Biomedical subjects

R C Ritter

Publications and source records attributed to R C Ritter.

At least 73 records · Page 4Linked to original sources

PubMed1991

Vagotomy attenuates suppression of sham feeding induced by intestinal nutrients.

The ability of intraintestinal nutrient infusions to suppress sham feeding was examined in intact rats and in rats with total subdiaphragmatic vagal transections. Vagotomy abolished the suppression of sham feeding by intraintestinal infusion of maltose or oleate. Suppression of sham feeding by intraintestinal L-phenylalanine was reduced but not abolished by vagotomy. The results of this examination indicate that the vagus nerve mediates suppression of the sham feeding by intraintestinal maltose and oleate but is only partially responsible for suppression of food intake produced by L-phenylalanine. Taken together with previously published data these results suggest that effects on feeding by specific nutrients may be mediated by anatomically distinct populations of visceral afferent neurons.

Animal Nutritional Physiological Phenomena↗

PubMed1991

Fourth ventricular capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.

Systemic treatment with capsaicin, a neurotoxin that destroys small unmyelinated primary sensory neurons, causes degeneration of vagal sensory fibers and attenuates suppression of sham feeding by exogenous cholecystokinin (CCK) or intraintestinally infused nutrients. To determine whether capsaicin-sensitive neurons or fibers in the hindbrain mediate suppression of feeding by intestinal nutrients, we examined nutrient-induced suppression of sham feeding in rats pretreated with fourth ventricular capsaicin. Capsaicin treatment abolished the suppression of sham feeding induced by intraperitoneal injection of CCK octapeptide or by intraintestinal maltose. Oleate-induced suppression of sham feeding also was significantly attenuated in capsaicin-treated rats. Capsaicin treatment, however, did not attenuate suppression of sham feeding by intraintestinal L-phenylalanine. These results indicate that capsaicin-sensitive substrates, located near the fourth ventricle, participate in the suppression of sham feeding by CCK and by some intestinal stimuli. Taken together with previously reported data, these results suggest that suppression of sham feeding by some intestinal nutrients is mediated by a neuronal substrate similar or identical to one that mediates suppression of feeding by exogenous CCK.

Animals↗

PubMed1990

Experimental determination of the force required for insertion of a thermoseed into deep brain tissues.

Our laboratories are developing a new technique for delivering localized hyperthermia to deep-seated brain tumors. In this technique, a spherical thermoseed is stereotactically navigated through the brain and tumour tissues via the noncontact application of an external magnetic force. The force required to produce motion of a 3 mm diameter sphere through in vitro brain tissues was measured to be 0.07 +/- 0.03 N. This result was obtained from a series of experiments performed on whole brain specimens extracted from adult canines. Data were also taken with a 3 mm x 3 mm cylinder and a 5 mm sphere. An experimental procedure simulating physiological conditions was developed prior to testing. Evaluations of systematic effects included determinations of the calibration uncertainties, tests of the dependence of the measured force on temperature, and studies of the effects of method of storage of the tissue specimens. The results obtained are compared with (and confirmed by) two different series of experiments performed in vivo on adult canines and with another series of experiments using brain phantom gelatin.

Animals↗

PubMed1990

Magnetic stereotaxis: a technique to deliver stereotactic hyperthermia.

Advances in imaging techniques and computer software over the past decade now define brain abnormalities such as tumors in precise, three-dimensional images. We have taken advantage of these technological improvements in designing a system capable of performing magnetic manipulation of an object in a nonlinear trajectory and able to deliver hyperthermia to highly specific targets within the brain. This device relies on external magnets to pull a small metal pellet (thermoceptor) through the brain, and on biplane fluoroscopy to localize the thermoceptor with respect to previously obtained magnetic resonance images. A radiofrequency tuned circuit serves as the hyperthermia applicator and selectively heats the thermoceptor. This paper describes experiments conducted in a series of dogs showing that all three components of the system (magnetic drive, stereotactic real time imaging, and hyperthermia) can be achieved. Integration of the system was accomplished in one animal. These encouraging results need further detailed substantiation in each of the components, yet demonstrate the feasibility of such a device.

