarly journals Calcium and Facilitation at Two Classes of Crustacean Neuromuscular Synapses

1973 ◽  
Vol 61 (1) ◽  
pp. 56-73 ◽  
Author(s):  
Thomas M. Linder
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Conditioning Stimulus ◽  
Critical Factor ◽  
The Other ◽  
Double Logarithmic Plot ◽  
Neuromuscular Synapses ◽  
Logarithmic Plot ◽  
Synaptic Region ◽  
The Relationship

The closer muscle of the crab, Chionoecetes, has at least two classes of excitatory neuromuscular synapses. In one class of synapses an action potential depolarizing the synaptic region releases much more transmitter if it has been preceded recently by another action potential. The other class of synapses shows this property, called facilitation, to a far lesser extent. Immediately after one conditioning stimulus the level of facilitation is similar in both classes. The rate of the ensuing decay of the facilitation is the critical factor differentiating the two classes of synapses. The relationship between external Ca++ concentration and transmitter release is similar for both classes of synapses. The slope of a double logarithmic plot of this relationship varies from 3.1 between 5 and 10 mM Ca++ to 0.9 between 30 and 40 mM Ca++. Facilitation does not significantly change when tested in external Ca++ concentrations ranging from 7 to 30 mM. The extracellularly recorded nerve terminal action potential does not increase in amplitude during facilitation. The results suggest that the mechanism of synaptic facilitation is similar for both classes of synapses and occurs after the stage in transmitter release involving Ca++.

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