Long-term facilitation alters transmitter releasing properties at the crayfish neuromuscular junction

1986 ◽  
Vol 55 (3) ◽  
pp. 484-498 ◽  
Author(s):  
J. M. Wojtowicz ◽  
H. L. Atwood

Synaptic transmission at the neuromuscular junction of the excitatory axon supplying the crayfish opener muscle was examined before and after induction of long-term facilitation (LTF) by a 10-min period of stimulation at 20 Hz. Induction of LTF led to a period of enhanced synaptic transmission, which often persisted for many hours. The enhancement was entirely presynaptic in origin, since quantal unit size and time course were not altered, and quantal content of transmission (m) was increased. LTF was not associated with any persistent changes in action potential or presynaptic membrane potential recorded in the terminal region of the excitatory axon. The small muscle fibers of the walking-leg opener muscle were almost isopotential, and all quantal events could be recorded with an intracellular microelectrode. In addition, at low frequencies of stimulation, m was small. Thus it was possible to apply a binomial model of transmitter release to events recorded from individual muscle fibers and to calculate values for n (number of responding units involved in transmission) and p (probability of transmission for the population of responding units) before and after LTF. In the majority of preparations analyzed (6/10), amplitude histograms of evoked synaptic potentials could be described by a binomial distribution with a small n and moderately high p. LTF produced a significant increase in n, while p was slightly reduced. The results can be explained by a model in which the binomial parameter n represents the number of active synapses and parameter p the mean probability of release at a synapse. Provided that a pool of initially inactive synapses exists, one can postulate that LTF involves recruitment of synapses to the active state.

2010 ◽  
Vol 108 (2) ◽  
pp. 369-377 ◽  
Author(s):  
Susmita Chowdhuri ◽  
Irina Shanidze ◽  
Lisa Pierchala ◽  
Daniel Belen ◽  
Jason H. Mateika ◽  
...  

We hypothesized that episodic hypoxia (EH) leads to alterations in chemoreflex characteristics that might promote the development of central apnea in sleeping humans. We used nasal noninvasive positive pressure mechanical ventilation to induce hypocapnic central apnea in 11 healthy participants during stable nonrapid eye movement sleep before and after an exposure to EH, which consisted of fifteen 1-min episodes of isocapnic hypoxia (mean O2 saturation/episode: 87.0 ± 0.5%). The apneic threshold (AT) was defined as the absolute measured end-tidal Pco2 (PetCO2) demarcating the central apnea. The difference between the AT and baseline PetCO2 measured immediately before the onset of mechanical ventilation was defined as the CO2 reserve. The change in minute ventilation (V̇I) for a change in PetCO2 (ΔV̇I/ ΔPetCO2) was defined as the hypocapnic ventilatory response. We studied the eupneic PetCO2, AT PetCO2, CO2 reserve, and hypocapnic ventilatory response before and after the exposure to EH. We also measured the hypoxic ventilatory response, defined as the change in V̇I for a corresponding change in arterial O2 saturation (ΔV̇I/ΔSaO2) during the EH trials. V̇I increased from 6.2 ± 0.4 l/min during the pre-EH control to 7.9 ± 0.5 l/min during EH and remained elevated at 6.7 ± 0.4 l/min the during post-EH recovery period ( P < 0.05), indicative of long-term facilitation. The AT was unchanged after EH, but the CO2 reserve declined significantly from −3.1 ± 0.5 mmHg pre-EH to −2.3 ± 0.4 mmHg post-EH ( P < 0.001). In the post-EH recovery period, ΔV̇I/ΔPetCO2 was higher compared with the baseline (3.3 ± 0.6 vs. 1.8 ± 0.3 l·min−1·mmHg−1, P < 0.001), indicative of an increased hypocapnic ventilatory response. However, there was no significant change in the hypoxic ventilatory response (ΔV̇I/ΔSaO2) during the EH period itself. In conclusion, despite the presence of ventilatory long-term facilitation, the increase in the hypocapnic ventilatory response after the exposure to EH induced a significant decrease in the CO2 reserve. This form of respiratory plasticity may destabilize breathing and promote central apneas.


