Effects of a thioreactive agent, diamide, on neuromuscular transmission in lobster

1982 ◽  
Vol 242 (1) ◽  
pp. C59-C64 ◽  
Author(s):  
C. A. Colton ◽  
J. S. Colton
Keyword(s):  
Transmitter Release ◽  
Neuromuscular Transmission ◽  
Similar Response ◽  
Free Solution ◽  
Frequency Increase ◽  
Short Term ◽  
Excitatory Junction Potential ◽  
Sites Of Action ◽  
Potential Frequency ◽  
Junction Potential

Diamide[diazine-dicarboxylic acid-bis(dimethylamide)], a thiol-oxidizing agent, has both pre- and postsynaptic actions on the glutaminergic neuromuscular junction of the lobster walking leg. Postsynaptically, diamide produced an increase in the response to exogenously applied glutamate, whereas the effect of diamide on presynaptic transmitter release involved two major changes: 1) a decrease in excitatory junction potential amplitude and 2) an increase in miniature junction potential frequency. Short-term facilitation also decreased. Equilibration with 1,4-dithiothreitol (a sulfhydryl-reducing agent) reversed the decline in excitatory junction potential frequency, and the fall in short-term facilitation. The miniature junction potential frequency increase induced by diamide was independent of external Ca2+, as diamide in a Ca2+-free solution produced a similar response to that in a Ca2+-containing solution. We propose that the action of diamide on transmitter release is similar to the action of polyvalent cations, i.e., diamide has two sites of action, a blockade of inward Ca2+ flux and an increased release of Ca2+ inside the terminal.

scholarly journals Reversible control of synaptic transmission in a single gene mutant of Drosophila melanogaster.

1983 ◽  
Vol 96 (6) ◽  
pp. 1517-1522 ◽  
Author(s):  
J H Koenig ◽  
K Saito ◽  
K Ikeda
Keyword(s):  
Drosophila Melanogaster ◽  
Elevated Temperature ◽  
Synaptic Transmission ◽  
Transmitter Release ◽  
Flight Muscle ◽  
Single Gene ◽  
Gene Mutant ◽  
Excitatory Junction Potential ◽  
Excitatory Junction Potentials ◽  
Junction Potential

Synaptic transmission of the single gene mutant, shibirets1 (shi), of Drosophila melanogaster is reversibly blocked by elevated temperature. The presynaptic mechanism of transmission was studied in the neuromuscular junction of the dorsal longitudinal flight muscle of this mutant. It was observed that when the temperature was raised to 29 degrees C in shi flies, the amplitude of the excitatory junction potential (EJP) greatly diminished, the frequency of spontaneously released miniature excitatory junction potentials (MEJP's) was greatly reduced, and almost complete vesicle depletion was observed. These conditions were reversible if the temperature was lowered to 19 degrees C. These data suggest that the block in transmission is a result of vesicle depletion. It is suggested that depletion occurs not as a result of excessive release of transmitter but rather as a result of a block in the recycling of vesicles, which causes depletion as exocytosis (transmitter release) proceeds normally.

scholarly journals Post-tetanic decay of evoked and spontaneous transmitter release and a residual-calcium model of synaptic facilitation at crayfish neuromuscular junctions.

1983 ◽  
Vol 81 (3) ◽  
pp. 355-372 ◽  
Author(s):  
R S Zucker ◽  
L O Lara-Estrella
Keyword(s):  
Transmitter Release ◽  
Calcium Concentration ◽  
Neuromuscular Junctions ◽  
Slow Component ◽  
Nonlinear Relationship ◽  
Time Constants ◽  
Excitatory Junction Potential ◽  
Excitatory Junction Potentials ◽  
Presynaptic Calcium ◽  
Junction Potential

The post-tetanic decay in miniature excitatory junction potential (MEJP) frequency and in facilitation of excitatory junction potentials (EJPs) was measured at crayfish neuromuscular junctions. A 2-s tetanus at 20 Hz caused the MEJP frequency to increase an average of 40 times and the EJP amplitude to increase an average of 13 times. Both MEJP frequency and EJP facilitation decayed with two time constants. The fast component of MEJP frequency decay was 47 ms, and that of EJP facilitation was 130 ms. The slow component of MEJP frequency decay was 0.57 s, and that of EJP facilitation was approximately 1 s. These results were consistent with the predictions of a residual calcium model, with a nonlinear relationship between presynaptic calcium concentration and transmitter release.

