Publications by authors named "Eldridge F"

This paper reports the results of two experiments designed to test predictions from the mood-as-input hypothesis about the factors that contribute to the ending of a worry bout. Experiment 1 looked at changes in self-reported mood across a catastrophising interview task. Experiment 2 investigated whether there were any changes in stop rule deployment between the beginning and end of a catastrophising interview task.

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The phase-dependent plasticity of carotid chemoafferent signaling was studied with electrical stimulation of a carotid sinus nerve during either inspiration or expiration in anesthetized, glomectomized, vagotomized, paralyzed, and ventilated rats. Stroboscopic and interferometric analyses of the resulting phase-contrast disturbances of the respiratory rhythm revealed that carotid chemoafferent traffic was dynamically filtered centrally by a parallel bank of leaky integrators and differentiators, each being logically gated to the inspiratory or expiratory phase in a stop-and-go manner as follows: 1) carotid short-term potentiation of inspiratory drive was mediated by dual integrators that both shortened inspiration and augmented phrenic motor output cooperatively in long and short timescales; 2) carotid short-term depression of respiratory frequency was mediated by a (possibly pontine) integrator that lengthened expiration with a relatively long memory; and 3) carotid "chemoreflex" shortening of expiration was mediated by an occult fast integrator, which, together with carotid short-term depression, formed a differentiator. These effects were modulated anteriorly by integrators in the nucleus tractus solitarius that were "auto-gated" to, or recruited by, the carotid sinus nerve input.

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The anatomical structure of central respiratory chemoreceptors in the superficial ventral medulla of rats was studied by using hypercapnia-induced c-fos labeling to identify cells directly stimulated by extracellular pH or PCO(2). The distribution of c-fos-positive cells was found to be predominantly perivascular to surface vessels. In the superficial ventral medullary midline, parapyramidal, and ventrolateral regions where c-fos-positive cells were concentrated, we found a common, characteristic, anatomical architecture.

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Repetitive stimulation of the carotid sinus nerve (CSN) elicits a short-term potentiation (STP) of the reflex response in respiratory motor output in mammals. The input-output transformation approximates a leaky integrator with a time constant of several seconds. Here, we showed that STP induced by CSN stimulation in rats was manifested in the reflex response in the amplitude of rhythmic phrenic nerve activity as well as its duration.

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1. Stimulation of the carotid sinus nerve causes an increase in inspiratory (I) and expiratory (E) neural activities. If central respiratory oscillation is generated by an attractor-cycle process, an increase in its activity can be caused by a centrifugal perturbation of state.

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In 16 decerebrated unanesthetized cats, we studied effects of neural inputs from upper airway on firing of 62 mesencephalic neurons that also developed respiratory-associated (RA) rhythmic firing when respiratory drive was high [Z. Chen, F. L.

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It is well known that rebreathing relieves the respiratory distress of maximal breathholding despite worsening blood gases, and it has been suggested that vagal input has a role in ameliorating this sensation via activation of pulmonary stretch receptors (PSR). However, it is believed by divers that expiration can lead to partial relief of distress of breathholding at total lung capacity (TLC) allowing a prolongation of breathholding. We studied the independent effects of an expiration and an inspiration on relief of respiratory distress of breathholding.

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Many hypotheses have been advanced to explain the hyperpnea of exercise and its close relations to the level of metabolic work, expressed as oxygen uptake (VO2) and carbon dioxide production (VCO2). Evidence is presented that a neural central command mechanism from the hypothalamus is important in the driving of both respiration and circulatory adjustments during locomotion or exercise, and that short-term potentiation of neurons in the medulla makes an important contribution. Both are probably augmented by receptors in working muscle and by the effects of increased [K+] acting on the carotid bodies.

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The respiratory distress of breathholding has been shown to be relieved by breathing, even without correction of worsening blood gases (Fowler, 1954). We repeated the study by having untrained normal subjects perform maximal breathholds which were followed by the rebreathing of a gas mixture containing 7.5% CO2 and 8.

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We recorded phrenic nerve activity and thalamic single unit firing in unanesthetized, suprathalamically decerebrated, paralyzed and ventilated cats, in which vagi and carotid sinus nerves (CSN) had been ablated. Seventy-six (14%) of 545 neurons in regions of the thalamus related to the ascending reticular system, which had been tonically firing at low respiratory drives, developed rhythmic increases of firing associated with each respiration when drive had been increased by CSN stimulation or hypercapnia. The increases of neuronal firing occurred in late inspiration/post-inspiration but sometimes lasted into expiration; the magnitude of change was graded according to the magnitude of respiratory activity.