1994 ◽  
Vol 72 (2) ◽  
pp. 778-784 ◽  
Author(s):  
F. Zhang ◽  
J. R. Goldsmith ◽  
J. H. Byrne

1. An in vitro analogue of long-term sensitization training was used to gain insights into the mechanisms and time course of the memory for long-term sensitization in Aplysia. The analogue, consisting of four blocks of shocks, was delivered to peripheral nerves of the isolated pleural-pedal ganglia, which contain the sensory neurons and motor neurons that mediate the tail withdrawal reflex. 2. Long-term facilitation of the connections between the sensory neurons and motor neurons was produced by the conjoint stimulation of two peripheral nerves, P8 and P9. Long-term facilitation, however, was not observed after conjoint stimulation of three nerves, P7, P8, and P9. 3. The preparation was viable and stable (no changes in the amplitudes of excitatory postsynaptic potentials (EPSPs) and membrane properties in controls) for at least 48 h. Moreover, the long-term facilitation persisted for at least 48 h. 4. We observed no significant long-term changes in the resting membrane potentials of the sensory and motor neurons or in the input resistance of the motor neurons 24 and 48 h after the conjoint stimulation of nerves P8 and P9. Thus changes in these biophysical properties do not appear to contribute to the expression of long-term facilitation. 5. The finding that conjoint stimulation of three nerves, P7, P8, and P9, produced no long-term facilitation raised the possibility that stimulation of nerve P7 alone might produce long-term inhibition that opposes the facilitatory effects induced by conjoint stimulation of nerves P8 and P9. Stimulation of nerve P7 alone, however, had no long-term inhibitory effect on the EPSPs.(ABSTRACT TRUNCATED AT 250 WORDS)


1974 ◽  
Vol 63 (2) ◽  
pp. 168-186 ◽  
Author(s):  
M. Orentlicher ◽  
J. P. Reuben ◽  
H. Grundfest ◽  
P. W. Brandt

The nonionic detergent Brij 58 eliminates irreversibly the capability of the sarcoplasmic reticulum (SR) of skinned crayfish muscle fibers to sequester Ca and to release it under appropriate stimulation. In contrast to deoxycholate (DOC) which causes an irreversible diminution of tension as well, Brij 58 does not affect the contractile proteins. Comparison of the time-course of tension development before and after Brij treatment demonstrates that Ca is accessible to the contractile proteins more rapidly after the SR is destroyed but, nevertheless, much more slowly than is predicted for free diffusion of Ca in the myoplasm. Slowing apparently results because of the presence of ca 1 mmol/kg fiber of myoplasmic Ca-binding sites that remain after Ca uptake of the SR is eliminated. A theoretical model is presented which allows for the effects of binding sites and of an unstirred layer in the vicinity of the fiber on Ca diffusion into the myoplasm.


2005 ◽  
Vol 34 (6) ◽  
pp. 387-396 ◽  
Author(s):  
Maria Julia Marques ◽  
Zarif T. R. Mendes ◽  
Elaine Minatel ◽  
Humberto Santo Neto

2003 ◽  
Vol 94 (1) ◽  
pp. 399-409 ◽  
Author(s):  
Ryan W. Bavis ◽  
Gordon S. Mitchell

