Antibiotic resistance pattern of enterotoxigenic Escherichia coli isolated from infants and young adults in Israel.

The aim of this study was to describe antibiotic resistance rates of enterotoxigenic Escherichia coli in Israel in order to facilitate the empirical choice of antibiotic treatment or prophylaxis for traveler's diarrhea and infantile diarrhea in our region. A total of 281 enterotoxigenic Escherichia coli isolates were tested: 144 from Bedouin infants and 137 from Israeli soldiers. Antibiotic-resistant isolates were prevalent in both groups, but higher resistance rates were found in the pediatric group. Strains producing heat-labile toxin showed higher resistance rates than strains producing heat-stable toxin. The results obtained in Israel preclude the use of many commonly used antibiotics for the treatment of traveler's diarrhea. Quinolones, however, are still effective.

Transmitter release modulation in nerve terminals of rat neocortical pyramidal cells by intracellular calcium buffers.

1. Dual whole-cell voltage recordings were made from synaptically connected layer 5 (L5) pyramidal neurones in slices of the young (P14-P16) rat neocortex. The Ca2+ buffers BAPTA or EGTA were loaded into the presynaptic neurone via the pipette recording from the presynaptic neurone to examine their effect on the mean and the coefficient of variation (c.v.) of single fibre EPSP amplitudes, referred to as unitary EPSPs. 2. The fast Ca2+ buffer BAPTA reduced unitary EPSP amplitudes in a concentration dependent way. With 0.1 mM BAPTA in the pipette, the mean EPSP amplitude was reduced by 14 +/- 2.8% (mean +/- s.e.m., n = 7) compared with control pipette solution, whereas with 1.5 mM BAPTA, the mean EPSP amplitude was reduced by 72 +/- 1.5% (n = 5). The concentration of BAPTA that reduced mean EPSP amplitudes to one-half of control was close to 0.7 mM. 3. Saturation of BAPTA during evoked release was tested by comparing the effect of loading the presynaptic neurone with 0.1 mM BAPTA at 2 and 1 mM [Ca2+]o. Reducing [Ca2+]o from 2 to 1 mM, thereby reducing Ca2+ influx into the terminals, decreased the mean EPSP amplitude by 60 +/- 2.2% with control pipette solution and by 62 +/- 1.9% after loading with 0.1 mM BAPTA (n = 7). 4. The slow Ca2+ buffer EGTA at 1 mM reduced mean EPSP amplitudes by 15 +/- 2.5% (n = 5). With 10 mM EGTA mean EPSP amplitudes were reduced by 56 +/- 2.3 % (n = 4). 5. With both Ca2+ buffers, the reduction in mean EPSP amplitudes was associated with an increase in the c.v. of peak EPSP amplitudes, consistent with a reduction of the transmitter release probability as the major mechanism underlying the reduction of the EPSP amplitude. 6. The results suggest that in nerve terminals of thick tufted L5 pyramidal cells the endogenous mobile Ca2+ buffer is equivalent to less than 0.1 mM BAPTA and that at many release sites of pyramidal cell terminals the Ca2+ channel domains overlap, a situation comparable with that at large calyx-type terminals in the brainstem.

Voltage dependent switch in the activity mode of the K+ channel in presynaptic nerve terminals.

The bursting K+ channel is the most common channel in fused Torpedo presynaptic nerve terminals. It possesses the property of 'statistical memory', demonstrated by non-random probability of channel opening. We examined the voltage dependence of the statistical memory and report that removal of channel inactivation by hyperpolarization abolishes it. Addition of the potassium channel blocker 4-aminopyridine to the bath solution led to disappearance of statistical memory, while raising extracellular potassium concentration had the opposite effect. Another common channel at Torpedo nerve terminals which is a non-selective channel did not exhibit statistical memory. We conclude that statistical memory is a channel-specific phenomenon and speculate regarding its possible role in cellular and network properties of the nervous system.