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Biomedical subjects

B G Stanley

Publications and source records attributed to B G Stanley.

At least 19 recordsLinked to original sources
PubMed1992

Differential effects of galanin and neuropeptide Y on extracellular norepinephrine levels in the paraventricular hypothalamic nucleus of the rat: a microdialysis study.

Evidence suggests that the peptides galanin (GAL) and neuropeptide Y (NPY) interact with the amine norepinephrine (NE) in the hypothalamic paraventricular nucleus (PVN) to stimulate feeding behavior. To directly investigate the nature of these interactions, extracellular levels of PVN NE were monitored in freely-moving rats using the microdialysis/HPLC technique. Following PVN administration of GAL (0.3 nmol), NPY (78 pmol) or Ringer's solution, local NE levels were measured at 20-min intervals for 2 hrs postinjection, under two feeding conditions, namely, in the presence or absence of food. The results demonstrate different effects of these peptides on endogenous NE levels. Following GAL administration, PVN NE levels were enhanced by 80 to 90%, up to 40 min postinjection, independent of food availability. In contrast, following NPY injection, NE levels were significantly reduced 20 min postinjection with food absent, and when food was available, NE levels tended to be enhanced. These results, consistent with pharmacological and biochemical studies, reveal different patterns of peptide-amine interactions in the PVN.

Animals↗
PubMed1990

Peptide-amine interactions in the hypothalamic paraventricular nucleus: analysis of galanin and neuropeptide Y in relation to feeding.

The neuropeptide galanin (GAL) has been found to elicit feeding after injection into the paraventricular hypothalamic nucleus (PVN), where it coexists with norepinephrine (NE), a neurotransmitter believed to be important in the control of natural feeding behavior. Using pharmacological tools, this study investigated the possibility that PVN GAL influences food intake via its direct interaction with the noradrenergic system localized in this nucleus. Tests with alpha-adrenergic receptor blockers demonstrated that GAL-induced feeding, similar to NE-stimulated feeding, depends specifically upon functional alpha 2-receptor sites. Further, experimentation with the catecholamine synthesis inhibitors, alpha-methyl-p-tyrosine and Fla-63, suggested that GAL's action also depends upon the release of endogenous NE. This is in contrast to another hypothalamic peptide, neuropeptide Y, which is also a strong stimulant of food intake and coexists with NE in the PVN. Neuropeptide Y remains effective in eliciting feeding in the presence of alpha 2-receptor antagonists and catecholamine-synthesis inhibitors, suggesting that, unlike GAL, it can act independently of endogenous NE.

Adrenergic alpha-Antagonists↗
PubMed1989

Suppression of neuropeptide Y-elicited eating by adrenalectomy or hypophysectomy: reversal with corticosterone.

Neuropeptide Y (NPY) injected into the paraventricular hypothalamus (PVN) stimulates a robust eating response in the satiated rat. To examine whether the NPY-feeding system interacts with the pituitary-adrenal axis, the eating response to PVN injections of NPY (78 pmol) was tested in adult male rats before and after sham surgery, adrenalectomy (ADX), hypophysectomy (HYPX), and/or corticosterone (CORT) replacement therapy. In unoperated or sham groups, NPY elicited 5.7-8.8 g of food intake in 1 h as compared to 0.4-1.1 g for vehicle-injected animals. In ADX groups, the NPY-elicited response was reduced by 60-71%, to between 2.4 and 2.8 g. Likewise, the average response of the HYPX group was reduced by 69%, to 1.7 g. Corticosterone replacement, via subcutaneous implant of a 100 mg CORT pellet, normalized the NPY-induced feeding response in both the ADX and HYPX groups. These findings suggest that the hypothalamic NPY-feeding system is largely dependent upon circulating CORT and that no other adrenal or pituitary hormone is essential.

Animals↗
PubMed1989

Patterns of extracellular norepinephrine in the paraventricular hypothalamus: relationship to circadian rhythm and deprivation-induced eating behavior.

