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Biomedical subjects

L L Bellinger

Publications and source records attributed to L L Bellinger.

At least 19 recordsLinked to original sources
PubMed2005

Specificity of meal pattern analysis as an animal model of determining temporomandibular joint inflammation/pain.

Analyzing feeding behavior, and in particular meal duration, can be used as a biological marker for temporomandibular joint (TMJ) inflammation/pain. The present study determined the specificity of meal duration as a measure of TMJ inflammation/pain in a rodent model. The model was also used to test the efficacy of dexamethasone (DEX) as a treatment for TMJ inflammation/pain that was induced by TMJ injection of complete Freund's adjuvant (CFA). In the first study, anesthetized male Sprague-Dawley rats housed in computerized feeding modules received bilateral intra-articular knee injections of CFA or saline. The next day, CFA-injected rats had significant knee swelling and impaired mobility. Food intake in the CFA-injected group was reduced over the next two days and this was due to reduced meal number with no change in meal size. Notably, meal duration was normal in both the CFA and saline knee-injected groups. In the second study, male rats were assigned to one of four groups: Group 1, no CFA and no DEX treatment; Group 2, no CFA and treatment with DEX (0.4 mg/kg i.m. once daily); Group 3, bilateral TMJ CFA injection and no DEX treatment; and Group 4, bilateral TMJ CFA injection and treatment with DEX. CFA significantly increased TMJ swelling and stress-induced chromodacryorrhea in Group 3, but treatment with DEX attenuated these effects in Group 4. Compared to the controls, meal duration was significantly lengthened 24 and 48 h post-CFA injection in Group 3, whereas DEX treatment attenuated TMJ swelling, chromodacryorrhea and normalized meal duration. The data demonstrate that meal pattern analysis, and in particular meal duration, can be used as a non-invasive specific measure of TMJ inflammation/pain and can be used as a marker of DEX treatment efficacy.

Animals↗
PubMed2003

Meal pattern changes associated with temporomandibular joint inflammation/pain in rats; analgesic effects.

Establishing a valid animal model to study temporomandibular joint (TMJ) pain has proven extremely difficult. Using complete Freund's adjuvant (CFA) to induce TMJ inflammation, we recently showed that meal pattern analysis could be used as a noninvasive biological marker to study TMJ pain in an animal model. The purpose of this study was to further validate our animal model by determining whether aspects of CFA-induced TMJ inflammation/pain are reversed with ibuprofen (IBU) treatment. In the first trial, 48 male rats were used and in the second trial, 32 female ovariectomized rats, given 17beta-estradiol replacement, were used. The rats were assigned to one of four groups: control (CON-CON); control+IBU (CON+IBU); CFA-CON; and CFA+IBU. In the male trial, CFA injection (P<.01) caused TMJ swelling and chromodacryorrhea (CFA-CON); IBU eliminated these changes in the CFA+IBU group. Meal pattern analysis showed the pertinent CFA-induced change and the IBU effect was that meal duration was increased in the CFA-CON group (P<.01), but normal in the CFA+IBU-treated group on the first, but not second, day postinjection. In the female trial, CFA increased TMJ swelling, but did not cause significant chromodacryorrhea (CFA-CON); IBU eliminated swelling in the CFA+IBU group. Meal duration was increased (P<.01) in the CFA-CON group, but was normal in the CFA+IBU-treated group on both the first and second days postinjection. In both trials, interleukin-1beta (IL-1beta) levels were increased similarly in CFA-CON and CFA+IBU groups (P<.01). This study shows that CFA-induced TMJ inflammation/pain can cause changes in meal patterns (i.e., meal duration), which may be used as a behavioral marker for TMJ inflammation/pain.

Animals↗
PubMed2003

A determination of tumor necrosis factor expression in TMJ inflammation with the use of microarray analysis.

