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Biomedical subjects

R A Jaffe

Publications and source records attributed to R A Jaffe.

At least 37 records · Page 2Linked to original sources

Stimulation of cutaneous mechanoreceptors by 60-Hz electric fields.

Chronic exposure of animals to 60-Hz electric fields is known to affect the nervous system in a variety of subtle ways. The mechanism whereby these effects are produced remains unknown. One hypothesis is that the effects are a result of direct interaction between neuronal membranes and induced currents. Alternatively, the effects could be produced indirectly, as a result of sensory stimulation and the resulting low-level stress. To test these hypotheses, a system was developed to expose the surface of an anesthetized cat's paw to surface electric fields up to 600 kV/m while simultaneously measuring, in dorsal root fibers, afferent nerve impulses originating from various receptor types in the exposed paw. Of the 245 receptor units tested, comprising ten cutaneous receptor types, ten responded to the electric field with an increase in firing rate. The most sensitive receptor type was the rapidly adapting field receptor (RAF); eight of 20 (40%) were sensitive to the electric field, with thresholds as low as 160 kV/m. One of 35 rapidly adapting high-frequency receptors and one of 22 type T hair-follicle receptors were also sensitive to the electric field. Follow-up tests on the RAF receptors showed that hair removal reduced but did not eliminate the electric field sensitivity, suggesting that at least one other mechanism was involved in addition to stimulation via hair movement. The most likely mechanism is field-induced vibrations of the skin, since a further reduction in firing rate occurred following application of mineral oil to the depilated paw. Direct interaction with neuronal membranes is not supported by our evidence.

Animals↗

Perinatal exposure to 60-Hz electric fields: effects on the development of the visual-evoked response in rats.

Two independent series of experiments were performed on 114 male Sprague-Dawley-derived, albino rat pups, which represented 61 litters in experimental series I and 53 litters in experimental series II. Animals were exposed for 20 h/day from conception to testing (postnatal days 11-20) to a vertical, 65-kV/m, 60-Hz electric field or sham-exposed. Recordings of the visual-evoked response (VER) were obtained using a small silver ball electrode placed epidurally over the visual cortex. Visual stimuli consisted of 10-microseconds light flashes delivered at 0.2 Hz. Computer-averaged VERs were obtained and power spectral analyses (fast Fourier transform) were performed on the tapered (split cosine-bell window), averaged VERs. The expected age-related changes were clearly evident; however, a detailed analysis of VER component latencies, peak-to-peak amplitude, and power spectra failed to reveal any consistent, statistically significant effect of exposure to 60-Hz electric fields.

Animals↗

Chronic exposure to a 60-Hz electric field: effects on neuromuscular function in the rat.

Neuromuscular function in adult male rats was studied following 30 days of exposure to a 60-Hz electric field at 100 kV/m (unperturbed field strength). Isometric force transducers were attached to the tendons of the plantaris (predominantly fast twitch), and soleus (predominantly slow twitch) muscles in the urethan-anesthetized rat. Square-wave stimuli were delivered to the distal stump of the transected sciatic nerve. Several measurements were used to characterized neuromuscular function, including twitch characteristics, chronaxie, tetanic and posttetanic potentiation, and fatigue and recovery. The results from three independent series of experiments are reported. Only recovery from fatigue in slow-twitch muscles was consistently and significantly affected (enhanced) by electric-field exposure. This effect does not appear to be mediated by field-induced changes in either neuromuscular transmission, or in the contractile mechanism itself. It is suggested that the effect may be mediated secondary to an effect on mechanisms regulating muscle blood flow or metabolism.

Age Factors↗

Chronic exposure to a 60-Hz electric field: effects on synaptic transmission and peripheral nerve function in the rat.

Several reports have suggested that the nervous system can be affected by exposure to electric fields and that these effects may have detrimental health consequences for the exposed organism. The purpose of this study was to investigate the effects of chronic (30-day) exposure of rats to a 60Hz, 100-kV/m electric field on synaptic transmission and peripheral-nerve function. One hundred forty-four rats, housed in individual polycarbonate cages were exposed to uniform, vertical, 60-Hz electric fields in a system free of corona discharge and ozone formation and in which the animals did not receive spark discharges or other shocks during exposure. Following 30 days of exposure to the electric field, superior cervical sympathetic ganglia, vagus and sciatic nerves were removed from rats anesthetized with urethan, placed in a temperature-controlled chamber, and superfused with a modified mammalian Ringer's solution equilibrated with 95% O2 and 5% CO2. Several measures and tests were used to characterize synaptic transmission and peripheral-nerve function. These included amplitude, area, and configuration of the postsynaptic or whole-nerve compound-action potential; conduction velocity; accommodation; refractory period; strength-duration curves; conditioning-test (C-T) response, frequency response; post-tetanic response; and high-frequency-induced fatigue. The results of a series of neurophysiologic tests and measurements indicate that only synaptic transmission is significantly and consistently affected by chronic (30-day) exposure to a 60-Hz, 100-kV/m electric field. Specifically, and increase in synaptic excitability was detected in replicated measurements of the C-T response ratio. In addition, there are trends in other data that can be interpreted to suggest a generalized increase in neuronal excitability in exposed animals.