In order to clarify the physiological role of norepinephrine (NE) in the hypothalamic paraventricular nucleus (PVN), changes in extracellular levels of endogenous NE were measured in 11 freely-moving rats using microdialysis and high pressure liquid chromatography with electrochemical detection. To determine whether there was a circadian pattern of extracellular NE in freely-eating subjects, samples of dialysate from the vicinity of the PVN were collected and assayed for NE every 2 hrs for 48 hrs. The pattern of NE averaged across subjects was similar during both 24-hr periods, with a reliable peak at the beginning of the dark cycle and relatively stable levels at all other times. When these animals were subsequently deprived of food for 24 hrs, a gradual rise in extracellular NE was observed, ultimately increasing to 215% of the predeprivation level. When the animals were refed and NE measurements were continued at more frequent intervals, extracellular levels were found to decline during the first 20 min of eating, as well as over the next 3 hrs as food intake diminished. These patterns of extracellular NE, together with previous evidence, suggest that endogenous NE in the PVN plays a role in the initiation and/or maintenance of normal eating behavior at the beginning of the nocturnal feeding period, as well as after food deprivation.

Animals↗
PubMed1989

Repeated hypothalamic stimulation with neuropeptide Y increases daily carbohydrate and fat intake and body weight gain in female rats.

Neuropeptide Y (NPY), repeatedly injected in the hypothalamic paraventricular nucleus (PVN), produces dramatic obesity and overeating in female rats maintained on a single nutritionally complete diet. In the present study, we investigated whether these effects could also be obtained in animals with a choice of three pure macronutrients: protein, carbohydrate, and fat. Female rats with indwelling PVN cannulas were injected with NPY (235 pmol) or its saline vehicle every 8 hr for 6 days. A third group was left undisturbed. Consumption of each macronutrient and body weight were measured every 24 hr for 6 days preinjection, 6 days during injections, and 21 days after the injections were terminated. Relative to vehicle or preinjection rates of body weight gain (approximately 1.5 g/day), NPY dramatically enhanced weight gain to a rate of 9.3 g/day and more than doubled total daily food intake. This augmentation was accounted for by increases in carbohydrate intake (+26.4 kcal/day) and fat intake (+48.5 kcal/day), with no significant potentiation of protein consumption. When the NPY injections were terminated, body weight and macronutrient intake returned to control levels within 1 or 2 weeks. These findings are consistent with a role for NPY in hypothalamic mechanisms of macronutrient intake and body weight regulation and suggest that disturbances in brain NPY may contribute to the development of eating and weight disorders.

Animals↗
PubMed1989

Patterns of extracellular 5-hydroxyindoleacetic acid (5-HIAA) in the paraventricular hypothalamus (PVN): relation to circadian rhythm and deprivation-induced eating behavior.

Daily rhythms in extracellular levels of the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), were examined in the region of the paraventricular nucleus (PVN), using intracerebral microdialysis combined with high performance liquid chromatography and electrochemical detection. Samples of PVN dialysate, from 11 rats on a 12/12 hr light/dark cycle, were collected and assayed for 5-HIAA every 2 hr for 3 days. During the first 2 days the rats were given free access to food. During the 3rd day they were deprived of food for a 24-hr period and then given food for 4 hr. The results showed that in freely-feeding rats, there was a 24-hr rhythm in the levels of 5-HIAA, with a marked transient peak just after the beginning of the dark portion of the light/dark cycle and stable levels at all other times. When the animals were food-deprived, PVN levels of this metabolite remained stable, and the early dark peak was abolished, suggesting that it might have been consequent to the eating behavior which normally occurred at this time. In the 4-hr refeeding period, there were no changes in 5-HIAA levels, despite the intense eating behavior which occurred during this time. These patterns of 5-HIAA in the PVN region, taken together with previous evidence, suggest that PVN serotonin metabolism may increase in association with feeding specifically in the early portion of the nocturnal eating period, when it may play a role in controlling food intake and macronutrient selection.

