1 The responses of excitatory junctions on locust skeletal muscle fibres to iontophoretically applied L-glutamic acid and DL-ibotenic acid, a rigidly extended analogue of glutamate, were recorded by means of intracellular microelectrodes.2 Iontophoresis of L-glutamate to junctional sites produced transient depolarizations. Ibotenate applied iontophoretically to these sites usually evoked small hyperpolarizations which probably resulted from the activation of glutamate H-receptors on the extrajunctional membrane surrounding the junctions. However, at a minority ( approximately 20%) of junctions, ibotenate iontophoresis evoked transient depolarizations.3 Iontophoretically applied glutamate desensitized the ibotenate receptors, and vice versa. In experiments performed at junctional sites at which ibotenate depolarizations were absent, ibotenate had no effect on the responses to glutamate.4 Glutamate and ibotenate junctional currents had similar reversal potentials, measured under voltage-clamp, suggesting that the ionic bases for these currents are identical.5 It is proposed that the excitation caused by ibotenate results from the activation of receptors for extended L-glutamate and that these receptors co-exist on the post-junctional membranes of locust excitatory nerve-muscle synapses with ibotenate-insensitive glutamate receptors activated by glutamate in partially folded conformation.

Animals↗

PubMed1979

Desensitization of glutamate receptors on innervated and denervated locust muscle fibres.

Depolarizations to L-glutamate, applied locally by microinophoresis to the extrajunctional membrane of locust extensor tibiae muscle fibres and measured either in current clamp or voltage clamp, increased in amplitude for equivalent doses of glutamate following chronic denervation of the muscle. 2. A two-pulse method was used to examine recovery from desentization of junctional and extrajunctional receptors. A 'response ratio', i.e. the amplitude of response to the second (test) of a pair of glutamate pulses over to the pulses. The 'response ratio' for extrajunctional depolarizations of innervated fibres increased exponentially with pulse interval, with a time constant of 15.6 +/- 4.7 sec (n = 11). Recovery of extrajunctional receptor populations from desensitization was accelerated after denervation. The recovery kinetics for responses from fibres 6-22 days after denervation were generally described by two exponential terms, with time constants in the range 0.5-10 sec which were inversely related to the glutamate sensitivity of the extrajunctional membrane. For junctional receptors on both innervated and denervated fibres the recovery kinetics were described by a single exponential with a time constant of 0.2-1 sec. 3. The results suggest that the increased extrajunctional glutamate sensitivity which occurs after denervation results from the 'appearance' of glutamate receptors with properties similar to those found at the post-junctional membrane on locust muscle fibres.

Animals↗

PubMed1979

Glutamatergic synapses and glutamate receptors on locust muscle.

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Animals↗

PubMed1979

Agonist-dependent desensitization of glutamate receptors at locus nerve-muscle junctions [proceedings].

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Animals↗

PubMed1978

Two components of extracellularly-recorded photoreceptor potentials in the cephalopod retina: differential effects of Na+, K+ and Ca2+.

The ERG of the isolated, superfused half-eye of the cephalopod Sepiola atlantica, evoked by a brief (10 micro second) light flash, has been studied by recording intraretinal potentials with glass microelectrodes. The intensity-response characteristics of the potentials recorded at an electrode fixed at the surface (Vs) can be fitted by a simple equation derived from an equivalent circuit model based on a sodium conductance increase mechanism. Raising the external potassium level reduces the maximal response (deltaVm), but does not alter the half-saturation intensity value (I0). Reducing external sodium does not affect deltaVm, but increase I0. Reducing external calcium also does not affect delta Vm, but decrease I0. These effects are adequately described by the model if it is also assumed (a) that changing the external sodium does not significantly alter the transmembrane sodium gradient, and (b) that sodium and calcium ions compete for the sensitivity control mechanism. Differential-depth recording between the fixed electrode at the surface and another electrode that could be moved into the retina revealed that the two component appearance of the transretinal ERG arose from the superposition of two vitreal-negative waveforms. An initial "fast" component was mainly recorded in the photoreceptive distal segments while a "slow" component was prominent in the more proximal regions of the retina. Perfusion with high K+ salines resulted in a decrease in the amplitudes of both fast and slow components of the response whereas reducing external Na+ reduced the amplitude of the fast component at all light intensities but reduced the amplitude of the slow component only at low intensities. The amplitudes of both the fast and slow components increased on reducing external calcium, but the rate of rise and fall of the fast component was independent of external calcium. The rate of rise of the slow component was also independent of the external Ca2+ level but a minimum in the recovery time (tF) was shifted to a lower intensity value at lower calcium concentrations. The shift of the minimum was to a higher intensity value with lowered sodium perfusing solutions. On the basis of the differential sensitivity of the two components to ion changes, as well as stimulus intensity and intraretinal distribution of the components, it is suggested that they reflect two distinct processes in the light-evoked potential of the photoreceptor cells.

Animals↗

PubMed1978

Metabolites of meperidine in serum.

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Animals↗

PubMed1978

Preoperative oral antacid therapy for patients requiring emergency surgery.

Preoperative oral antacid therapy has been used effectively to reduce the number of emergency obstetric patients "at risk" of developing acid-aspiration syndrome. Thirty-three nonobstetric adult patients requiring emergency surgery were selected to determine whether the protective effects of antacid therapy could also be derived in this high-risk group. Maalox-treated patients had a mean gastric pH of 6.46 +/- 0.5 and gastric volume 21.5 +/- 3.6 ml, with none at risk, whereas control patients had mean pH of 3.71 +/- 0.43, gastric volume 71.5 +/- 16.5 ml, and 42.1% at risk. This report suggests that preoperative antacid therapy should reduce the incidence of acid aspiration and subsequent morbidity and mortality in patients requiring emergency surgery.

Administration, Oral↗

PubMed1978

Endogenous GTP and the regulation of epinephrine stimulation of adenylate cyclase.

Epinephrine increased adenylate cyclase activity 10 to 15 fold in lysates of the cultured human astrocytoma cell line 132-1N1. GTP had little effect on adenylate cyclase activity of lysed cell preparations either with or without added epinephrine. However, the epinephrine stimulation of adenylate cyclase was essentially lost (less than 90%) when a washed nuclei-free membrane preparation of the cyclase was assayed. A 10 to 15 fold epinephrine stimulation of the membrane adenylate cyclase could be demonstrated if cytosol of GTP were added to the assay with the hormone. The criteria of anion exchange, cation exchange, gel exclusion and paper chromatography indicated that the cytosolic agents which acted synergistically with hormones were GTP and GDP. The apparent Kact's for the synergistic action of GDP and GTP were essentially identical (1.0 muM) and of all the other nucleotides examined only GDP had a potency similar to GTP. However, the effect of GDP was apparently due to its rapid conversion to GTP even in the absence of a regenerating system. With epinephrine pretreatment of the intact 132-1N1 cells there was a specific loss of epinephrine stimulation of adenylate cyclase activity. The hormone pretreatment did not alter the capacity of the cytosol from these desensitized cells to potentiate epinephrine stimulation of the cyclase. Rather, the alteration was in the particulate fraction of the lysate. The desensitization of the membranous cyclase was stable and not reversed by GTP.

Adenylyl Cyclases↗

PubMed1978