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J Mambrini

Publications and source records attributed to J Mambrini.

At least 19 recordsLinked to original sources
PubMed1990

[Heptaminol hydrochloride as an epithelium transporter].

Electrophysiological and transport effects induced by heptaminol hydrochloride were studied in frog epithelium. This tissue, which can easily be maintained in vitro, is a valuable model for studying sodium active transport with hormone-dependent characteristics that reproduce mammalian nephron behavior (notably in areas with tight gap junctions). The two following techniques were used: the Ussing short-circuit current method and the swept-frequency impedance measurement method. Our findings indicate the following. (i) Heptaminol hydrochloride significantly increases the short-circuit current and transepithelial polarization. (ii) This effect develops progressively as the molecule is introduced on the serous side (3Na+/2K+ active countertransport sites). Time to maximum development is approximately 20 min and the electrophysiological effect lasts from 60 to 90 min. (iii) The mean equivalent cationic current rise is larger in sulfate-Ringer (+23 +/- 4.6 microA, p less than 0.01) than in chloride-Ringer (+14 +/- 4.9 microA, p less than 0.05). The increase in short-circuit current is approximately 0.9 muequiv. cm-2 h-1 in sulfate-Ringer. (iv) The increase in mean polarization is greater in chloride (+21 +/- 6.2 mV, p less than 0.02) than in sulfate (+6 +/- 1.5 mV, p less than 0.01) following a diphasic effect on potential. (v) Changes in apical impedance Z are small (-454 +/- 323 omega, nonsignificant) compared with transepithelial resistance in sulfate (-1065 +/- 359 omega, p less than 0.05). (vi) Changes in membrane capacitance reflect changes in the membrane surface. However, no significant capacitance changes are produced in sulfate and chloride solution by heptaminol hydrochloride (-0.04 +/- 0.11 microF and 0.05 +/- 0.11 microF, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Alcohols↗
PubMed1989

Synaptic current between neuromuscular junction folds.

Measurements of membrane infoldings of vertebrate subsynaptic membranes were taken to evaluate the possible electrophysiological implications. The shapes of standard interfolds of different neuromuscular junctions were established from micrographs available in the literature. Electrical properties were estimated using published fibre membrane and myoplasm electrical values. Models of synaptic current pathways were designed taking into account the small size of the postsynaptic patch activated by a transmitter quantum. This analysis reveals a resistance "in series" between the ACh-sensitive interfold crest and the remainder of the muscle fibre. The calculated cytoplasmic resistance of an interfold is between 0.2 and 3 Mohms which is in the same range as the fibre DC input resistance. The calculated interfold resistance appears to be dependent on the fibre type, the age and the pathology. Functional roles of junctional folds and dendritic spines are discussed.

Acetylcholine↗
PubMed1988

[The effects of heptaminol chlorhydrate on neuromuscular transmission].

6-Amino-2-methyl-2-heptanol chlorhydrate, heptaminol chlorhydrate, blocks the response to indirect stimulation of the mouse diaphragm in vitro. This effect is due to a dose-dependent pre- and post-synaptic block of neuromuscular transmission starting at 1 mM heptaminol (HEPT). The complete block of neuromuscular transmission occurs at 10 mM. At 2 mM, the decrease in quantal size is more significant in the presence of d-tubocurarine than when the extracellular calcium is lowered. At this concentration, heptaminol also prolongs the depolarization time of the motor end plate potential. Slightly higher concentrations of heptaminol produce a decrease in quantal content. This latter effect is associated with an increase in synaptic delay.

Amino Alcohols↗
PubMed1981

[Characteristics of the unitary end-plate potential of the frog (author's transl)].