Episodic hypoxia elicits a long-lasting augmentation of phrenic inspiratory activity known as long-term facilitation (LTF). We investigated the respective contributions of carotid chemoafferent neuron activation and hypoxia to the expression of LTF in urethane-anesthetized, vagotomized, paralyzed, and ventilated Sprague-Dawley rats. One hour after three 5-min isocapnic hypoxic episodes [arterial Po 2(PaO2 ) = 40 ± 5 Torr], integrated phrenic burst amplitude was greater than baseline in both carotid-denervated ( n = 8) and sham-operated ( n = 7) rats ( P < 0.05), indicating LTF. LTF was reduced in carotid-denervated rats relative to sham ( P < 0.05). In this and previous studies, rats were ventilated with hyperoxic gas mixtures (inspired oxygen fraction = 0.5) under baseline conditions. To determine whether episodic hyperoxia induces LTF, phrenic activity was recorded under normoxic (PaO2 = 90–100 Torr) conditions before and after three 5-min episodes of isocapnic hypoxia (PaO2 = 40 ± 5 Torr; n = 6) or hyperoxia (PaO2 > 470 Torr; n= 6). Phrenic burst amplitude was greater than baseline 1 h after episodic hypoxia ( P < 0.05), but episodic hyperoxia had no detectable effect. These data suggest that hypoxia per se initiates LTF independently from carotid chemoafferent neuron activation, perhaps through direct central nervous system effects.


2007 ◽  
Vol 292 (1) ◽  
pp. R505-R515 ◽  
Author(s):  
Marika L. Armstrong ◽  
Ashok K. Dua ◽  
Coral L. Murrant

To characterize the vasodilatory response in the transition from a single skeletal contraction to a series of contractions, we measured the response of hamster cremaster muscle arterioles associated with four to five skeletal muscle fibers stimulated to contract for one, two, three, or four contractions (250-ms train duration) at 4-s intervals [15 contractions per minute (CPM)] for up to 12 s, at stimulus frequencies of 4, 10, 20, 30, 40, 60, and 80 Hz. To investigate the contribution of contraction frequency, we stimulated muscle fiber bundles at 30 or 60 CPM for 12 s at stimulus frequencies of 4, 20, and 60 Hz. Arteriolar diameters at the site of overlap with the stimulated muscle fibers were measured before and after each contraction. At 15 CPM at 4, 20, and 60 Hz, we observed a peak change in diameter following the first contraction of 1.1 ± 0.1, 1.6 ± 0.2, and 2.1 ± 0.2 μm that almost doubled in response to the second contraction (2.0 ± 0.1, 3.0 ± 0.1, and 3.8 ± 0.1 μm, respectively), but there was no further dilation following the third or fourth contraction. A similar response occurred at all stimulus and contraction frequencies tested. At 30 and 60 CPM at 60 Hz, the plateau after two contractions was followed by a further increase in diameter to a second plateau at 7–8 s. Therefore, the vasodilatory response in the transition from single to multiple contractions had components that were stimulation parameter dependent and independent and showed a plateauing behavior indicative of rapid changes in either the nature and/or concentration of vasodilators released or changes in vascular reactivity.


1999 ◽  
Vol 354 (1391) ◽  
pp. 1803-1810 ◽  
Author(s):  
Keith M. Martin–Smith ◽  
Lindsay M. Laird ◽  
Luke Bullough ◽  
Matthew G. Lewis

Community resistance to, and resilience from, perturbation will determine the trajectory of recovery from disturbance. Although selective timber extraction is considered a severe disturbance, fish communities from headwater streams around Danum Valley Field Centre, Sabah, Malaysia, showed few long–term changes in species composition or abundance. However, some species showed short–term (< 18 months) absence or decrease in abundance. These observations suggested that both resistance and resilience were important in maintaining long–term fish community structure. Resistance to perturbation was tested by monitoring fish communities before and after the creation of log–debris dams, while resilience was investigated by following the time–course of recolonization following complete removal of all fish. High community resistance was generally shown although the response was site–specific, dependent on the composition of the starting community, the size of the stream and physical habitat changes. High resilience was demonstrated in all recolonization experiments with strong correlations between pre– and post–defaunation communities, although there was a significant difference between pool and riffle habitats in the time–course of recovery. These differences can be explained by the movement characteristics of the species found in the different habitats. Resilience appeared to be a more predictable characteristic of the community than resistance and the implications of this for ensuring the long–term persistence of fish in the area are discussed.


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