A series of controlled seismic experiments performed in a limestone quarry demonstrate the utility of high-precision electronic detonators in studying source characteristics of multiple explosive ...arrays. At near-source ranges (80–130m), where source dimensions are on the same order as source-receiver distances, the influence of the difference in travel path-length among individual explosions on the seismograms is significant. Focusing of the seismic energy is observed as a function of station location with respect to the source array and is attributed to the extended source length (68–94 m) and firing time of the source (380–544 ms). We examine two methods for modelling ripple-fired explosions at near-source ranges using the principles of superpositioning. The first method is based primarily on acquisition of an adequate single shot signal and requires well-constrained shot times. Amplitude variations which result from travel path differences are not modelled, which restricts use of this technique for purposes of blast vibration reduction to larger distances (>2–3 source dimensions) where the spatial finiteness effects of the source begin to diminish. For near-source distances (<2 source dimensions), we successfully model multiple-source seismograms by convolving a synthetic seismic source signal for a single explosion with individual half-space Green's functions calculated for each explosion in the array. Our single-source model for a cylindrically shaped single charge (borehole length of 17.5 m and diameter of 90 mm) of 68 kg consists of a modified Mueller-Murphy approximation which utilizes source parameter estimates taken from chemical explosion study results. Model parameters include a final cavity radius of 0.25 m and an elastic radius of 18 m. The final model is obtained by convolving the simulated single-source time series with half-space Green's functions calculated for several source depths and superposed to approximate the spatial extent of the borehole. The relative amplitude and phase characteristics of the observed single-source signal at the same distance (80.6 m) are reproduced by this model. Multiple-source synthetic seismograms contain individual Green's functions for each source-receiver distance but utilize identical sources for the explosive array. Focusing effects are shown to be due to the effect of propagation path differences between individual explosions in agreement with the results of Anderson & Stump (1989) in simulating multiple-source seismograms. Good fits to the measured production shot amplitude spectra are obtained with the synthetic spectra. Spectral peaks are well-matched due to precision of the firing times which were controlled by electronic detonators. Our example of delay time variances for 32 ms production shot (Appendix) argues for better constraint of firing times for contolled seismic experiments. Such constraint requires a 1 per cent error or less in cap firing times which can be realized by the use of firing systems with an order-of-magnitude increase in precision compared to pyrotechnic detonators.
B-HT 920 (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo-4,5-dazepine), an agonist at alpha 2-adrenoceptors and at dopamine autoreceptors, was tested with respect to stimulation of postsynaptic brain ...dopamine receptors in mice, rats and rhesus monkeys. In mice B-HT 920 (0.2-20 mg/kg s.c.) injected 4 h after reserpine did not stimulate locomotor activity; this was in contrast to apomorphine (0.1-10 mg/kg s.c.) which elicited locomotor activity in a dose-dependent manner. However, B-HT 920 was effective in inducing locomotor activity when injected 12, 24 and 48 h after reserpine. This effect was dose-dependent and increased with the duration of reserpine pretreatment. In naive rats, B-HT 920 (0.02-2.0 mg/kg s.c.) only decreased exploratory activity and did not elicit stereotyped activity in doses up to 4 mg/kg s.c. This was in contrast to the stereotypy-inducing effect of apomorphine (2.0 and 4.0 mg/kg s.c.). In rats with unilateral striatal ibotenic acid lesion, B-HT 920 (0.2-2.0 mg/kg s.c.) was ineffective in producing significant ipsilateral rotation, whereas apomorphine (0.5-10.0 mg/kg s.c.) was very potent in this model. In rats with unilateral 6-OH-dopamine lesions of the medial forebrain bundle B-HT 920 elicited strong contralateral rotation in a dose-dependent manner (0.02-1.0 mg/kg s.c.). In this model B-HT 920 was equi-effective but long acting when compared with apomorphine. The contralateral rotation produced by B-HT 920 was antagonized by the D2-antagonist sulpiride but not by the D1-antagonist SCH 23390. In rhesus monkeys with severe parkinson-like symptoms induced by MPTP, B-HT 920 in doses of 10 micrograms/kg i.m. and higher restored normal behavior, resulting in complete relief of parkinson symptoms in all animals with 100 micrograms/kg i.m. It is concluded that the property of B-HT 920 to stimulate the 'denervated' supersensitive (reserpine, 6-OH-dopamine, MPTP) but not the normosensitive postsynaptic dopamine receptor in the striatum may represent a novel principle for a specific approach to dopamine substitution treatment of Parkinson's disease.
The effect of neuraminidase on synaptic transmission was studied at cholinergic and noncholinergic contacts in the buccal and cerebral ganglion of Aplysia. The amplitudes of monosynaptic unitary ...postsynaptic potentials generated by intracellular stimulation of identified presynaptic neurones were measured as indication for the efficacy of synaptic transmission. Neuraminidase was either intrasomatically injected into a presynaptic neurone, or the whole ganglion was incubated with the enzyme. Intrasomatic injection of the enzyme resulted in complete failure of synaptic transmission. This effect occurred independently of the transmitter used. The synaptic failure was presynaptic in origin. The biophysical characteristics of an injected neurone, particularly the amplitude and propagation of its action potential, did not appear to be affected by neuraminidase. Synaptic transmission and biophysical membrane properties were unaffected by extracellular neuraminidase. We conclude that the synaptic blockade is due to the enzyme's action inside the presynaptic nerve ending. It seems most likely that neuraminidase cleaves sialic-acid-containing-compounds associated with the nerve terminal surface membrane, probably thus causing failure of transmitter release.
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