Animals↗
PubMed1988

Multiple brain sites sensitive to feeding stimulation by opioid agonists: a cannula-mapping study.

Evidence suggests that brain opioid receptors of the mu, delta and kappa subtypes may be involved in the control of feeding behavior. However, limited information is available regarding the specific anatomical location of these feeding relevant opioid receptors. To address this problem, we microinjected three opioid agonists, morphine, (D-Ala2)-Met-enkephalinamide (DALA) or MR 2034, into one of 15 different brain areas and measured the subsequent feeding responses of satiated rats. Morphine (25 nmol) and DALA (6.8 nmol) both elicited strong feeding responses from the same five brain areas, namely, the paraventricular, dorsomedial and lateral hypothalamus, as well as from sites within the septum and amygdala. No other brain sites yielded significant responses to these opioid receptor agonists. In contrast to this anatomically specific pattern of effects, the opioid agonist MR 2034 (8.6 nmol) produced a feeding response which was generally smaller in magnitude and had little anatomical specificity. These findings suggest that opioid receptor systems for stimulating feeding exist in multiple discrete brain areas. Of the regions tested, specific sites within the hypothalamus, septum and amygdala are distinguished as being most sensitive to feeding stimulation by morphine and DALA.

Animals↗
PubMed1986

A small, removable microdialysis probe.

A miniaturized, concentric, microdialysis probe is described. It is constructed from 36 gauge stainless steel tubing inside of 26 gauge tubing, with a cellulose hollow fiber tip 0.2 mm in diameter and 2 mm long. It has a 6000 molecular weight cut off that excludes enzymes but collects monoamines, their metabolites, and other small neurochemicals. In vitro tests show relative recovery rates of 5-10%. Absolute recovery measured in picograms was independent of the perfusate flow rate inside the probe. Tests in awake rats with probes in the nucleus accumbens showed stable amounts of catecholamines and metabolites collected during repeated 20 min samples. After ip amphetamine, release of dopamine in the accumbens increased from 20 to 40 pg per sample while DOPAC and HVA decreased from about 1500 to 500 pg. Tests of multiple site sampling succeeded in obtaining norepinephrine and dopamine plus three metabolites (DOPAC, HVA and 5HIAA) from four probes simultaneously in four different brain sites in each rat. Five day continuous samples or monthly intermittent samples can be obtained with this microdialysis probe.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Flexor tendon injuries: late solution. Therapist's management.

Tenolysis and staged flexor tendon reconstruction are two viable alternatives in managing flexor tendon injuries when primary repair is unsatisfactory or no longer indicated. Successful results depend upon postoperative management that influences scar formation, encourages motion, and restores function. Close cooperation between the surgeon, therapist, and patient is essential for optimal results.

Exercise Therapy↗
PubMed1985

Suppression of norepinephrine-elicited feeding by neurotensin: evidence for behavioral, anatomical and pharmacological specificity.

Neurotensin (NT) injected into the paraventricular hypothalamic nucleus (PVN) has been shown to suppress feeding behavior. To investigate whether this suppression generalizes to feeding elicited by norepinephrine injection, rats with bilateral PVN cannulas were injected with NT (3.0 nmol/cannula) or vehicle followed by norepinephrine (20.0 nmol/cannula). Pretreatment with NT caused a 48% reduction in feeding elicited by norepinephrine. To determine whether NT's effect resulted from non-specific behavioral effects or leakage into the periphery, NT (0.25, 1.25 or 6.0 nmol) was injected ipsilateral or contralateral to a unilateral norepinephrine (40.0 nmol) injection. Ipsilateral NT produced a dose-dependent suppression of norepinephrine-elicited feeding which was significantly greater than the effect of contralateral NT, suggesting that NT's effect was at least partially behaviorally and anatomically specific. To investigate the pharmacological specificity of the suppression, rats that ate in response to PVN norepinephrine (40.0 nmol) were given prior injections of NT or one of six NT fragments at 0.25, 1.25, 6.0 or 30.0 nmol. NT and the C-terminal fragments 3-13 and 6-13 caused a dose-dependent suppression of feeding. In contrast, none of the N-terminal fragments (i.e. 1-8, 1-11 or 1-12) were effective. This specificity rules out non-specific changes in parameters such as pH or osmotic pressure and suggests that the anorectic effect may have been mediated by NT receptors.

