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Biomedical subjects

S Peters

Publications and source records attributed to S Peters.

At least 235 records · Page 13Linked to original sources
PubMed1986

Neurons containing NADPH-diaphorase are selectively resistant to quinolinate toxicity.

Exposure of cultures of cortical cells from mouse to either of the endogenous excitatory neurotoxins quinolinate or glutamate resulted in widespread neuronal destruction; but only in the cultures exposed to quinolinate, an N-methyl-D-aspartate agonist, was there a striking preservation of the subpopulation of neurons containing the enzyme nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). Further investigation revealed that neurons containing NADPH-d were also resistant to the toxicity of N-methyl-D-aspartate itself but were selectively vulnerable to the toxicity of either kainate or quisqualate. Thus, neurons containing NADPH-d may have an unusual distribution of receptors for excitatory amino acids, with a relative lack of N-methyl-D-aspartate receptors and a relative preponderance of kainate or quisqualate receptors. Since selective sparing of neurons containing NADPH-d is a hallmark of Huntington's disease, the results support the hypothesis that the disease may be caused by excess exposure to quinolinate or some other endogenous N-methyl-D-aspartate agonist.

Animals↗
PubMed1986

Prognostic importance of hypodiploid hemopoietic precursors in myelodysplastic syndromes.

It has been suggested that a poor prognosis and the development of leukemia in patients with myelodysplasia may be related to chromosomal abnormalities. We measured the DNA content of bone marrow cells with flow cytometry in 19 hematologically normal subjects and in 70 patients who had recently been diagnosed as having myelodysplasia. Thirty-four of the patients were found to have aneuploidy. This was not related to the percentage of blast cells in the bone marrow, and there was no demarcation in terms of DNA content between patients with a high percentage of blast cells and those with a low percentage of such cells. Patients with hypodiploid marrow cells had a significantly shorter survival time than other patients (P = 0.001). Patients with hyperdiploid marrow and those whose marrow had a normal DNA content had similar survival times. Hypodiploidy appears to be a better indicator of poor survival than the marrow blast-cell count. Patients with sideroblastic anemia invariably had cells with a normal or high DNA content; none of these patients died during the study. Our data suggest that there is a relation between the loss of chromosomal material and progression toward a leukemic phenotype. It is tempting to speculate that this process may involve a loss of negative regulatory genes ("anti-oncogenes").

Aneuploidy↗
PubMed1986

Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension.

Radial distension of the large intestine produced a slow depolarization in a population of neurons in the inferior mesenteric ganglion of the guinea pig. The slow potentials often occurred simultaneously with cholinergic fast potentials [( excitatory postsynaptic potentials (EPSPs]) yet persisted in the presence of nicotinic and muscarinic cholinergic antagonists when all fast EPSPs were absent. The amplitude of the distension-induced noncholinergic slow depolarization increased with increasing distension pressure. For distensions of 1-min duration at pressures of 10-20 cm of water, the mean depolarization amplitude was 3.4 mV. The slow depolarization was associated with an increase in membrane resistance, and prolonged periods of colon distension resulted in a tachyphylaxis of the depolarization. Desensitization of ganglion cells to the peptide substance P attenuated the distension-induced slow potential by an average of 49% +/- 17%. Thus, two colonic mechanosensory afferent pathways converge on principal ganglion cells in the inferior mesenteric ganglion: one was previously described to be mediated by acetylcholine, and the other is described here, whose transmitter remains to be determined but which preliminary evidence suggests is mediated in part by substance P. The noncholinergic afferent pathway may enhance the intestinal inhibitory reflex mediated by cholinergic mechanosensory afferent input to the abdominal prevertebral sympathetic ganglia.

Animals↗
PubMed1986

Non-cholinergic transmission in a sympathetic ganglion of the guinea-pig elicited by colon distension.