Many different factors can lead to inflammatory changes within temporomandibular joint tissues. This investigation examined if the expression of TNF-alpha and its receptors was altered in TMJ tissues during inflammation. Adult male rats were injected bilaterally with complete Freund's adjuvant (CFA) into the TMJ or served as uninjected controls and were killed two days after CFA treatment. TMJ tissues were removed, and expression of TNF-alpha and its receptors was examined via gene microarray analysis, RT-PCR, Western blot, and ELISA. Gene microarray analysis provided evidence for changes in gene expression, notably that TNF-alpha and TNF-R1, but not TNF-R2, were significantly elevated in CFA-treated TMJ tissues. However, protein levels of TNF-alpha, TNF-R1, and TNF-R2 were all significantly increased in CFA-treated TMJ tissues. These results indicate that the pro-inflammatory cytokine TNF-alpha may play a significant role in the onset of inflammatory conditions associated with adjuvant-induced arthritis of the TMJ.

Animals↗
PubMed2001

Modulation of the inflammatory response in the rat TMJ with increasing doses of complete Freund's adjuvant.

OBJECTIVES: Acute inflammation stresses the physiological system, which must respond in order to reestablish homeostasis. The purpose of this study was to determine whether bilateral temporomandibular joint (TMJ) injections of different doses of Complete Freund's Adjuvant (CFA) produced dose-dependent changes in biologic markers of acute inflammation. The ability to establish an animal model with varying degrees of joint inflammation would allow evaluation of agents or conditions that could modulate the severity of the disease. DESIGN: The TMJs of three groups of male Sprague-Dawley rats were injected with CFA containing varying doses of Mycobacterium tuberculosis (MT). A group of non-injected and a group of saline injected rats were used as controls. Food intake, body weights, swelling and chromodacryorrhea were recorded daily. Interleukin-1 beta (IL-1 beta) and corticosterone levels were assayed and condylar cartilage thickness was measured 48 h after injections. RESULTS: Twenty-four hours post-injection, bilateral TMJ swelling and chromodacryorrhea were significantly (P< 0.05) increased following 10 microg of MT and further increased with elevated MT dose. In the CFA groups food intake was attenuated (P< 0.01) 24 and 48 h post-injection and negatively correlated with dose at 24 h. Body weight was also negatively correlated with dose. TMJ retrodiscal tissues IL-1 beta was increased (P< 0.05) in a dose-dependent manner. CFA increased corticosterone (P< 0.05), but this elevation was not dose dependent. Condylar cartilage thickness was decreased in a dose-dependent manner. CONCLUSIONS: These data suggest that an intermediate dose of CFA can be used to effect submaximal levels of TMJ inflammation that will allow experimental modulation in future studies.

Acute-Phase Reaction↗
PubMed2000

Differential effects of selective vagotomy and tropisetron in aminoprivic feeding.

Both total subdiaphragmatic vagotomy (TVAGX) and serotonin(3) receptor blockade with tropisetron or ondansetron attenuate amino acid-imbalanced diet (Imb) anorexia. Total vagotomy is less effective than tropisetron in reducing Imb-induced anorexia and also blunts the tropisetron effect. With the use of electrocautery at the subdiaphragmatic level of the vagus, we severed the ventral and dorsal trunks as well as the hepatic, ventral gastric, dorsal gastric, celiac, and accessory celiac branches separately or in combination to determine which vagal branches or associated structures may be involved in these responses. Rats were prefed a low-protein diet. On the first experimental day, tropisetron or saline was given intraperitoneally 1 h before presentation of Imb. Cuts including the ventral branch, i.e., TVAGX, ventral vagotomy (above the hepatic branch), and hepatic + gastric vagotomies (but not hepatic branch cuts alone) caused the highest (P < 0.05) Imb intake on day 1 with or without tropisetron. The responses to tropisetron were not affected significantly. On days 2-8, groups having vagotomies that included the hepatic branch recovered faster than sham-treated animals. Because the hepatic and gastric branches together account for most of the vagal innervation to the proximal duodenum, this area may be important in the initial responses, whereas structures served by the hepatic branch alone apparently act in the later adaptation to Imb.

Adaptation, Physiological↗
PubMed2000

Meal pattern analysis in response to temporomandibular joint inflammation in the rat.