When the transmitter release is reduced in physiological solutions with low calcium and high magnesium content (70% of transmission failure), most of the end-plate potentials are evoked by the release of one quantum. Observing a short sequence of the unitary potentials (10-30), one can see that they distribute into a few patterns of similar amplitude, latency and time to peak. The amplitude and latency frequency distributions show successions of peaks frequently set at regular intervals. The average number of peaks is 11 for the amplitude distribution and 14.5 for the latency distributions. Lowering the temperature (20-10 degrees C) lengthens the interval between the latency peaks (Q10 = 2). These observations suggest the existence of a limited number of releasing sites set at regular intervals (10-20 micrometers) along the branches of the nerve terminal. This hypothesis is discussed with regard to the well-known interpretation of the amplitude sub-units of the unitary response and the sub-miniature potentials. The time-distribution of the unitary-evoked potentials of identical latency is frequently periodic (about 60 s at 4 HZ of frequency stimulation). Slightly different frequencies can be observed at different latency values. Through our interpretation of the sub-units, these facts mean that the few active zones follow a periodic process which can explain the periodic oscillation already shown for the total activity of the neuromuscular junction.

Action Potentials↗
PubMed1979

[Evolution in time of transmitter release at frog neuromuscular junction].

It has previously been shown that the unitary quantal end-plate potentials observed at synapses blocked by low Ca++ high Mg++ ringer, belong to distinct clusters according to their amplitude, time to peak and latency characteristics. These clusters correspond probably to distinct releasing units dispersed along the presynaptic terminal branches. The distribution versus time of the occurence of unitary potentials belonging to one latency cluster has been studied over long lasting evoked nerve activity (stimulation frequencies: 1 to 10 Hz). It was observed that transmitter release at one releasing site is statistically periodic with emitting periods separated by rest periods. At a given end-plate the period of emitting activity seems to be independent from one emitting site to another.

Animals↗
PubMed1979

[Existence of different populations of unitary evoked postsynaptic potentials at the frog neuromuscular junction].

The postsynaptic response to monoquantic evoked transmitter release (mean quantal content about 0.3) has been studied at temperatures from 10 to 23 degrees C. The delay between nerve stimulation (1 to 10 Hz) and the unitary postsynaptic potentials fluctuates by steps. The existence of preferential delay sites can always be detected (mean number 13.5 +/- 3.1). Identical delay unitary postsynaptic potentials often shows identical amplitude and identical time to peak. These results suggest that few emitting sites are preferentially activated along the nerve terminal at low level release during long lasting stimulation. The "single process" assumption used in statistical studies of transmitter release is probably oversimplified.

Animals↗
PubMed1979

[A critical study of the relations between superficial or profound electrical potentials and regeneration in vertebrates (author's transl)].

It has been claimed that the action of the central and peripheral nervous systems on the regeneration process could be mediated through an electrical field which can be detected at the superficial limit of the animal tested. In this paper, it is demonstrated that superficial d. c. potentials detected on the skin of an amphibian are strickly correlated to the well-known skin ionic active transport mechanism and are quite independent of deep innervation. Moreover, reinforcing the deep electrical field through an amputated limb of a mammal (Wistar rat) doex not initiate regeneration, as has been claimed. We demonstrate that the insertion of d.c. generator does not significantly increase tritiated thymidine incorporation into the DNA of amputated animals as compared to control ones. Furthermore, wound healing proceeds in the same way in both groups. It is concluded that an electric field regeneration relationship remains to be demonstrated.

Animals↗
PubMed1979

[Effects of a neurotoxin isolated from the sea anemone, Anemonia sulcata, at frog neuromuscular junction (author's transl)].

ATX II is a toxin extracted from tentacles of Anemonia sulcata. It was known that this protein displays neurotoxic effects on frog isolated neuromuscular preparation (Fig. 1, 2) and that muscular contractures observed with ATX II are blocked by d-tubocurarine (Fig. 3) or on a 40-days-denervated gastrocnemius (Fig. 4). Part of these experiments has already appeared. 1. These effects of ATX II depend on calcium concentration in the bathing medium, as is the case for transmitter release. The same results were observed when we substituted strontium to calcium. 2. On an intact sciatic sartorius preparation, ATX II does not act on the amplitude of the miniature endplate potentials (mepps, Fig. 6). The muscular action potential is not modified by this toxin. 3. ATX II increases the frequency of the mepps (Fig. 5). The evoked transmitter release (quantal content) after ATX II is also largely increased (Fig. 7). 4. In conclusion, it is suggested that ATX II acts indirectly on the muscle through an increase in acetylcholine release from the motor nerve terminals.