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We recorded phrenic nerve activities and single unit firings of mesencephalic neurons in 19 decerebrate, paralyzed and ventilated cats, in which the spinal cord had been transected at C7-T1 and carotid sinus nerves cut but vagus nerves left intact. After we had found neurons with respiratory-associated rhythmic activity, we tested the effect of changing pulmonary vagal input by (1) stopping and restarting the ventilator; (2) changing the ventilator's tidal volume; (3) progressively cooling the vagus nerves to 6-7 degrees C; and (4) vagal section. All methods of testing yielded results that showed that vagal input, probably from pulmonary stretch receptors, tonically inhibits the respiratory-associated firing of the mesencephalic neurons by a direct mechanism that is independent of a vagal effect on medullary respiratory drive.

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Seizure activity can lead to profound respiratory stimulation in spontaneously breathing animals with intact respiratory feedback mechanisms (Paydarfar et al., Am. J.

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Phrenic and cervical sympathetic nerve responses to hypercapnia were examined before and after anesthesia in twelve midcollicularly decerebrated, vagotomized, glomectomized, paralyzed and ventilated cats. We measured responses of integrated phrenic and cervical sympathetic nerve activities to increases in end-tidal PCO2 (PETCO2) from apneic threshold to approximately 30 torr above threshold. All cats were studied first in the unanesthetized state.

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1. We recorded phrenic nerve activities and single unit firing of mesencephalic neurones in unanaesthetized supracollicularly decerebrated, paralysed and ventilated cats, in which vagi and carotid sinus nerves had been ablated. We made these measurements first at low levels of respiratory drive associated with normal PCO2 levels, then with increased respiratory drive and levels of phrenic activity produced by hypercapnia or by carotid sinus nerve stimulation.

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We studied the effects on breathing of seizures induced by focal injection of penicillin G into the parietal cortex in 13 anesthetized cats. Electrocorticograms, ventilation, end-tidal PCO2, and intrapleural and arterial pressures were monitored; changes of these variables were related to the stages of motor seizure. The first respiratory responses, tachypnea and hyperpnea, usually occurred before any peripheral muscular contractions developed.

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Development of short-term potentiation (STP) of respiration, which leads to the respiratory 'afterdischarge', was studied in anesthetized, paralyzed, vagotomized and glomectomized cats. Phrenic nerve activity was used as an index of respiratory output. Respiratory output was increased and the potentiating mechanism activated by electrical stimulation of a carotid sinus nerve (CSN).

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Bovine spermatozoa were assessed indirectly for the presence of a Y chromosome by monitoring expression of the H-Y antigen. Spermatozoa labeled with a monoclonal H-Y antibody (MoAb) and fluorescein-conjugated goat antibody to mouse F(ab)2 were counted with both a fluorescent microscope and a fluorescence-activated cell sorter (FACS). Of ejaculated spermatozoa, 40% to 60% fluoresced by this procedure compared to 1% to 15% of sperm reacted with nonimmune serum.

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We studied the effect of changing drive on resetting of respiratory rhythm in anesthetized cats and in a model (Van der Pol) of a limit-cycle oscillator. In cats, rhythm was perturbed by brief mesencephalic stimuli. Stimulus time in the cycle (old phases) and times of onset of rescheduled breaths (cophases) were measured.

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The recently released drug buspirone is an anxiolytic agent that appears not to have the sedating effects of barbiturates and benzodiazepines, both known to have respiratory depressant effects. Because of its increasing clinical use, we desired to study the effects of buspirone on respiratory control. We therefore determined central neural respiratory responses, measured from phrenic nerve activity, after intravenous administration in paralyzed, vagotomized, and glomectomized cats whose end-tidal PCO2 and body temperature were kept constant.

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1. The effects on activities and rhythms of the two opposing phrenic nerves (C5 roots) of mid-line sagittal splitting of the medulla were determined in anaesthetized or decorticate, vagotomized, paralysed and ventilated cats. 2.

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We induced generalized seizures by cortical injection of penicillin in anesthetized, paralyzed cats. After they had developed recurrent ictal-interictal ECoG cycling and fictive tonic-clonic motor convulsions (status epilepticus), we studied the effect of systemically administered neuropharmacological agents on the seizure cycling. Antagonists of adenosine receptors, theophylline and 8-cyclopentyltheophylline, increased the cycle period due to marked prolongation of duration of ictal discharge, often to more than 30 min.

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