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J C Bornstein

Publications and source records attributed to J C Bornstein.

107 records · Page 6Linked to original sources
PubMed1980

Selective antagonist activity of 5-aminohex-2-enedioic acid on amino acid excitation of cat spinal neurones.

D- and L-5-aminohex-2-enedioic acid (AHED) and the DL-2-bromo derivative, which are conformationally restricted analogues of the excitatory amino acid antagonist D-alpha-aminoadipic acid (D alpha AA), were tested microelectrophoretically on cat spinal neurones. D-AHED reduced the excitatory action of N-methyl-D-aspartate (NMDA) to a greater extent than that of L-glutamate and the potency of this action was a half to a third that of D alpha AA. The DL-2-bromo derivative excited neurons, an effect greater than that of L-glutamate and not blocked by either D alpha AA or L-glutamic acid diethyl ester.

2-Aminoadipic Acid↗
PubMed1980

The effects of anaesthetic and convulsant barbiturates on the efflux of [3H]D-aspartate from brain minislices.

The effects have been investigated of anesthetic and convulsant barbiturates on the spontaneous and potassium-stimulated efflux of [3H]D-aspartate from rat cortex minislices. In concentrations (100 microM) which have previously been shown to alter calcium ATPase activity in synaptosomes, anaesthetic barbiturates depressed and convulsant barbiturates stimulated the spontaneous efflux of [3H]D-aspartate in a dose-dependent manner. The effects on the efflux of [3H]D-aspartate evoked by 44.7 mM KCl were similar, although one convulsant barbiturate (1,3M1B) was without effect. The results are discussed in terms of entry and removal of calcium ions from nerve terminals.

Amobarbital↗
PubMed1979

Inhibition of the evoked release of acetylcholine by the porphyrin precursor delta-aminolevulinic acid.

The effect of delta-aminolevulinic acid (ALA) on neuromuscular transmission were studied. High concentrations (0.6 to 18 mM) of ALA caused significant reductions in the amplitudes of curarized end-plate potentials (epps). Changing the ratio of calcium to magnesium in the bathing solution allowed the quantal content of the epps to be directly measured. Under these conditions, ALA reduced the quantal content of epps without affecting the depolarization produced by a single quantum of acetylcholine. It was concluded that ALA, in high concentrations, inhibits the release of acetylcholine evoked by a nerve impulse but is unlikely to be the cause of the neurological defects of acute porphyria.

Acetylcholine↗
PubMed1979

Morphine presynaptically inhibits a ganglionic cholinergic synapse.

The effects of morphine on synaptic transmission through the inferior mesenteric ganglion (IMG) were studied using intracellular recording techniques. Morphine produced a reversible, dose-dependent reduction in the quantal content of the synaptic potentials with little or no effect on quantal size or the properties of the ganglion cells. This effect of morphine was antagonized by naloxone suggesting the presence of specific preganglionic opiate receptors.

Animals↗
PubMed1979

Kainate neurotoxicity and glutamate inactivation.

Dihydrokainate, an inhibitor of high affinity L-glutamate as an excitant of cat spinal neurones in vivo. This action of dihydrokainate was selective in that the effects of excitants taken up actively in vitro by CNS tissue (L-aspartate, D- and L-glutamate and L-homocysteate) were enhanced whereas those of other substances not taken up (acetylcholine, D-homocysteate, kainate and N-methyl-D-aspartate) were not. Since kainate and dihydrokainate have similar potencies as inhibitors of L-glutamate uptake, interference with the inactivation of synaptically released L-glutamate may contribute to the neurotoxic effects of kainate.

Amino Acids↗
PubMed1979

Role of pain in placebo analgesia.

The hypothesis that perceived pain intensity can influence placebo analgesia was tested. One hundred and seven subjects rated their pain from from 0 to 10 on a visual analog scale after a standard wisdom tooth extraction. The expected course of such postoperative pain in the absence of therapy or placebo is a steady increase; this was confirmed by blind administration of the placebo. When placebos were given intravenously in view of the patients, some (placebo nonresponders) reported that their pain increased, whereas others (placebo responders) reported that their pain either decreased or remained the same over the next 60 min. A placebo response was more likely to occur if the pain rating 5 min prior to placebo administration (initial pain) was greater than 2.6. Furthermore, placebo responders with initial pain above this 2.6 level reported significantly greater mean analgesia than those with lower initial pain. Indeed, responders with initial pain less than 2.6 reported no change in pain during the 60 min after administration of a placebo. When their initial pain level was greater than 2.6, they reported a steady decline in pain over this period. However, above the 2.6 level there was no obvious relationship between the magnitude of the placebo analgesia and the initial pain.

Analgesia↗
PubMed1979

Some effects of hypertonic solution on the properties of spontaneous transmitter release in the hypogastric ganglia of guinea-pigs.

1. The effects of hypertonic solutions on spontaneous transmitter release at synapses in the hypogastric ganglia of guinea-pigs were studied using intracellular recording techniques. 2. Hypertonic solutions were found to cause a marked hyperpolarization of the ganglion cells and this was accompanied by an increase in both the threshold and input resistance of these cells. 3. The frequency of spontaneous quantal release was found to depend exponentially on the tonicity of the bathing solution with a 50% increase in tonicity producing a 7-9 fold increase in the frequency of release. 4. Hypertonic solutions were also found to increase the degree of bursting within the spontaneous process so that the proportion of multiquantal spontaneous potentials was found to be increased in such solutions. 5. Two different models, the 'charge-screening' model (Van der Kloot & Kita, 1973) and the 'Ca-increase' model (Shimoni, Alnaes & Rahamimoff, 1977), for the mechanism underlying the effects of hypertonic solution were considered.