Sensory transmission from the colon was studied using a preparation of inferior mesenteric ganglion (i.m.g.) attached to a segment of distal colon in guinea-pigs, in vitro. Electrical responses to colon distension were recorded intracellularly from neurones of the i.m.g. Distension of the distal colon up to an intraluminal pressure of 20 cmH2O caused an increase in resting asynchronous synaptic activity and a concomitant slow depolarization. The asynchronous synaptic activity, but not the slow depolarization, was abolished by cholinergic antagonists. Distension-induced non-cholinergic depolarizations were elicited in 44% of i.m.g. neurons sampled. For distensions of 1 min at 10-20 cmH2O, depolarizations reached a mean amplitude of 3.4 +/- 0.3 mV and lasted 108 +/- 7 s. Continuous distension resulted in a tachyphylaxis of the depolarization. Tetrodotoxin (3 X 10(-7) M) superfused over the i.m.g. reversibly abolished the distension-induced non-cholinergic depolarization. Distension-induced non-cholinergic depolarizations were accompanied by an increase in input resistance of 21%. Neuronal excitability also increased, as sub-threshold potentials produced by intracellular current injection reached threshold for firing action potentials during colon distension. The amplitude of non-cholinergic depolarizations increased with colonic intraluminal pressure between 2 and 20 cmH2O, although the slope of the mean amplitude-pressure curve decreased progressively at higher pressures. The amplitude of distension-induced non-cholinergic depolarizations increased as membrane potential was manually hyperpolarized to approximately -80 mV, whereupon further hyperpolarization resulted in a decrease in response amplitude. Non-cholinergic slow excitatory post-synaptic potentials (e.p.s.p.s) evoked by repetitive presynaptic nerve stimulation were reversibly attenuated by 19 +/- 8% during depolarizations produced by distension. Systemic administration of capsaicin (50-350 mg/kg) reduced the number of i.m.g. neurones exhibiting the non-cholinergic mechanosensory response; direct superfusion of capsaicin over the i.m.g. attenuated the response in some neurones but had no effect in others. These results demonstrate the existence of a non-cholinergic mechanosensory pathway from the colon to the i.m.g., and suggest that non-cholinergic transmission in the ganglion participates in mediating gastrointestinal reflexes. One transmitter utilized by the non-cholinergic mechanosensory pathway may be substance P.

Action Potentials↗
PubMed1985

Mediator release during nasal provocation. A model to investigate the pathophysiology of rhinitis.

The pathogenesis of rhinitis was investigated using a model of nasal provocation with different types of stimuli. Allergic subjects had an immediate response to antigenic challenge with symptoms of rhinitis highly correlated with increments in the concentrations of histamine, prostaglandin D2, kinins and kininogens, leukotrienes, and toluene sulfonyl arginine methyl ester esterase activity in their nasal secretions. This reaction was abated by a tricyclic antihistamine also capable of inhibiting mediator release from human mast cells in vitro and, in some subjects, by disodium cromoglycate. In a number of patients, symptoms reappeared three to 12 hours after nasal provocation. This late reaction also involves release of all of the aforementioned mediators except for prostaglandin D2, and preliminary data suggest that it can be inhibited by oral or topical steroids. Cold, dry air can induce rhinitis with mast cell mediator release from selected subjects. The pathogenesis of this reaction is unclear, but there are indications that osmolarity changes are responsible for mast cell activation. Thus, mast cells can be induced to release mediators and cause nasal symptoms by both immunologic and physical mechanisms, which may account for the pathophysiology of several types of rhinitis.

Air↗
PubMed1985

Vasopressin-mediated slow EPSPs in a mammalian sympathetic ganglion.

Vasopressin is one of numerous neuropeptides contained in sympathetic ganglia, but whose function remains unresolved. In this report, we present electrophysiological evidence that arginine-vasopressin (AVP) is a neurotransmitter in guinea pig inferior mesenteric ganglion (IMG). AVP superfused over the IMG, in vitro, produced in a population of neurons a membrane depolarization accompanied by a resistance increase, both of which were blocked by a specific V1 receptor antagonist. Moreover, slow excitatory postsynaptic potentials (EPSPs) elicited by repetitive nerve stimulation were attenuated in 75% of cells tested in the presence of excess AVP, and occasionally in the presence of the antagonist. Thus, AVP joins substance P as a putative transmitter of slow potentials in the guinea pig IMG.

Animals↗