Action Potentials↗

Effects of droperidol on activity of carotid body chemoreceptors in cat.

1 The effect of droperidol on the spontaneous activity of carotid body chemoreceptors and on their response to various stimuli was studied in 21 anaesthetized, paralyzed and artificially ventilated cats. Carotid body blood flow was controlled with a perfusion pump, and drugs were injected into the perfusion circuit. 2 In low doses, droperidol transiently increased the rate of spontaneous chemoreceptor activity, but in higher doses it depressed chemoreceptor activity after an initial stimulation. 3 Droperidol reduced or abolished the normal increase in chemoreceptor activity produced by stagnant asphyxia. This effect did not depend solely on the ability of droperidol to suppress spontaneously occurring impulses. Chemoreceptor responses to sodium cyanide, and to dopamine were also inhibited. 4 Dopamine antagonists other than droperidol were also studied for their effect on chemocreceptor activity. Chlorpromazine depressed spontaneous chemoreceptor activity and also reduced the chemoreceptor responses to sodium cyanide and dopamine, as did pimozide. The effects of these dopamine antagonists were much briefer and less marked than those of droperiodol. 5 Although the influence that we have shown droperidol to have on peripheral chemoreceptor activity has an uncertain basis, it may have important implications in human and veterinary medicine.

Animals↗

Analysis of inhibitory effect of dopamine on carotid body chemoreceptors in cats.

The inhibitory effect of dopamine on carotid body chemoreceptors was studied in anesthetized cats to determine whether it was dependent on changes in blood flow in the vicinity of the receptors. The blood supply to the carotid body was isolated, and flow was controlled with a perfusion pump. Single- or few-fiber recordings were made from the peripheral end of the cut carotid sinus nerve in seven cats. The rate of discharge of 68 chemoreceptor strands increased when flow through the carotid body was stopped. This response was reduced or abolished by dopamine in animals ventilated with either room air (15 strands) or a gas mixture of 95% O2 and 5% CO2 (53 strands). These results suggest that dopamine exerts its inhibitory effect primarily through a direct action on the chemoreceptors rather than by a vasomotor effect in the carotid body.

Animals↗

Analysis of passive and active electrophysiologic properties of neurons in mammalian nodose ganglia maintained in vitro.

1. We studied the passive and active electrical properties of the soma membrane of neurons in nodose ganglia removed from cats and rabbits and maintained in vitro. The ganglia were superfused at 37 degrees C with a solution formulated to approximate the extracellular fluid of each species. The solution was buffered to pH 7.34, continuously equilibrated with 95% O2 and 5% CO2, and contained dialyzed calf serum and glucose. We also examined these properties in nodose ganglion neurons in vivo. Intracellular recordings were obtained with glass micropipettes filled with either 3 M KCl or 5 M K acetate. 2. We determined mean values for a variety of passive and active electrophysiologic properties. Values obtained in vitro did not differ significantly from those obtained in vivo. Based on the passive electrical properties of the soma membrane, neurons in the nodose ganglion appear to be a uniform population, despite the different sensory modalities conveyed by the afferent fibers. 3. Cell bodies of neurons generated action potentials in response to impulses in their afferent fibers. Somatic spikes could be evoked by stimulation of either the supranodose or infranodose vagus nerve, and an inflection point could be seen on their rising phase. When the vagus nerve was stimulated at frequencies greater than 10-20 Hz, the generation of somatic spikes often became progressively delayed and then failed completely, leaving a smaller potential (IS spike) which was apparently generated in the initial complex. The afterhyperpolarization was associated only with the somatic spike. 4. Many neurons, both in vitro and in vivo, developed a persistent hyperpolarization when repetitive action potentials occurred in the soma. This hyperpolarization was apparent at frequencies as low as 1-2 Hz, persisted for up to 5 s after the occurrence of the last somatic spike, and sometimes caused failure of somatic spikes to be generated. 5. Neurons in both species differed in their responses to suprathreshold depolarization applied through the recording electrode. Some neurons produced a train of action potentials which lasted for the duration of the depolarizing pulse, the frequency of the train being related to the magnitude of depolarization. The trains were characterized by gradually decreasing spike amplitudes and increasing interspike intervals. Other neurons responded with only a single spike or brief burst of action potentials at the beginning of depolarization to threshold. 6. It is suggested that the adaptive properties of the soma membrane of a peripheral sensory neuron are similar to those of its sensory ending, and that electrophysiological studies of the soma membrane may provide an opportunity to examine mechanisms of receptor adaptation.