Synapsin Regulates Basal Synaptic Strength, Synaptic Depression, and Serotonin-Induced Facilitation of Sensorimotor Synapses in Aplysia

2007 ◽  
Vol 98 (6) ◽  
pp. 3568-3580 ◽  
Author(s):  
Diasinou Fioravante ◽  
Rong-Yu Liu ◽  
Anne K. Netek ◽  
Leonard J. Cleary ◽  
John H. Byrne
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Vesicle ◽  
Transmitter Release ◽  
Computational Analysis ◽  
Spontaneous Recovery ◽  
Synaptic Strength ◽  
Short Term ◽  
Homosynaptic Depression ◽  
Heterosynaptic Plasticity

Synapsin is a synaptic vesicle-associated protein implicated in the regulation of vesicle trafficking and transmitter release, but its role in heterosynaptic plasticity remains elusive. Moreover, contradictory results have obscured the contribution of synapsin to homosynaptic plasticity. We previously reported that the neuromodulator serotonin (5-HT) led to the phosphorylation and redistribution of Aplysia synapsin, suggesting that synapsin may be a good candidate for the regulation of vesicle mobilization underlying the short-term synaptic plasticity induced by 5-HT. This study examined the role of synapsin in homosynaptic and heterosynaptic plasticity. Overexpression of synapsin reduced basal transmission and enhanced homosynaptic depression. Although synapsin did not affect spontaneous recovery from depression, it potentiated 5-HT–induced dedepression. Computational analysis showed that the effects of synapsin on plasticity could be adequately simulated by altering the rate of Ca2+-dependent vesicle mobilization, supporting the involvement of synapsin not only in homosynaptic but also in heterosynaptic forms of plasticity by regulating vesicle mobilization.

Postsynaptic Induction and Presynaptic Expression of Group 1 mGluR-Dependent LTD in the Hippocampal CA1 Region

2002 ◽  
Vol 87 (3) ◽  
pp. 1395-1403 ◽  
Author(s):  
Ayako M. Watabe ◽  
Holly J. Carlisle ◽  
Thomas J. O'Dell
Keyword(s):  
Synaptic Transmission ◽  
Transmitter Release ◽  
Metabotropic Glutamate Receptors ◽  
Calcium Influx ◽  
Pyramidal Cells ◽  
Excitatory Synapses ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Group I ◽  
Sites Of Action

Activation of metabotropic glutamate receptors (mGluRs) with the group I mGluR selective agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) induces a long-term depression (LTD) of excitatory synaptic transmission in the CA1 region of the hippocampus. Here we investigated the potential roles of pre- and postsynaptic processes in the DHPG-induced LTD at excitatory synapses onto hippocampal pyramidal cells in the mouse hippocampus. Activation of mGluRs with DHPG, but not ACPD, induced LTD at both Schaffer collateral/commissural fiber synapses onto CA1 pyramidal cells and at associational/commissural fiber synapses onto CA3 pyramidal cells. DHPG-induced LTD was blocked when the G-protein inhibitor guanosine-5′- O-(2-thiodiphosphate) was selectively delivered into postsynaptic CA1 pyramidal cells via an intracellular recording electrode, suggesting that DHPG depresses synaptic transmission through a postsynaptic, GTP-dependent signaling pathway. The effects of DHPG were also strongly modulated, however, by experimental manipulations that altered presynaptic calcium influx. In these experiments, we found that elevating extracellular Ca2+ concentrations ([Ca2+]o) to 6 mM almost completely blocked the effects of DHPG, whereas lowering [Ca2+]o to 1 mM significantly enhanced the ability of DHPG to depress synaptic transmission. Enhancing Ca2+ influx by prolonging action potential duration with bath applications of the K+ channel blocker 4-aminopyridine (4-AP) also strongly reduced the effects of DHPG in the presence of normal [Ca2+]o (2 mM). Although these findings indicate that alterations in Ca2+-dependent signaling processes strongly regulate the effects of DHPG on synaptic transmission, they do not distinguish between potential pre- versus postsynaptic sites of action. We found, however, that while inhibiting both pre- and postsynaptic K+ channels with bath-applied 4-AP blocked the effects of DHPG; inhibition of postsynaptic K+channels alone with intracellular Cs+ and TEA had no effect on the ability of DHPG to inhibit synaptic transmission. This suggests that presynaptic changes in transmitter release contribute to the depression of synaptic transmission by DHPG. Consistent with this, DHPG induced a persistent depression of both AMPA and N-methyl-d-aspartate receptor-mediated components of excitatory postsynaptic currents in voltage-clamped pyramidal cells. Together our results suggest that activation of postsynaptic mGluRs suppresses transmission at excitatory synapses onto CA1 pyramidal cells through presynaptic effects on transmitter release.