Inflammation of the temporomandibular joint (TMJ) can alter behavioral responses such as food intake and mobilize stress hormones. The hypothesis of this study was that food intake and diurnal corticosterone analysis can be used as indicators of adjuvant-induced TMJ inflammation. Groups of rats received adjuvant or no injections at the beginning of the resting (AM) or activity (PM) phase. Forty-eight hours (early) or 6 weeks (late) after adjuvant injection, plasma corticosterone was assayed and food intake was recorded. Food intake was suppressed up to 4 days post-injection. As expected, the non-injected group showed low AM and high PM corticosterone. AM corticosterone was elevated, but PM corticosterone was attenuated in both early- and late-stage-injected rats. A computerized pair-fed experiment showed that adjuvant-induced hypophagia did not alter corticosterone levels. Meal pattern analysis revealed decreased food intake due to a decrease in the number of meals taken. Notably, meal size remained the same but meal duration increased. This model demonstrated that food intake and stress hormone analysis could be used as indicators for sequelae of adjuvant-induced TMJ inflammation.

Analysis of Variance↗
PubMed1999

Effect of dorsomedial hypothalamic nuclei knife cuts on ingestive behavior.

Previous findings show that rats with electrolytic or excitotoxic lesions in the dorsomedial hypothalamic nucleus (DMN) are hypophagic and hypodipsic and have reduced ponderal and linear growth but normal body composition. DMN-lesioned (DMNL) rats also show altered ingestive responses to naloxone. The present study investigated the intrahypothalamic nerve pathways involved in these DMNL effects and the response of the pathways to deprivation challenges by placing knife cuts posterior (Post), lateral (Lat), ventral (Vent), dorsal, or anterior to the DMN or by administering sham operations. One major finding was that rats with Post or Vent were hypophagic (P < 0. 05) and had reduced body weight but responded normally to deprivation challenges. Post and Lat groups were hypodipsic (P < 0. 05), but plasma Na+, K+, and osmolality and 24-h post-water-deprivation drinking responses were similar in all groups. Naloxone did not suppress the intake of Post rats. It appears that the hypophagia and the reduced body weight after DMNL involve fibers entering or leaving the DMN from ventral and posterior directions, and they may be part of an opioid feeding system.

Animals↗
PubMed1999

Effects of dorsomedial hypothalamic nuclei lesions on intake of an imbalanced amino acid diet.

Within 3 h of ingesting an imbalanced amino acid diet (Imb), rats show attenuated intake, which can be ameliorated by prior administration of the serotonin receptor antagonist tropisetron (Trop). Earlier work in which the dorsomedial hypothalamic nucleus (DMN) was electrolytically lesioned (DMNL) determined that this structure plays a role in the early detection of and subsequent adaptation to Imb. However, that study did not address whether cell bodies in the DMN, fibers of passage, or both were involved in the DMNL response to Imb. In the present investigation in experiment 1, rats were given electrolytic DMNL or a sham operation (Sham). The rats were injected with saline (Sal) or Trop just before introduction of Imb. By 3 h Sal-DMNL rats consumed more Imb than did the Sal-Sham rats; intake was normal by 12 h. Trop enhanced Imb intake, with Trop and DMNL being additive. By day 4 the DMNL rats were eating and gaining weight less than were Sham rats. In experiment 2, DMN cell bodies were destroyed by ibotenic acid (Ibo). Sal-injected Ibo-lesioned and Sham rats showed similar food intake depression on Imb; Trop similarly increased Imb intake in both groups. By day 4 both Ibo-L rats were eating and gaining weight less than were Sham rats. In experiment 3, groups of rats were given knife cuts posterior, lateral, ventral, dorsal, or anterior to the DMN. During the first 3 h of consuming Imb, all cuts except posterior enhanced the intake of Imb. Over the next 24 h the anterior cut group continued to eat more Imb than did the Sham rats. In experiment 4 DMNL rats were given novel diets; the DMNL rats did not display a neophilic response. The data suggest that fiber tracts that pass through the DMN may be involved in the early detection of Imb. DMN cell bodies, or fibers of passage, are not involved in the Trop effect. Finally, DMN cell bodies are necessary for proper long-term adaptation to Imb.

Amino Acids, Essential↗
PubMed1998

Dorsomedial hypothalamic lesions alter intake of an imbalanced amino acid diet in rats.