Action Potentials↗

A pharmacological analysis of neurally induced inhibition of carotid body chemoreceptor activity in cats.

Experiments were performed to determine the mechanism by which centrifugal impulses in the carotid sinus nerve (CSN) reduce the frequency of impulse traffic in afferent chemoreceptor fibers from the carotid body in cats. Recordings of chemoreceptor activity were made from single- or few-fiber preparations dissected off the CSN, while the remainder of the CSN was stimulated electrically to produce neurally induced inhibition of chemoreceptor activity. Various drugs were injected either intravenously or directly into the arterial blood supply to the carotid body. We found that catecholamines (dopamine, norepinephrine and epinephrine) inhibited spontaneous chemoreceptor activity, and that alpha adrenergic antagonists abolished both this inhibition and that produced by electrical stimulation of the CSN in the same preparation. Atropine, but not nicotinic antagonists of acetylcholine, consistently blocked neurally induced inhibition but not that produced by catecholamines. Muscarinic agonists had no effect on spontaneous chemoreceptor activity. We conclude that centrifugal activity in the CSN causes release of endogenous catecholamines in the carotid body, and that these catecholamines mediate neurally induced inhibition of chemoreceptor activity is due to the vasomotor effects of acetylcholine.

Acetylcholine↗

Influence of centrifugal sinus nerve activity on carotid body catecholamines: microphotometric analysis of formaldehyde-induced fluorescence.

The effects of centrifugal activity in the carotid sinus nerve (CSN) on the intensity of formaldehyde-induced fluorescence of carotid body were examined in cat. Measurements of intensity were obtained from 21 to 56 sections of each carotid body with a microscope photometer attached to a fluorescence microscope. Comparisons were made between the two carotid bodies removed from each cat. In one series of experiments, one carotid body (CSN intact) served as control, while the experimental carotid body was on the side on which centrifugal activity was increased by electrical stimulation of the peripheral end of the cut CSN. In a second series, centrifugal CSN activity was increased by hypoxemia; one CSN was transected (control) and the other was left intact (experimental). In untreated cats, fluorescence intensity was significantly higher on the side with increased centrifugal CSN activity. In cats treated with either MK486, which inhibits conversion of L-DOPA to dopamine, or reserpine, increased centrifugal CSN activity caused a significant decrease in intensity of type I cells. These findings indicate that centrifugal discharges regulate, in part, the synthesis and release of catecholamines by type I cells of the carotid body.

Carbidopa↗

Dynamics of venous-arterial testosterone transfer in the pampiniform plexus of the rat.

The dynamics of venous-arterial testosterone transfer in the pampiniform plexus of the rat have been studied using [3-H] testosterone in controlled perfusion in the pampiniform plexus isolated from its testicle in vivo. The rate of transfer of testosterone increased in direct proportion to the testosterone concentration in spermatic vein blood over the range 0-100 ng/ml. When the venous-arterial concentration gradient was reversed by infusing [14-C] testosterone into the spermatic artery proximal to the pampiniform plexus, the label was transferred from the artery to the adjacent spermatic vein. Transfer of [3-H] methoxy-inulin infused concomitantly with the [14-C] testosterone was relatively insignificant in either direction. The testosterone transfer rate generally increased with increasing blood flow over the range 0.01-0.36 ml/min. However, transfer rate became less dependent on blood flow at the high end of the range. A comparison of transfer rates from whole blood and dextran (6% in saline) each containing 24-27 ng [1,2-3-H] testosterone/ml and flowing at 0.36 ml/min for one hour resulted in a maximum of 6.1% transfer from blood and 46% transfer from dextran. Transfer from blood reached plateau levels in less than 10 min, whereas transfers from dextran peaked between 30 and 40 min. At lower rates testosterone transfer from dextran reached equilibration levels, whereas transfer from blood rarely exceeded 5% of spermatic venous levels. We concluded that venous-arterial steroid transfer in the pampiniform plexus behaves like a passive countercurrent diffusion system that is concentration limited, depending principally on the concentration gradient of diffusible steroid between the closely juxtaposed spermatic vein and artery.

Animals↗