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Biomedical subjects

R J Contreras

Publications and source records attributed to R J Contreras.

44 records · Page 3Linked to original sources
PubMed1980

Central origins of cranial nerve parasympathetic neurons in the rat.

The location of central neurons that contribute preganglionic parasympathetic axons to cranial nerves VII, IX, and X in rats has been identified using horseradish peroxidase (HRP) tracing methods. Collectively, these neurons form an uninterrupted dorsal column that extends over the entire length of the medulla. The cephalic end of this column turns ventrally with neurons scattered in the parvicellular reticular formation between the rostral pole of the nucleus of the solitary tract (NST) and the facial motor nucleus. Applying HRP crystals to the cut cervical vagus labels neurons in the classically defined dorsal motor nucleus. Rostrally, this distribution continues along the medial edge of NST, ending just caudal to neurons exiting in the lingual-tonsilar branch of IX. At the rostral pole of the NST and ventral to it, neurons occur that serve the lingual-tonsilar and tympanic branches of IX, as well as the chorda tympani and greater superficial petrosal (GSP) branches of VII. Central neurons of the chorda tympani and tympanic nerves spread ventrally from NST into a sparse but largely coextensive distribution in the reticular formation lateral to the ascending radiations of the facial motor nucleus. Immediately ventral to this distribution, a dense accumulation of GSP efferent neurons appears rostrolateral to the facial motor nucleus. Although they vary considerably in number and packing density, the neurons of the dorsal efferent column and those extending from it into the reticular formation have similar morphological characteristics. The somata are medium-sized, fusiform, or multipolar, but with usually no more than five or six major processes.

Animals↗
PubMed1979

Sodium deprivation alters neural responses to gustatory stimuli.

The effects of sodium deprivation for 10 d, a period sufficient to induce sodium appetite, on gustatory nerve discharges in rats were determined. Chorda tympani responses to concentration series of sodium chloride, sucrose, hydrochloric acid, and quinine hydrochloride were recorded and analyzed without the experimenter knowing the animal's deprivation condition. After deprivation, both whole nerve and single nerve fiber responses to sodium chloride were smaller; NaCl-best fibers, those more responsive to sodium chloride than to sucrose, hydrochloric acid, or quinine, were most affected. Thresholds had not changed; however, slopes of the stimulus-response functions for sodium chloride were lowered. Comparable changes in responses to the other stimuli did not occur. These results were discussed with respect to a possible relationship between changes in sodium chloride responsivity and changes in sodium intake, differences between methods of inducing sodium appetite, coding of taste quality and intensity, and mechanisms which might effect the responsivity change.

Animals↗
PubMed1978

Salt taste and disease.

Sodium appetite reflects the importance of sodium homeostasis and the relative scarcity of sodium for many terrestrial animals. Man, for various reasons, also seems to have a specific preference for salt which he consumes in excess of need, and this has been characterized as an important contributor to hypertension. Gustatory sensibility is necessary for the development of sodium appetite. Thus, research on the possible role salt taste sensitivity plays in controlling NaCl consumption in the sodium deficient rat was reviewed as a potential model for the study of salt taste and hypertension in man. Taste acuity experiments began first by examining salt taste thresholds. These studies found that thresholds were not altered by sodium deficiency in rat and the results in hypertensive humans were inconclusive. Threshold determinations may not reveal true sensitivity differences because they varied significantly across experiments and because they are restricted to a small portion of the intensity domain. When research was directed to suprathreshold stimuli, concentrations a rat or man might normally experience, the evidence suggested that hypertensive humans, like sodium-deficient rats, were less sensitive to the taste of salt. This reduced sensitivity may account, in part, for the fact that these two groups consume more salt.

Adrenal Glands↗
PubMedDate not supplied

Gustatory neuron types in the periphery: a functional perspective.

Robert P. Erickson's research and writings formed the intellectual backdrop and guiding force for much of the major research on sensory coding in taste. As articulated best by Erickson, consideration focused on the relative merits of labeled-line and across-fiber pattern theory. The present article focuses primarily on a review of the electrophysiological and behavioral studies on salt taste and salt taste-mediated behavior in rodents. The evidence clearly shows that the peripheral gustatory system consists of a few neuron types/groups with well-defined physiological response characteristics. Electrophysiological studies of the chorda tympani nerve define a physiological group of narrowly tuned neurons selectively responsive to NaCl stimuli. It appears that this is a sodium-sensing module that functions primarily in the detection, recognition, and ingestion of NaCl.

Animals↗
PubMedDate not supplied

High dietary NaCl early in development enhances mean arterial pressure of adult rats.

We investigated the long-term influence of early dietary NaCl on adult mean arterial pressure (MAP) and heart rate (HR), assessed continuously for 7 weeks when fed water and chow containing 1% NaCl (weeks 1, 4, 7), 0% NaCl (weeks 2-3), and 3% NaCl (weeks 5-6) while on a 12:12 light/dark cycle. Subjects were offspring of female Sprague-Dawley rats fed solid chow consisting of either 0.1% (basal), 1% (intermediate), or 3% (high) NaCl throughout pregnancy and lactation. After weaning on postnatal day (PD) 21, offspring were fed the same NaCl diet of their mother until PD 30, at which time all offspring were given Purina 5001 diet (1% NaCl) as their solid chow. On PD 60, 22 adult male offspring (eight basals, six intermediates, eight highs) were implanted with an aortic electronic sensor for transmitting blood-pressure signals by telemetry. MAP and HR varied significantly across the 7-week testing period in association with dietary NaCl levels. The three perinatal salt groups had similar HR levels on normal 1% NaCl chow. However, HR increased in all groups during 0% NaCl and decreased in all groups during 3% NaCl. In contrast, the average MAP levels were significantly greater in the highs compared to both the intermediate and basal groups during both dark and light periods. MAP increased in high and basal groups during both 0% and 3%; however, the increase was more pronounced in the highs. In conclusion, exposure to high levels of dietary NaCl early in development led to a persistent increase in MAP in adulthood.

Animals↗