Within 3 h of ingesting an imbalanced amino acid diet (IAAD), rats show attenuated intake. The associated conditioned taste aversion can be ameliorated by giving the serotonin3 receptor blocker, tropisetron (TROP). A recent c-fos study indicated that the dorsomedial hypothalamic nucleus (DMN) may be activated 2-3 h after ingestion of IAAD. In Experiment 1, DMN-lesioned rats (DMNL) or sham-operated (SHAM) rats were injected with saline (SAL) or TROP just before introduction of IAAD. By 3 h, SAL-DMNL rats consumed more (P < 0.01) of the IAAD than did the SAL-SHAM rats. Thereafter, over the next 21 h, the intake of the SAL-DMNL group returned to control levels. TROP treatment enhanced the intake of the treated groups; the TROP and the lesion effect were additive (P < 0.01). By d 4 of receiving the IAAD, the DMNL groups were eating less than SHAM rats (P < 0.05). The data suggest that the DMN may be involved in the early detection of the amino acid deficiency induced by IAAD, is not involved in the TROP effect and is necessary for proper long-term adaptation to an IAAD.

Amino Acids↗
PubMed1998

The dorsomedial hypothalamic nucleus revisited: 1998 update.

This article reviews data that have accumulated since the early 1970s on the role of the dorsomedial hypothalamic nucleus (DMN) in neuroendocrine and autonomic homeostasis. Both the ventromedial hypothalamic nucleus (VMN) and the lateral hypothalamic area (LHA) project to the DMN, which in turn projects to the paraventricular nucleus of the hypothalamus (PVN), thus placing the DMN at an important nodal point of neuroendocrine/autonomic circuitries. The DMN is composed of cells and fibers containing neuropeptide Y (NPY), and the nutritional status (starvation-refeeding) is reflected in NPY levels of both VMN and DMN in Sprague-Dawley, Zucker (fa/fa), and corpulent rats (cp/cp JCR:LA). The DMN is involved in the final common pathway of corticotrophin-releasing hormone (CRH) secretion by the PVN, sympathetic nervous system outflow to the adrenal gland, and brown adipose tissue (BAT) thermogenesis. The DMN is also part of a "fear circuitry" regulating cardiovascular responses to stress such as myocardial blood flow and the tachycardia associated with the defense reaction. This appears to be mediated by a gamma amino butyric acid (GABA) mechanism. Although exhibiting reduced ponderal and linear growth and hypophagia and hypodipsia, the rat with DMN lesions (DMNL rat) has normal body composition, anabolic hormone levels, and intermediary metabolism, and it responds normally to numerous endocrine, nutritional, intra- and extracellular thirst and body weight-regulatory challenges. The DMNL rat shows normal efficiency of food utilization, but shows an attenuated response to the feeding-stimulatory effect of insulin. The only other lesion-induced abnormalities are hyperprolactinemia and a disrupted circadian corticosterone rhythm. The hyperprolactinemia in DMNL rats appears to be related to an attenuation of dopamine (DA). Rats with DMNL are capable of mating and can bear offspring, but there is a dramatic effect on litter size and other litter parameters that only improves when one parent is a DMNL rat. Antiaging effects produced by DMNL are evident in the prevention of age-associated microalbuminuria and kidney lesions, as well as, in prevention of the age-related decline in circulating insulin-like growth factor I (IGF-I). Recent evidence suggests that DMN, together with the VMN and the arcuate nucleus (ARC) of the hypothalamus, may be part of the circuitry that is responsive to the feedback signal from adipose tissue by the hormone leptin. The above findings and others suggest that the DMN plays a diverse role in physiological regulatory processes.

Animals↗
PubMed1997

Meal patterns prior to and following liver transplantation in rats.

Afferent nerves of the liver have been suggested to have a major influence on feeding behavior. Nevertheless, total liver denervations (TLD) in rats, that were verified by histofluorescence technique, did not change short or long term meal patterns. However, these studies have been criticized that the TLD procedures may have missed some liver innervation. In the present study meal patterns were conducted prior to and following liver transplantation in rats using a transplant procedure with arterialization. The transplanted rats recovered their pre-operative body weight in 7.5 +/- 0.6 days and meal pattern analysis was conducted two days later. In comparison with pre-surgery there was no differences in 24 h food intake (gms); dark phase: intake (gms), meal size (gms), meal duration (min), inter-meal interval (min), and frequency; and light phase: intake (gms), meal size (gms), meal duration (min), inter-meal interval (min), and frequency. These data, like earlier work in TLD rats showing that the animals consumed normal meals (when offered a variety of diets), starting with the first meal post-surgery, question the importance of liver afferents in the control of feeding behavior.

