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R Rahamimoff

Publications and source records attributed to R Rahamimoff.

80 records · Page 5Linked to original sources
PubMedDate not supplied

Is extracellular calcium buffering involved in regulation of transmitter release at the neuromuscular junction?

During synaptic activity at the neuromuscular junction, sodium, potassium and calcium ions flow through both the postsynaptic and presynaptic membrane. These ionic fluxes can cause changes in the local extracellular concentration in the synaptic gap: a decrease in the concentration of the inwardly flowing ions (sodium and calcium) and an increase in the outwardly flowing potassium ions. To check whether depletion of calcium ions in the synaptic gap is involved in transmitter release, we have used calcium buffers to keep the extracellular calcium concentration almost constant. The expectation was that if depletion does occur, transmitter release will increase; if no depletion occurs, there will be no change in quantal release when the calcium concentration is the same in buffered and unbuffered bathing solutions. We report here that, surprisingly, perfusing the frog neuromuscular preparation with a calcium-buffered solution caused a decrease in transmitter release compared with that in an unbuffered solution with the same calcium concentration. This presumably indicates that the calcium level in the synaptic cleft is higher than that in the bulk extracellular medium. If such a mechanism operates physiologically, it may provide an energetically economical way to determine the level of evoked transmitter release and thus synaptic efficiency.

Acetylcholine↗
PubMedDate not supplied

Activation of protein kinase C augments evoked transmitter release.

In view of the emerging role of the phosphoinositide system in cellular communication we examined its involvement in quantal-transmitter release, which is a key element in synaptic transmission. Transmitter release is normally activated by an increase in intracellular calcium, achieved either by entry of calcium ions through the presynaptic membrane or by intracellular calcium liberation. One of the targets of the phosphoinositide signalling system is the enzyme protein kinase C (PKC), which can be activated experimentally by tumour promoting phorbol esters, including 12-O-tetradecanoylphorbol-13-acetate (TPA). Such activation of PKC may be implicated in transmitter release in two ways. First, phorbol esters were found to increase secretion and enhance calcium currents; it might therefore be expected that they would increase synaptic transmitter release. But phorbol esters also inhibit the calcium current in dorsal root ganglion neurones. We report that the phorbol ester TPA augments synaptic transmission at the neuromuscular junction by increasing transmitter liberation. Activation of PKC also depends synaptic depression.

Animals↗
PubMedDate not supplied

Confocal microscopy of the lizard motor nerve terminals.

Confocal imaging was performed on the ceratomandibularis nerve muscle preparation of the lizard Anolis carolinensis, using 4-Di-2-ASP as a fluorescent probe. The imaging system consisted of a Sarastro Phoibos 1000 (Molecular Dynamics) scanning system and a Zeiss Universal microscope. The data were analyzed using the VANIS set of programs on a Silicon Graphics Personal Iris computer. A three dimensional reconstruction of the nerve terminals was performed using look-through and depth-coded projections. The volume of the nerve terminal was estimated in 15 neuromuscular junctions and found to be 84,835 microns 3 (+/- 8558 SEM). The largest diameter in each one of the 178 individual boutons was estimated from the look-through projections of 17 nerve terminals in 9 preparations. It was found to be 4.71 microns (+/- 0.08 SEM). The diameter perpendicular to the largest diameter in the same projection at 0 degrees was 3.3 microns (+/- 0.054 SEM). Thus it seems that the synaptic boutons of the ceratomandibularis are suitable for combined optical and electrophysiological recordings.

Animals↗
PubMedDate not supplied

The methodology for studying coordinated calcium concentration changes in a pancreatic beta cell line.

Intracellular calcium concentration was imaged in beta Tc cells with the aid of Fluo-3 indicator and the Meridian ACAS 570 interactive laser cytometry. This cell line does not respond by an elevation in [Ca2+]in to increase in extracellular [glucose], but does respond to 10 microM forskolin. It was found that forskolin increases the mean [Ca2+]in and produces calcium spikes. Time series analysis was performed on individual pixels. Autocorrelation revealed that forskolin induces oscillation in [Ca2+]in. Cross-correlation analysis showed that all the intracellular pixels along the line scan are highly correlated, indicating that the increase in [Ca2+]in encompasses the entire cell.

Aniline Compounds↗
PubMedDate not supplied

Pathophysiology of the neuromuscular junction in diabetic rats.

Using electrophysiological methods, we examined transport and transmission properties of the neuromuscular synapse in normal and diabetic rats. The stereospecific glucose transport system in the presynaptic nerve terminal was examined in two diabetic models and compared to the control. In both the streptozotocin (STZ) model and the Cohen model, a significant reduction was observed in the rates of glucose transport. A semiquantitative index for glucose transport, the glucose uptake factor, was 61 +/- 18% (SD) in the control group, 17 +/- 9% in the STZ group, and 15 +/- 10% in the Cohen group. Diabetes also affects the liberation of acetylcholine from the presynaptic motor nerve endings. The mean number of acetylcholine quanta liberated by the nerve impulse [quantal content (QC)] was reduced by 43% after 3.5 months of STZ diabetes. Thus, both the metabolic and the transmission functions of the neuromuscular junction are affected by the diabetic state.

Acetylcholine↗