Animals↗
PubMed1985

Feeding and drinking elicited by central injection of neuropeptide Y: evidence for a hypothalamic site(s) of action.

Neuropeptide Y (NPY), which exists in very high concentrations in the brain, has been shown to elicit a powerful feeding response and a small drinking response in satiated rats. In order to delineate the brain sites sensitive to these effects, NPY was injected through chronic guide cannulas into seven different brain regions, and the food and water intake of satiated rats was measured one hr postinjection. Injection of NPY (78 pmoles) into hypothalamic areas, namely the paraventricular nucleus (PVN), ventromedial hypothalamus (VMH), and lateral hypothalamus (LH), elicited a strong feeding response; in contrast, injections into extra-hypothalamic areas, namely the amygdala, thalamus, and periaqueductal gray, were completely ineffective. Administration of NPY into the PVN and VMH also elicited a small drinking response; however, all other areas, including the LH, were insensitive to this effect. The findings that NPY was effective in the hypothalamus, as opposed to sites anterior, posterior, lateral or dorsal to this structure, suggest a hypothalamic site(s) of action for this neuropeptide.

Animals↗
PubMed1985

Neuropeptide Y injected in the paraventricular hypothalamus: a powerful stimulant of feeding behavior.

Neuropeptide Y (NPY) was injected directly into the paraventricular nucleus of the hypothalamus (PVN) of satiated, brain-cannulated rats, and food and water intake were measured 0.5, 1, 2, 4, and 22 hr postinjection. NPY (24, 78, 235, 783, and 2351 pmol/0.3 mul) produced a large, dose-dependent increase in food intake as well as small increase in water intake. The latency to eat was about 10 min, with substantial feeding occurring in the first 30 min. At dose below 78 pmol, the eating generally occurred only within the first hour. At doses above 235 pmol, however, the subjects' food intake continued to increase such that by 4 hr postinjection they had consumed the equivalent of normal 22-hr intake, and 22 hr postinjection they had also eaten significantly more than control subjects. Previous studies have shown that norepinephrine injected into the PVN stimulates feeding through alpha-adrenergic receptors. To investigate a possible interaction, subjects were given PVN injections of phentolamine (60 nmol) prior to injections of either NPY (78 pmol) or norepinephrine (20 nmol). Phentolamine pretreatment significantly decreased feeding elicited by norepinephrine without affecting feeding elicited by NPY. This suggests that NPY does not stimulate feeding through the release of endogenous norepinephrine. The powerful stimulation of feeding elicited by this neuropeptide suggests an important role for hypothalamic NPY, or a structurally related peptide, in the regulation of feeding behavior.

Animals↗
PubMedDate not supplied

Paraventricular nucleus injections of peptide YY and neuropeptide Y preferentially enhance carbohydrate ingestion.