Animals↗
PubMed1996

Satietin: Fos mapping of putative brain sites of action.

A purified extract of a blood-borne satiety factor, called satietin, was injected into the cerebral ventricles of rats that were either fed ad libitum or were food deprived. The animals were killed 2 h after injection and their brains subsequently sectioned and stained for Fos-like immunoreactivity (Fos-IR) to determine the putative sites of action for satietin in the brain. Fos-IR was induced in only a few locations, the most prominent sites being the bed nucleus of the stria terminalis, the central nucleus of the amygdala, and the parvocellular division of the paraventricular nucleus of the hypothalamus. Each of these areas has previously been implicated in the control of feeding behavior. Sites in the hindbrain that are associated with nausea were devoid of satietin-induced Fos-IR. Finally, these sites of action of satietin show some differences from sites that are prominently activated by other classes of anorectic agents.

Amygdala↗
PubMed1996

The lateral hypothalamic area revisited: ingestive behavior.

This article discusses the role of the lateral hypothalamic area (LHA) in feeding and drinking and draws on data obtained from lesion and stimulation studies and neurochemical and electrophysiological manipulations of the area. The LHA is involved in catecholaminergic and serotonergic feeding systems and plays a role in circadian feeding, sex differences in feeding and spontaneous activity. This article discusses the LHA regarding dietary self-selection, responses to high-protein diets, amino acid imbalances, liquid and cafeteria diets, placentophagia, "stress eating," finickiness, diet texture, consistency and taste, aversion learning, olfaction and the effects of post-operative period manipulations by hormonal and other means. Glucose-sensitive neurons have been identified in the LHA and their manipulation by insulin and 2-deoxy-D-glucose is discussed. The effects on feeding of numerous transmitters, hormones and appetite depressants are described, as is the role of the LHA in salivation, lacrimation, gastric motility and secretion, and sensorimotor deficits. The LHA is also illuminated as regards temperature and feeding, circumventricular organs and thirst and electrolyte dynamics. A discussion of its role in the ischymetric hypothesis as an integrative Gestalt concept concludes the review.

Animals↗
PubMed1996

Innervated liver plays an inhibitory role in regulation of food intake.

BACKGROUND: With the onset of eating, the associated rise of dopamine in the lateral hypothalamus (LHA-DA) is thought to regulate quantity of food consumed per meal. Early release of LHA-DA induced by eating is facilitated by oronasal stimulation; we propose that the subsequent LHA-DA response induced by nutrients in the portal vein is dampened by the innervated liver. This was tested by measuring LHA-DA in normal rats: during parenteral feeding to bypass oronasal stimulation, while eating during parenteral feeding, and while eating only. METHODS: Rats had either total liver denervation or sham operation, with placement of a jugular vein catheter and LHA-DA microdialysis cannula. After a 3-week recovery period total liver denervated rats were randomized to parenterally fed, food only, and parenteral plus food groups each with sham-operated controls in which LHA-DA was measured. RESULTS: No difference in LHA-DA release in food only groups occurred between total liver denervated or sham-operated rats. A significantly higher rise in LHA-DA was observed in total liver denervated versus sham-operated rats in parenterally fed (129% +/- 4% versus 116% +/- 2%; p < 0.05) and parenteral plus food (151% +/- 4% versus 134% +/- 4%; p < 0.05) groups. CONCLUSIONS: In total liver denervation versus sham operation, an increase in LHA-DA release occurs during parenteral feeding and eating during parenteral feeding, suggesting that innervated liver inhibits LHA-DA release.

Animals↗
PubMed1995

Meal patterns and plasma liver enzymes and metabolites after total liver denervations.