Animals↗
PubMed1977

[Periodic variations in motor endplate potentials].

The amplitudes of motor end-plate potentials in the Frog have been measured during repetitive stimulations of the motor nerve at frequencies between 0,5 and 30 Hz. A serial analysis showed that cyclic variations of these amplitudes were superimposed on the random fluctuation of epp due to the quantal nature of transmitter release. The period of these cyclic variations varied between 3 and 10 stimulations. This period was not significantly related to the frequency of the stimulation. The frequency spectrum analysis of the epp amplitudes showed similar values for the period of the cyclic variation of epp. The same kind of analysis applied to a binomial series of random numbers did not significantly present periodic fluctuations. The same analysis was applied to mean amplitudes of groups of 5 to 120 successive epps at the same end-plate. Periodic fluctuations were identified with periods of about 10 to 180 sec. It is suggested that periodic failures of nerve spike propagation in nerve terminals at sites of low safety factor, as at branchings, are responsible for the observed cyclic variation of epp.

Animals↗
PubMed1977

[Origin of the differences of superficial potentials in Rana esculenta].

The spatial distributions of superficial D.C. potentials on the skin of Rana esculenta have been compared to those of the intensity of short-circuit current (S.C.C.) expressing the transcutaneous active transport of sodium ions. It has been observed that the sites of maximum D.C. potentials coincide with the localisations of maximum S.C.C. values. Moreover, superficial D.C. potentials and S.C.C. are similarly modified by the depression of metabolic activity due to lowered temperature or poisoning by dinitrophenol (DNP). It is thus proposed that the spatial distribution of the transcutaneous active transport system for sodium ions is the origin of the electric generator of superficial D.C. potentials.

Animals↗
PubMed1977

[Variation of the time constant (tau) of the decay of end-plate current during focalized transmitter release].

The variations of the time constant tau of the end-plate current (epc) have been studied at the clamped neuromuscular junction of the frog while transmitter release was focalised by local iontophoretic application of Ca++. In the absence of any anticholinesterasic drug, tau varies according to the variations of the intensity of epc (Iepc) due to pre or postsynaptic experimental procedure. It is suggested that focalisation of transmitter release induces local acetylcholinesterase inhibition by an excess of substrate; then the transmitter life time in the synaptic cleft is momentarily increased, allowing repeated binding of Ach to postsynaptic receptors.

Acetylcholinesterase↗
PubMed1970

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

1. The action of ions which increase the nerve spike duration at Ranvier's node has been studied at the neuromuscular junction of the frog.The duration of the presynaptic action potential is increased by UO(2), Ni, Nz and TEA ions.2. The release of transmitter after a nerve impulse is delayed and prolonged in the presence of the four ions, but the amount of evoked transmitter release estimated from the mean quantal content of e.p.p. is increased only by UO(2) (2+) and TEA. Both Ni(2+) and Zn(2+) decrease it.3. The frequency of m.e.p.p.s is increased by UO(2) (2+) and decreased by Ni(2+) and Zn(2+) at KCl-depolarized junctions. It is not affected by TEA.4. It has been concluded that the increased presynaptic spike duration is responsible for the delayed and prolonged transmitter release in the presence of ions which increase the nerve spike duration at Ranvier's node. It is demonstrated that some ;specific' effects possibly resulting from ionic competition for presynaptic sites between UO(2) (2+), Ni(2+) or Zn(2+) and other ions present in the Ringer may increase, interfere with, or hide the increased transmitter release that may be predicted from the lengthened presynaptic depolarization.

Action Potentials↗