Action Potentials↗
PubMed1978

Spontaneous multiquantal release at synapses in guinea-pig hypogastric ganglia: evidence that release can occur in bursts.

1. A study was made of some properties of the spontaneous synaptic potentials recorded in cells of the hypogastric ganglia of guinea-pigs. 2. The distribution of the amplitudes of the spontaneous synaptic potentials arising from a single preganglionic fibre was found to be multimodal, with peaks at roughly integral multiples of a unit peak. 3. It was found that the amplitudes of the larger spontaneous potentials were consistent with them being the result of synchronous or near-synchronous release of two or more unit-sized quanta (multiquantal release). 4. The proportion of multiquantal potentials observed was found to be dependent on the extracellular calcium ion concentration. 5. When the stochastic properties of the spontaneous potentials were examined, it was found that the spontaneous release process was not random and independent but appeared to be clustered. Indeed, the probability of occurrence of a unit spontaneous synaptic potential was greatly enhanced during the 40--60 msec immediately following any given spontaneous synaptic potential. 6. When unit spontaneous potentials were excluded from the analysis, the multiquantal potentials were still found to be clustered although the clustering was less marked than that seen in the over-all process. 7. These results suggested that the multiquantal spontaneous potentials arose from the release of unit quanta in short high frequency bursts and it was found that a mathematical model incorporating such a mechanism could describe the spontaneous quantal release process.

Animals↗
PubMed1974

The effects of physostigmine on synaptic transmission in the inferior mesenteric ganglion of guinea-pigs.

1. Synaptic potentials were recorded with intracellular electrodes from cells in the inferior mesenteric ganglion of the guinea-pig.2. Half-widths of the synaptic potentials recorded fell into two groups: type L cells had long synaptic potentials (11.6-15.2 msec) and low thresholds (14.6 mV mean), type S cells had short synaptic potentials (6.1-9.3 msec) and high thresholds (29.9 mV mean).3. Physostigmine (1.2 x 10(-6)M) caused a significant increase in the half-width of both types of synaptic potential.4. Physostigmine caused a significant increase in the half-width of spontaneous synaptic potentials and an increase in their amplitude.5. Repetitive preganglionic stimulation, in the presence of physostigmine, led to a marked and prolonged depolarization in all cells. In most cells repetitive spontaneous firing of action potentials was then observed. This effect was blocked by atropine (1.4 x 10(-7)M).6. The effect of atropine on the half-width in a physostigmine-treated cell was inconsistent: although synaptic potentials in some cells were slightly shortened their half-widths were always greater than the control.7. It is concluded that cholinesterase plays a role in limiting the time course of the synaptic potential, by limiting the duration of action of acetylcholine.

Acetylcholine↗
PubMedDate not supplied

Electrophysiological analysis of the convergence of peripheral inputs onto neurons of the coeliac ganglion in the guinea pig.

The convergence of intestinofugal axons from different intestinal regions onto individual neurons in the coeliac ganglion of the guinea pig was investigated using intracellular recording methods in vitro. Peripheral nerve trunks from the distal ileum, the most proximal colon and the colon near the colonic flexure were electrically stimulated along with preganglionic fibres running in the splanchnic nerve. Fast cholinergic excitatory synaptic potentials (EPSPs) were seen in ganglion cells in response to stimulation of each nerve trunk. Roughly half of 78 neurons impaled received inputs from stimulation of peripheral nerves, and almost all of these received input from the proximal colon. Most cells responded to stimulation of more than one peripheral nerve indicating that coeliac neurons receive converging inputs from intestinofugal neurons located in more than one intestinal region. In a second series of experiments, segments of intestine were left attached to the ganglion and distended with saline to stimulate peripheral mechanosensory input to the coeliac ganglion. In each experiment, two segments were stimulated. A subgroup of ganglion cells exhibited spontaneous fast EPSPs and the frequency of these potentials was increased by distension of one or other of the attached intestinal segments. However, few neurons responded to distension of both of the attached intestinal segments suggesting that some of the intestinofugal inputs to the coeliac ganglion identified by electrical stimulation may be sensitive to sensory modalities other than distension. Hexamethonium (0.5 mM) applied to the intestine, and not to the coeliac ganglion, reduced the frequency of the spontaneous synaptic potentials seen in coeliac ganglion cells, but did not abolish the response to distension of the colon (n = 8). When the Ca2+ concentration of the solution bathing the proximal colon was reduced to block all synaptic transmission in the enteric plexuses the background synaptic input was further depressed, but again the response to distension was little changed (n = 4). This suggests that at least some of the neurons projecting from the colon to the coeliac ganglion are first order mechanosensory neurons.

Animals↗
PubMedDate not supplied

A simple mathematical model of second-messenger mediated slow excitatory postsynaptic potentials.

We have developed a novel and simple mathematical model of a slow excitatory postsynaptic potential (EPSP) based on an abstraction of the processes of activation, inactivation, and summation of a cAMP, protein kinase A (PKA)-dependent second-messenger cascade. The model describes the activation of receptors, G-proteins, and production of cAMP as the first stage and uses first-order, non-rate-limited kinetics. The second stage corresponds to the release of active, PKA catalytic subunit and can use first- or higher-order kinetics. The third stage represents simple phosphorylation of ion channels and is limited by the number of channels available. The decay of each stage is based on first-order, mass-action kinetics. These equations and some variations were solved numerically and values of the parameters were determined by fitting to a variety of experimental data from myenteric neurons of the guinea-pig ileum. The model produced a slow EPSP with a nonlinear stimulus-response relationship that resulted from the underlying kinetics of the signaling cascade. This system of equations is suitable for incorporation into a large-scale computer simulation, and the methodology should be generalizable to other pathways.

Animals↗