The liver by way of afferent nerves has been suggested to be a controller of food intake. However, long term meal pattern analysis of chow intake by rats has revealed that total liver denervation (TLD) did not affect the patterns. Nevertheless, these studies have been criticized because they may have missed initial subtle difference in meal patterns that were corrected later by redundant mechanisms. TLD also can alter physiological regulator mechanisms that could secondarily affect feeding behavior. Furthermore, the TLD procedure itself can produce pathologic changes if extreme care is not taken; if pathology does occur it could subsequently affect food intake measurements. In Experiment 1, male rats were given TLD or sham operations (SHAM) at the beginning of the light phase and food withheld until the onset of the dark period. Using a computer operated system, postsurgery onset on feeding, meal size, duration, and frequency were found to be comparable between the groups from the first meal onward. In Experiment 2, 21 days after TLD or SHAM feeding patterns were recorded; all meal parameters were similar between the groups. The rats were then killed and plasma analyzed for liver enzymes (a reflection of liver damage), nutrients and metabolites: no differences were found between the groups. The data suggests that TLD doesn't affect normal regulation of chow intake from the rats' first postsurgery meal onwards. The second study showed that the TLD technique, in our hands, did not produce an adverse effect on normal liver function.

Afferent Pathways↗
PubMed1995

Blood profile and balance study of rats given the putative anorectic agent satietin.

Satietin (SAT), a glycoprotein found in the plasma of a variety of animals, is a putative satiety agent. In experiments 1 and 2 rats received chronic third ventricle cannulas. At the start of the dark phase, in experiment 1, one group was infused with artificial cerebrospinal fluid (aCSF) and fed ad libitum (CON); a second group was infused with 100 micrograms/rat of human SAT and fed ad libitum in individual computerized pellet feeding modules; a third group was infused with aCSF and pair fed (PF) to the SAT-treated rats. The animals were killed 19.5 h later and blood was collected. Food and water intake and body weight were significantly, and comparably, reduced in the SAT-treated and PF group compared with the CON group. Plasma was assayed for a variety of nutrients, metabolites, enzymes, hormones, ions, and osmolality. Differential white cell counts were made. None of the above parameters differed significantly between the SAT and PF groups. Meal pattern analyses showed SAT treatment did not at any time alter meal size but significantly increased meal duration and intermeal interval during the first 6 h of the dark phase. In experiment 2 rats were placed in metabolic cages and infused with SAT or aCSF. Food and water intakes of the SAT group were suppressed for 1 day, whereas their body weights were significantly attenuated for 3 days. Urine volume and feces elimination were similar in the two groups over the 6-day measurement period. The normalcy of the data from experiment 1 is in accord with the possibility that SAT may act as a physiological satiety agent.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Effects of components derived from HPLC purification of human satietin on ingestion, body weight, and taste aversion in the rat.

The putative satiety agent human satietin (h-SAT) once thought to be homogenous has been separated by high-performance liquid chromatography (HPLC) into components designated peak A (P-A, 53%/w) and Peak B (P-B, 47%/w); P-B contains a putative satiety agent. In Experiment 1, male Sprague-Dawley rats were divided into six (n = 9-11) groups (Grps) and ICV infused: Grp 1, artificial cerebrospinal fluid (a-CSF), 10 microliters/rat; Grp 2, albumin (ALB), 53 micrograms/rat; Grp 3, semipurified (sp) h-SAT (parent compound), 100 micrograms/rat; Grp 4, P-A, 53 micrograms/rat; Grp 5, P-B, 47 micrograms/rat; and Grp 6, P-A+B, 53+47 micrograms/rat, respectively. Compared to Grp 1, food intake, the first day postinfusion, was suppressed in Grp 3 (p < 0.01) and equally attenuated (p < 0.06) in Grps 5 and 6. Body weight remained suppressed (p < 0.05) in Grps 3, 5, and 6 for 3 days and in Grps 3 and 6 (p < 0.05) for an additional 3 days; Grps 2 and 4 did not differ from Grp 1. These data show P-B suppresses food intake comparably to P-A+B and causes a prolonged weight loss. In Experiment 2, sph-SAT and a recombination of P-A and P-B was tested for aversiveness using the two-bottle test. Both sph-SAT and P-A+B significantly suppressed food intake, but only sph-SAT was found to be aversive. These data show that most likely during HPLC processing of sph-SAT an aversive component was lost.

Angiotensin II↗