Improved upper limit on flavor-changing neutral-current decays of the b quark.
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Biomedical subjects
Publications and source records attributed to S Stone.
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The properties of axon-bearing horizontal cells were studied by intracellular recording in the light-adapted Xenopus retina. In this adaptational state, the only receptor input was provided by red-sensitive cones. Measurements of response amplitude as a function of stimulus diameter indicated that different units were divisible into two compartments on the basis of their receptive field dimensions: one with a mean length constant, lambda, of 170 microns, the other with lambda = 450 microns. Lucifer Yellow dye injection revealed that units having small receptive fields invariably were cell bodies, whereas units having large receptive fields always were axons. For both horizontal cell bodies and axons, the waveform in response to large spots or annuli consisted of a hyperpolarizing on-transient, followed by a depolarizing rollback to a sustained plateau during light on, and a rapidly depolarizing off-transient that overshot the dark potential level. In contrast, in responses to small spots, the depolarizing rollback was much reduced or absent. However, for small field compartments only, when concentric annular stimuli were flashed around steadily illuminated, small, centered spots, the horizontal cell waveform consisted primarily of a depolarizing potential during light on. This depolarizing component was reduced selectively when the preparation was superfused with Ringer containing 5 mM gamma-aminobutyric acid (GABA). Following a brief exposure to 5-10 mM Sr2+, enhanced oscillatory potentials appeared in the horizontal cell light response during the depolarizing rollback and at light off. The modifications of the depolarizing rollback evoked by Sr2+ were antagonized by GABA. The strontium-induced alterations of the light response were not altered by 6 microM tetrodotoxin (TTX). The results are interpreted in terms of a feedback synaptic action exerted by horizontal cells upon cones, which is expressed as the depolarizing rollback component of the horizontal cell light-evoked waveform. The spatial properties of this component suggest that horizontal cell axons but not horizontal cell perikarya are capable of evoking a feedback signal in the cone. The actions of strontium indicate that calcium currents may play a role in shaping the feedback response. The ability of GABA to antagonize the Sr2+ effect upon the depolarizing rollback indicates that GABA may play a role in feedback.
Under mesopic conditions, the light-evoked waveform of horizontal cells in Xenopus retina reflects synaptic input from both rod and cone photoreceptors. These inputs interact non-linearly: the response to a weak red (cone-effective) flash is increased up to four-fold when the red stimulus falls on a green (rod-effective) background by reference to the response elicited by the same red flash on a dark field. We refer to this phenomenon as enhancement. It was not observed either when stimulus and field wavelengths were reversed or were of the same color. Enhancement was not altered by polarization of the horizontal cell membrane up to +/- 30 mV with extrinsic current. Enhancement could not be elicited with any combination of test and background wavelengths under photopic conditions. Superfusion of the retina with GABA resulted in a hyperpolarization of the horizontal cell membrane and an emphasis of the rod input to the horizontal cell light-evoked response. Picrotoxin depolarized the cell and favored the cone input. Enhancement was altered in predictable ways by these drugs. Glycine reduced selectively the cone input to the horizontal cell, whereas its antagonist, strychnine, increased the rod input. The results are interpreted to indicate that the excitability of the horizontal cell is modified both by distal and proximal retinal circuits; a glycinergic interplexiform cell probably plays a role in the latter pathway.
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The effects of naloxone infusion given together with an infusion of LRH on gonadotropin secretion, were studied in 6 normal male volunteers before and after pretreatment with the GABA-transaminase inhibitor, valproic acid. In concordance with previous studies, naloxone infusion augmented the LRH-stimulated secretion of LH. Baseline serum LH concentrations were not significantly different after valproic acid pretreatment compared to control values. Similarly, valproic acid pretreatment failed to blunt the naloxone-augmented LRH-stimulated secretion of LH. Our data suggest that the previously reported animal studies on the central suppressive effect of GABA on endogenous LRH release is less prominent than the suppressive effect of opioidergic regulatory mechanisms in the human male.
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The plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) response to acute exercise and the relationship of these opioid peptides to basal and luteinizing hormone-releasing hormone (LRH)-stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion was studied in eight normal male volunteers. Acute exercise resulted in a rise in plasma beta-LPH levels that returned to base line when measured 60 min after exercise. Plasma beta-EP levels did not demonstrate any rise when measured immediately after 20 min of exercise or at 60 min after exercise. Serum LH concentrations in individual volunteers declined to nadir values 60-180 min after exercise after which they showed a rebound to levels higher than the preexercise values in three of five volunteers in whom nadir LH levels were attained before the final (180 min) measurement. Serum FSH concentrations were unaltered by exercise. Acute exercise similarly did not alter the LH/FSH response to exogenous LRH stimulation. Pretreatment of the volunteers with the narcotic antagonist, naloxone, failed to alter the postexercise or LRH-stimulated LH and FSH release. The data suggest that beta-EP does not exert a suppressive effect on LH secretion after acute exercise in normal human males. Whether the suppression of LH secretion after acute exercise in unconditioned males is due to factor(s) cosecreted with beta-LPH, an increase in brain beta-EP or to alternate mechanisms such as alteration in central dopaminergic or GABAergic tone remains to be established.
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