Animals↗

PubMed1989

Lateral parabrachial lesions attenuate ingestive effects of area postrema lesions.

Lesions of the area postrema and adjacent nucleus of the solitary tract (AP lesions) cause rats to consume increased amounts of palatable food in short duration tests. Because the lateral parabrachial nucleus (lPBN) receives a prominent afferent projection from the AP and adjacent nucleus of the solitary tract, it is possible the lPBN plays a role in the altered ingestive behaviors observed in AP-lesioned rats. The present study examines the role of the lPBN in overingestion of highly palatable foods subsequent to AP lesions. We found that lesions of the lPBN alone did not cause rats to consume increased amounts of palatable food. Rather, when lPBN lesions were produced before AP lesions, increased intake of highly palatable food did not occur. Moreover, when AP-lesioned rats received subsequent lPBN lesions, the previously established overingestion of palatable foods was abolished. These results indicate that the lPBN is necessary in the pathogenesis of AP lesion-induced overingestion of highly palatable foods.

Animals↗

PubMed1989

Capsaicin attenuates hindbrain neuron responses to circulating cholecystokinin.

Capsaicin is a neurotoxin that destroys small sensory neurons with unmyelinated axons, including a subpopulation of vagal sensory neurons. Capsaicin treatment attenuates suppression of food intake induced by systemic administration of cholecystokinin (CCK) but not by gastric distension. However, both gastric distension and intravascular CCK alter the discharge of dorsal hindbrain neurons by a vagal mechanism. Therefore, it is plausible that some hindbrain neurons receive convergent input from capsaicin-sensitive vagal neurons that are responsive to CCK and also from capsaicin-insensitive neurons that are responsive to gastric distension. To investigate this possibility we made extracellular recordings from gastric distension-responsive hindbrain neurons during intra-arterial cholecystokinin octapeptide (CCK-8) administration in anesthetized intact and capsaicin-pretreated rats. We found that capsaicin-pretreated rats exhibit attenuated neuronal discharge responses to CCK-8 but not to gastric distension. These results are consistent with the existence of convergent CCK-sensitive and gastric distension-sensitive afferent inputs to hindbrain neurons and suggest that various gastrointestinal sensory modalities may be communicated to the brain by populations of neurons that can be distinguished by their sensitivity to neurotoxins.

Animals↗

PubMed1989

Magnetic movement of a brain thermoceptor.

Hyperthermia has significant potential as an adjuvant form of brain tumor therapy. Current intracranial hyperthermia methods, however, are limited in their ability to control spatiotemporal thermal distribution. A stereotaxic magnetic movement system that may be capable of heating discrete regions of brain to a preselected temperature is described. With this system, a ferromagnetic object (referred to as a thermoceptor) is directed through the brain by an external drive magnet. Real time thermoceptor position is monitored with biplanar fluoroscopy and superimposed on a preoperative magnetic resonance imaging scan using a computer. Once in position, the thermoceptor can be inductively heated by externally generated radiofrequency signals. Experiments on the magnetic drive and imaging aspects of this system have been conducted in vitro and in vivo. Mechanical studies of cadaver dog brains revealed that a mean force of 0.07 +/- 0.03 N was required to move a 3-mm diameter sphere through brain at a speed of less than 1 cm/15 s. A cranial phantom with mechanical properties similar to brain was constructed of gelatin and Plexiglas. With the use of a "neck loop" design drive magnet with a maximum magnetic field strength of 0.10 T, a 3 x 3 mm cylindrical neodymium iron boron thermoceptor was smoothly directed through the phantom in two dimensions. Additional experiments were conducted with a larger drive magnet in five anesthetized dogs. Neodymium iron boron and samarium cobalt thermoceptors of various shapes and sizes were placed into the cerebral cortex through a burr hole, then directed with the drive magnet. Fluoroscopy was used to follow the thermoceptor movements.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Reduction of CCK-8 binding in the nucleus of the solitary tract in unilaterally nodosectomized rats.

