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The teeth of putatively carnivorous dinosaurs are often blade-shaped with well-defined serrated cutting edges (Figure 1). These ziphodont teeth are often easily differentiated based on the morphology and density of the denticles [1, 2]. A tearing function has been proposed for theropod denticles in general [3], but the functional significance of denticle phenotypic variation has received less attention. In particular, the unusual hooked denticles found in troodontids suggest a different feeding strategy or diet compared to other small theropods. We used a two-pronged approach to investigate the function of denticle shape variation across theropods with both congruent body shapes and sizes (e.g., dromaeosaurids versus troodontids) and highly disparate body shapes and sizes (e.g., troodontids versus tyrannosaurids), using microwear and finite element analyses (Figure 1). We found that many toothed coelurosaurian theropods employed a puncture-and-pull feeding movement, in which parallel scratches form while biting down into prey and oblique scratches form as the head is pulled backward with the jaws closed. In finite element simulations, theropod teeth had the lowest stresses when bite forces were aligned with the oblique family of microwear scratches. Different denticle morphologies performed differently under a variety of simulated biting angles: Dromaeosaurus and Saurornitholestes were well-adapted for handling struggling prey, whereas troodontid teeth were more likely to fail at non-optimal bite angles. Troodontids may have favored softer, smaller, or immobile prey., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Eating disorders are associated with impaired decision-making and dysfunctional reward-related neurochemistry. The present study examined the potential contributions of dopamine and opioid signaling to these processes using two different decision-making tasks. In one task, Long Evans Rats chose between working for a preferred food (high-carbohydrate banana-flavored sucrose pellets) by lever pressing on a progressive-ratio schedule of reinforcement vs. obtaining less preferred laboratory chow that was concurrently available. In a second (effort-free) task, rats chose between the same two reinforcers when they were both available freely. Rats were trained in these tasks before receiving haloperidol (0.00, 0.05, 0.10mg/kg, intraperitoneally (i.p.)) or naloxone (0.0, 1.5, 3.0mg/kg, i.p.). In the first task, haloperidol decreased breakpoint, lever presses, number of reinforcers earned, and increased chow intake, whereas naloxone decreased breakpoint and number of reinforcers earned but had no effect on chow consumption. In the effort-free task, haloperidol reduced intakes of both foods without affecting preference, whereas naloxone selectively reduced the consumption of banana-pellets. The present findings support converging evidence suggesting that DA signaling affects processes more closely related to appetitive motivation, leaving other components of motivation unchanged. By contrast, opioid signaling appears to mediate aspects of hedonic feeding by selectively altering intakes of highly palatable foods. For preferred foods, both appetitive and consummatory aspects of food intake were altered by opioid receptor antagonism. Our findings argue against a general suppression of appetite by either compound, as appetite manipulations have been shown to unselectively alter intakes of both types of food regardless of the task employed., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Two skeletons of the large compsognathid Sinocalliopteryx gigas include intact abdominal contents. Both specimens come from the Jianshangou Beds of the lower Yixian Formation (Neocomian), Liaoning, China. The holotype of S. gigas preserves a partial dromaeosaurid leg in the abdominal cavity, here attributed to Sinornithosaurus. A second, newly-discovered specimen preserves the remains of at least two individuals of the primitive avialan, Confuciusornis sanctus, in addition to acid-etched bones from a possible ornithischian. Although it cannot be stated whether such prey items were scavenged or actively hunted, the presence of two Confuciusornis in a grossly similar state of digestion suggests they were consumed in rapid succession. Given the lack of clear arboreal adaptations in Sinocalliopteryx, we suggest it may have been an adept stealth hunter.