The development of transmission at an identified molluscan synapse. I. The emergence of synaptic plasticities

1988 ◽  
Vol 60 (6) ◽  
pp. 2196-2210 ◽  
Author(s):  
P. A. Pawson ◽  
R. Chase
Keyword(s):  
Transmitter Release ◽  
Mean Amplitude ◽  
Synaptic Depression ◽  
Progressive Increase ◽  
Excitatory Postsynaptic Potential ◽  
Developmental Trend ◽  
Chemical Synapse ◽  
Short Term ◽  
Embryonic Life ◽  
Frequency Facilitation

1. A monosynaptic, chemical synapse exists between two identified neurons in the subesophageal ganglia of the pulmonate mollusc, Achatina fulica. The snail undergoes a direct development, i.e., there is no intervening metamorphic period. The presynaptic (V2) and postsynaptic (RPr1) cells are two of the largest neurons found in the ganglia. The development of transmission at this synapse was studied from the last one-third of embryonic life to adulthood. 2. Synaptic transmission was studied by eliciting an action potential in V2 and recording the resultant excitatory postsynaptic potential (EPSP) in RPr1. In a train of repetitive stimuli, the ratio of the mean amplitude of the second EPSP to that of the first EPSP (EPSP2/EPSP1) is always greater than 1, indicating that short-term facilitation is present at all developmental ages studied. Following the initial short-term facilitation, embryonic synapses undergo a profound synaptic depression. Postembryonically there is a progressive increase in the amount of frequency facilitation with age, suggesting that the synapse shows a developmental trend towards an increased capacity for transmitter release. 3. In contrast to the progressive growth of frequency facilitation, the amplitude of the first EPSP in a series of responses (EPSP1) is not significantly related to age. 4. When transmitter release is reduced to approximately 25% of normal levels by a low-Ca2+/high-Mg2+ saline, the synaptic depression that is observed in the younger synapses disappears and is replaced by an adult-like frequency facilitation. 5. The adult synapse displays a phenomenon similar to posttetanic potentiation, which we refer to as the "retention of frequency facilitation." If an initial train of 150 stimuli at 0.2 Hz is followed by a second, identical train after an interval of 1 h, the postsynaptic response is greater during the second train than during the first. This phenomenon only becomes apparent in the second month after hatching, indicating that this separate synaptic plasticity develops at a different rate than does frequency facilitation.

Short-term daily exercise activity enhances endothelial NO synthesis in skeletal muscle arterioles of rats

1994 ◽  
Vol 76 (5) ◽  
pp. 2241-2247 ◽  
Author(s):  
D. Sun ◽  
A. Huang ◽  
A. Koller ◽  
G. Kaley
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Gracilis Muscle ◽  
Myogenic Tone ◽  
Control Group ◽  
Free Solution ◽  
Short Term ◽  
Daily Exercise ◽  
Exercise Activity ◽  
Dose Dependent

We aimed to test the hypothesis that as a consequence of short-term daily bouts of exercise the control of arteriolar smooth muscle by endothelium is altered. Rats ran on a treadmill once a day, 5 days/wk, for 2–4 wk (with gradually increasing intensity, up to 26 min at 22 m/min at a 1% grade by the beginning of the 3rd wk and up to 38 min at 28 m/min at a 2% grade by the beginning of the 4th wk) while a control group remained sedentary (SED). Cannulated and pressurized arterioles of rat gracilis muscle developed spontaneous myogenic tone, which was slightly enhanced in exercised (EX) compared with SED rat arterioles. At 80 mmHg pressure, the passive (Ca(2+)-free solution) and active diameters of SED and EX rat arterioles were 105.4 +/- 3.8 and 55.1 +/- 2.3 microns and 107.1 +/- 3.4 and 50.2 +/- 2.2 microns, respectively. Dose-dependent dilations to sodium nitroprusside (10(-8)-10(-6) M) and constrictions to norepinephrine (10(-8)-10(-6) M) were not affected in EX arterioles, whereas dilations to adenosine (10(-6)-10(-4) M) were significantly reduced. In contrast, dose-dependent dilations to acetylcholine (ACh; 5 x 10(-9)-10(-7) M) and L-arginine [precursor of nitric oxide (NO); 10(-4)-10(-3) M] were significantly enhanced (by 33–78 and 57–75%, respectively) in arterioles of EX compared with those of SED rats. Responses of arterioles to sodium nitrite were not different in SED and EX groups.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Role for Endocannabinoids in Spinal Manipulative Therapy Analgesia?

2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
Stephen M. Onifer ◽  
Randall S. Sozio ◽  
Cynthia R. Long
Keyword(s):  
Chronic Pain ◽  
Clinical Research ◽  
Circuit Breaker ◽  
Spinal Manipulative Therapy ◽  
Basic Research ◽  
Short Term ◽  
Significant Disabilities ◽  
Manipulative Therapy ◽  
Critical Knowledge ◽  
Sites Of Action

Chronic pain is quite prevalent and causes significant disabilities and socioeconomic burdens. Spinal manipulative therapy and other manipulative therapies are used to manage chronic pain. There is a critical knowledge gap about mechanisms and sites of action in spinal manipulative therapy pain relief, especially the short-term analgesia that occurs following a treatment. Endocannabinoids are an activity-dependent neurotransmitter system that acts as a short-term synaptic circuit breaker. This review describes both clinical research and basic research evidence suggesting that endocannabinoids contribute to short-term manipulative therapy analgesia. Determining endocannabinoids involvement in spinal manipulative therapy will improve its clinical efficacy when results from basic science and clinical research are translated.

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