Cholecystokinin octapeptide (CCK-8) binding sites were examined in the caudal hindbrain of unilaterally nodosectomized and intact rats by in vitro autoradiography with 125I-CCK-8. Unilateral nodosectomy caused a significant reduction in CCK-8 binding in the caudal medial nucleus of the solitary tract (NST) on the side ipsilateral to the nodose ganglionectomy. Examination of other caudal hindbrain regions exhibiting CCK-8 binding did not reveal changes in binding in nodosectomized animals compared to controls. These findings suggest that the CCK receptors in this brain region may be located on terminals of vagal afferent neurons.

Animals↗

PubMed1988

Capsaicin attenuates suppression of sham feeding induced by intestinal nutrients.

Satiety appears to be mediated in part by neurally transmitted signals from the gastrointestinal tract. Capsaicin is a neurotoxin that selectively destroys small unmyelinated primary sensory neurons including some of those innervating the abdominal viscera. Therefore, we examined suppression of sham feeding induced by cholecystokinin octapeptide (CCK-8) or intraintestinal nutrient infusions in capsaicin-treated rats. Suppression of sham feeding induced by CCK-8 was significantly attenuated in rats treated with capsaicin. Suppression of sham feeding induced by intraintestinal infusions of maltose, oleic acid, or L-phenylalanine was also attenuated in capsaicin-treated rats. In contrast, capsaicin treatment did not attenuate the suppression of sham feeding induced by intraintestinal casein hydrolysate (mixed amino acids). Intraintestinal infusions of octanoic acid or D-phenylalanine solutions did not significantly suppress sham feeding in either vehicle- or capsaicin-treated rats. These results indicate that the suppression of feeding by some intestinal stimuli may be mediated by nutrient or peptide-sensitive visceral afferent neurons that are sensitive to damage or destruction by capsaicin.

Animals↗

PubMed1988

Low-dose fourth ventricular bombesin selectively suppresses food intake.

Bombesin (BBS) administered into the lateral cerebral ventricles suppresses food intake. Suppression of food intake, however, is accompanied by arousal of competing behaviors such as grooming and increased locomotion, which are atypical of normal satiety. We have found that BBS infused into the fourth cerebral ventricle in rats reduces food intake at doses one-tenth to one-hundredth of those required via the lateral ventricle. In addition, the lowest fourth ventricular dose that significantly reduced food intake did not increase locomotor activity. These data suggest that the hindbrain may be a more sensitive site for BBS-induced suppression of feeding than forebrain sites and that feeding and locomotor effects of BBS may involve dissociable neural substrates.

Animals↗

PubMed1987

Paraquat-induced, dose-dependent conditioned taste aversions and weight loss mediated by the area postrema.

Paraquat's (PQ) effect on feeding behavior in the rat was examined using a conditioned taste aversion (CTA) paradigm. CTA is a learned avoidance of tastes closely associated with prior illness. Male Sprague-Dawley rats trained to drink an instant breakfast solution were subsequently offered a novel-flavored solution and consumption was measured over 30 min. Following consumption of the novel solution, PQ (0.48-48.0 mumol/kg) was injected subcutaneously. Peak blood PQ concentrations were measured by serially sampling blood (0.15 ml) from an indwelling jugular cannula between 10 and 35 min after injection. Two days later, the rats were offered the same novel-flavored solution. Paraquat produced dose-dependent avoidance of the novel solution when injected subcutaneously. A PQ dosage of 2.7 mumol/kg or less did not alter consumption. The ED50 for CTA production of 13.0 mumol/kg was determined by log-probit analysis. The minimum effective dosage was 4.2 micron/kg. The doses examined did not produce overt clinical or histological signs of toxicity. Peak blood paraquat concentration was linearly related (r = 0.995) to dosage. Additionally when administered by gavage CTAs occurred only with a much larger PQ dosage (480 mumol/kg). Thermal lesions of a hindbrain circumventricular organ, the area postrema (AP), prevented PQ-induced CTAs despite repeated PQ injections. Additionally, weight loss following PQ exposure was also attenuated by AP lesions. CTAs were induced in these same AP-lesioned rats by oral administration of copper sulfate. This substance conditions taste aversions by activating vagal afferent neurons. The fact that copper sulfate-induced aversions were not blocked by lesions of the area posterema indicates that the lesioned rats are capable of forming CTAs when treated with a toxicant which does not act via the AP. These data indicate that PQ produces CTAs in a dose-dependent manner. Furthermore, PQ-induced CTAs and weight loss are mediated by the AP. The AP may contain receptors which detect xenobiotics, enabling animals to avoid future contact with these compounds.