Neuropeptide Y (NPY) injected into the paraventricular nucleus (PVN) is known to elicit a powerful feeding response in satiated, brain-cannulated rats. The present experiment investigates the effect of peptide YY (PYY), a structurally-related peptide, on feeding behavior and, in addition, the effects of both PYY and NPY on the pattern of macronutrient selection. Injection of PYY directly into the PVN, in doses ranging from 7.8 to 235 pmol/0.3 microliters, caused a strong, dose-dependent stimulation of feeding behavior, as well as a small stimulation of drinking behavior, in satiated rats. The mean latency to eat was 9.3 min, with substantial feeding occurring within 30 min of the injection. At low doses, the increase in feeding was seen predominantly during the first hr. At the highest dose, in contrast, food intake continued to increase progressively over the next few hr. such that by 4 hr postinjection food intake was more than 20 g over vehicle baseline. In 1 hr tests with 3 pure macronutrient (protein, fat and carbohydrate) diets simultaneously available, PYY and NPY (78 pmol/0.3 microliters) both elicited a strong and selective increase in carbohydrate consumption, with little or no effect on protein or fat consumption. These results suggest that hypothalamic receptors sensitive to PYY and NPY may participate in the control of carbohydrate consumption.

Animals↗
PubMedDate not supplied

Neuropeptide Y chronically injected into the hypothalamus: a powerful neurochemical inducer of hyperphagia and obesity.

Neuropeptide Y (NPY), a putative neurotransmitter abundant in the brain, has recently been shown to act within the hypothalamus, inducing a powerful eating response and a specific appetite for carbohydrates. In the present study, NPY (235 pmol) injected bilaterally in the paraventricular nucleus three times a day for 10 days caused approximately a two-fold increase in daily food intake, a six-fold increase in the rate of body weight gain and a three-fold increase in the body fat of female rats. Subsequently, the food intake and body weight of these subjects decreased precipitously, reaching control levels 20 days postinjection. These findings, demonstrating that exogenous NPY is capable of overriding mechanisms of satiety and body weight control, suggest that disturbances in NPY function may play a role in some disorders of eating behavior and body weight regulation.

Adipose Tissue↗
PubMedDate not supplied

Bombesin-induced anorexia: sites of action in the rat brain.

To determine the brain sites at which centrally injected bombesin (BBS) may act to suppress feeding behavior, this peptide (1.0 micrograms/0.3 microliter) was microinjected into one of twelve brain regions in 6 hr food deprived rats, and food intake was measured 45 min postinjection. Bombesin produced its strongest suppression of feeding (47-65%) when injected into hypothalamic areas, namely, the paraventricular, dorsomedial, ventromedial nuclei and lateral hypothalamus, and also when administered into the amygdala and the periaqueductal gray. Insensitive areas included the septum, ventral tegmental area and reticular formation. In contrast to these somewhat site-specific effects on feeding behavior, observation of BBS' effects on other behaviors revealed that, in all brain areas tested, there was a significant increase in grooming behavior and decrease in time spent resting and sleeping. In conjunction with high levels of BBS-like immunoreactivity and BBS receptors in the brain areas where injected BBS suppresses feeding, these results suggest that the effects of centrally administered BBS on feeding behavior may be mediated by multiple hypothalamic and extra-hypothalamic brain regions.

Animals↗
PubMedDate not supplied

Stimulation of feeding by galanin: anatomical localization and behavioral specificity of this peptide's effects in the brain.

The neuropeptide galanin (GAL) has been found to elicit eating after injection into the hypothalamic paraventricular nucleus (PVN). To determine whether GAL's effect in the brain is anatomically specific, this peptide (0.1 or 0.3 nmol) was microinjected into one of 14 different brain areas of rats, and its impact on subsequent food intake was measured. Among the hypothalamic sites tested, only the PVN and the adjacent periventricular region yielded a significant eating response to GAL. With injection into the PVN, a feeding response was observed without apparent changes in other food-associated behaviors, e.g., drinking, grooming, resting and sleeping, or low and high levels of activity. All other hypothalamic and extrahypothalamic sites tested were unresponsive to GAL, with the exception of the amygdala where a significant eating response was observed. These findings suggest that central GAL elicits feeding by acting in an anatomically localized and behaviorally specific manner. In light of other pharmacological and anatomical evidence, it is suggested the PVN GAL, in modulating feeding behavior, may work in association with the catecholamine norepinephrine (NE) which is known to coexist with GAL in PVN neurons.

Animals↗