Animals↗

PubMed1986

Substance P-containing trigeminal sensory neurons project to the nucleus of the solitary tract.

Intense substance P-like immunoreactivity (SPLI) was identified in fiber bundles coursing between the spinal nucleus of the trigeminal nerve and the ventrolateral nucleus of the solitary tract at the level of the area postrema. These bundles were apparent only when tissue was stained for substance P immunoreactivity and were not visible in preparations treated with antisera to somatostatin or neurotensin. Following unilateral section of the trigeminal nerve, the SPLI-containing fiber bundles were absent ipsilateral to the nerve section. The fibers were absent bilaterally in rats which were previously injected with capsaicin. Unilateral removal of the nodose ganglion did not diminish the intensity or apparent number of SPLI fibers. These data indicate the presence of a trigeminosolitary projection which is composed of primary trigeminal sensory neurons containing substance P. The results provide an anatomical route by which substance P of trigeminal origin may modulate vagal or glossopharyngeal sensory information.

Animals↗

PubMed1986

Area postrema lesions: cause of overingestion is not altered visceral nerve function.

Rats with lesions of the area postrema and the immediately subjacent nucleus of the solitary tract (AP lesions) ingest greater quantities of palatable foods than intact rats. Because AP lesions destroy some abdominal vagal sensory terminals and may damage vagal motor neurons as well, it is possible that lesion-induced alteration of vagal function causes overingestion of palatable foods. To test this hypothesis, we have examined ingestion of a highly palatable solid food by AP- and sham-lesioned rats with total subdiaphragmatic vagotomies and examined ingestion of a highly palatable sucrose solution by AP- and sham-lesioned rats with open gastric fistulas (sham feeding). Vagotomy in sham-lesioned rats failed to cause overingestion of palatable food. Furthermore, vagotomy in AP-lesioned rats did not abolish their overingestion of palatable food, although AP lesion-induced overingestion was attenuated by vagotomy. Finally, sham-feeding AP-lesioned rats consumed significantly more sucrose solution than sham-lesioned rats. These results indicate that overingestion of palatable foods and solutions by AP-lesioned rats is not due to impaired abdominal visceral afferent function and probably is not due to altered vagal efferent function. The data are consistent with our previous suggestion that overingestion by AP-lesioned rats results from a primary change in responsiveness to orosensory cues.

Animals↗

PubMed1986

Dorsomedial hindbrain participation in cholecystokinin-induced satiety.

To study the role of the dorsomedial hindbrain in cholecystokinin (CCK)-induced satiety, lesions were produced in the region of the obex. We observed that lesions that were limited to the area postrema (AP) and immediately adjacent nucleus of the solitary tract (NST) did not attenuate the satietogenic effects of CCK. Similarly, lesions of the medial NST rostral to the AP had no effect on CCK-induced satiety. However, when the majority of the medial and commissural subnuclei of the NST as well as the AP were lesioned, there was a significant attenuation of the satietogenic effect of CCK. Since this lesion includes the bulk of the terminal field from the gastric branch of the vagus nerve, these results support the role of gastric afferent projections in the mediation of CCK-induced satiety. Although we do not rule out the possibility that the AP itself monitors circulating CCK, our data clearly show that the AP is not essential for induction of satiety by exogenous CCK.

Animals↗

PubMed1985

Capsaicin pretreatment attenuates suppression of food intake by cholecystokinin.

Capsaicin, the pungent principal in red pepper, has been shown to damage small-diameter peptide-containing sensory neurons. Suppression of feeding by cholecystokinin octapeptide (CCK OP) was attenuated after systemic pretreatment with capsaicin. Capsaicin pretreatment did not attenuate suppression of food intake by intragastric preloads. Pretreatment of rats with microgram quantities of capsaicin injected into the fourth ventricle, near the sites of vagal afferent termination, also attenuated CCK OP-induced suppression of food intake. These results suggest that the satiety-inducing effects of CCK OP are mediated, at least in part, by capsaicin-sensitive afferent neurons.

Animals↗

PubMed1984

Area postrema lesions cause overconsumption of palatable foods but not calories.

Rats with lesions of the area postrema and immediately adjacent solitary nucleus consume greater amounts of highly palatable food during short exposures than do control rats. When a highly palatable substance (cookies or glucose solutions) is available continuously along with laboratory chow, lesioned rats exhibit average 24 hour calorie intakes which are not different from those of control rats. Nevertheless, the lesioned animals ingest a significantly greater proportion of total calories as the highly palatable substances than do control rats. The data suggest that lesions involving the area postrema and adjacent nucleus of the solitary tract enhance intake of highly palatable food without causing overconsumption of calories.

Animals↗

PubMed1984

The role of the rat in research on control of ingestion: a commentary and review of recent advances in understanding brain control of food intake.

The majority of data concerning the control of food intake in mammals is derived from studies of laboratory rats. Some ingestive controls, identified in rats, seem to operate identically in most farm species. Other controls, which have been identified in nonrodent species, appear to be absent in the rat. Thinking about the neural control of ingestion in agricultural species is based almost entirely on inferences drawn from experiments performed with rats. Recent studies of brain substrates of ingestive control have revealed a prominent role for the caudal hindbrain. Recognition of the caudal hindbrain's participation in the control of ingestion emphasizes the longitudinal integration of brain control of ingestion. Consequently, we must refrain from assuming that the basal forebrain is the unique site for brain control of ingestion. Progress in the investigation of the neural controls of food intake will continue to depend heavily on studies in the rat. Such studies can speed the development of understanding of ingestive controls in farm species by prescribing critical comparative studies. Lack of circumspection prior to initiation and interpretation of such comparative studies can lead, however, to costly misreading of the pattern of ingestive physiology in farm species.

Animals↗

PubMed1983

Overconsumption of preferred foods following capsaicin pretreatment of the area postrema and adjacent nucleus of the solitary tract.

Lesions which destroy the area postrema (AP) and damage the adjacent nucleus of the solitary tract (NST) produce a constellation of behavioral signs which include overingestion of highly palatable food, exaggerated drinking in response to angiotensin II, diminished feeding in response to glucoprivation and chronically reduced body weight. The diversity of these signs, as well as the anatomical complexities of the AP and adjacent NST, suggest that more than one behaviorally relevant neural population may be damaged by lesions of these areas. Injections of the neurotoxin, capsaicin, made directly into the region of the AP and adjacent NST, cause rats to overconsume highly palatable foods when these foods are available during short (30 min) presentations or when they are available continuously. The capsaicin-treated animals, unlike rats with thermal lesions of the AP and adjacent NST, do not exhibit chronically reduced body weight or overdrink in response to angiotensin II. In addition, feeding in response to glucoprivation is undiminished in capsaicin-injected rats. These results suggest that thermal damage of the AP and adjacent NST causes overingestion of preferred foods by damaging a population of capsaicin-sensitive neurons. The other manifestations of thermal lesions of the AP and adjacent NST are probably mediated by neurons which are not susceptible to capsaicin-induced damage. Since small unmyelinated sensory neurons are most sensitive to damage by capsaicin, it may be that damage to small sensory neuron projections in the AP and/or adjacent NST produces the overconsumption of palatable foods.

Angiotensin II↗