Injections of the serotonin (5-HT)(1A) agonist, 8-hydroxy-2(di-n-propylamino)tetralin, (8-OH-DPAT), either systemically or into the midbrain raphe nuclei, elicit food intake in otherwise satiated rats. Lesions of the paraventricular nucleus of the hypothalamus are well known for producing long-term overeating, but past research has excluded this site as a potential locus for short-term 8-OH-DPAT feeding effects. More recent work shows that small lesions of the posterodorsal amygdala (PDA) elicit overeating in their own right. Since this and related regions of the amygdala receive 5-HT innervations from the dorsal raphe nucleus (DRN), we determined if PDA lesions might alter feeding after injecting 8-OH-DPAT into this midbrain region. Adult female rats received either bilateral electrolytic lesions of the PDA or sham lesions. After recording weight gains for over 1 month, all rats were implanted with DRN cannulae, then randomly tested every 3-4 days for 1 h intake of standard lab chow after 0, 0.4, 0.8 or 1.6 nmol injections of 8-OH-DPAT. Additional 90 min measures of intake were also made after 0 vs. 250 microg (760 nmol) 8-OH-DPAT s.c. At the two highest DRN doses tested, lesioned rats showed 50% less intake compared to shams. A similar profile emerged after the single s.c. dose. These results suggest that the PDA may be an important locus at which reduced release of endogenous 5-HT stimulates feeding. Alternatively, the PDA may represent part of a larger brain circuit whose integrity is necessary for eliciting intake in response to a variety of feeding stimuli.

Infusions of norepinephrine (NE), the gamma-aminobutyric acid agonist, muscimol (MUS), or neuropeptide Y (NPY) into the paraventricular nucleus (PVN) of the hypothalamus all increase food intake. Such feeding may be due to direct activation of behavioral processes driving ingestion and/or to alterations in nutrient metabolism that feeding serves to normalize. To examine these possibilities, male Sprague-Dawley rats received PVN infusions of vehicle, 20 nmol NE, 1 nmol MUS or 100 pmol NPY at dark onset, then food intake was measured under three feeding conditions: (1) 1 and 2 h immediately after injections, (2) 1 h after a 1 h delay between injections and access to food, and (3) 1 h after a 1 h feeding delay, but with injections occurring just before presenting food. Measures of energy expenditure (EE) and respiratory quotients (RQs) in the absence of food were made over 2 h in parallel experiments. Results confirmed that NE, MUS and NPY all increased dark-onset feeding, but only NPY increased intake above control levels after a 1 h feeding delay. No neurochemically-induced changes in EE were observed, nor were there changes in RQs after NE or MUS. However, NPY reliably enhanced RQs from 30 to 120 min of testing. Our findings imply that NE and MUS initiate relatively immediate, short-term feeding that is not associated with changes in nutrient metabolism and does not summate with cues stimulated by delayed access to food. NPY initiates more protracted feeding temporally linked to enhanced carbohydrate metabolism. This may indicate that part of NPY's feeding stimulatory effects are secondary to physiological processes driving ingestion.

The present study examined the impact of the 5-HT(2A/2C) agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on the feeding-stimulant action of neuropeptide Y (NPY) injected into three hypothalamic sites, the paraventricular nucleus (PVN), the perifornical hypothalamus (PFH) and the ventromedial nucleus (VMH). Injections of NPY (100-200 pmol) into each region potentiated food intake. Pretreatment with DOI (5-20 nmol) into the PVN effectively suppressed feeding elicited by PVN NPY (100 pmol). In contrast, DOI injections into the PFH and VMH failed to modify NPY-stimulated eating. This suggests that 5-HT(2A/2C) receptor modulation of NPY feeding within the hypothalamus is localized to the PVN.

Previous research has shown that both the paraventricular nucleus (PVN) of the hypothalamus and the perifornical hypothalamus (PFH) are sites at which microinjection of neuropeptide Y (NPY) can induce eating. The PVN has also been shown to be responsive to the effects of exogenous NPY on energy substrate utilization. Therefore, the objective of the present study was to further characterize and compare the effects of NPY on whole-body calorimetry and feeding after microinjection into either the PVN or the PFH. The metabolic effects of NPY (19.5-78 pmol) were determined using an open-circuit calorimeter by measuring the volumes of oxygen consumed and carbon dioxide expired in order to compute respiratory quotients (RQs). Following NPY injection into the PVN (n = 10) or PFH (n = 10), RQs and locomotor activity were monitored over three hours. Additional groups of rats with PVN (n = 10) or PFH (n = 10) cannulae were tested for their feeding responses to these same doses of peptide. While NPY injections into the PVN evoked dose-dependent increases in RQ within 30-40 min of treatment, PFH NPY did not alter RQ at any of the doses tested. Locomotor activity was unaffected by NPY in either site. NPY administration into both the PVN and PFH stimulated eating, although the PFH was found to be the more sensitive in terms of absolute amount of food consumed. These findings support the hypothesis that the PVN may regulate metabolic processes that either produce or coincide with NPY-induced feeding. This contrasts with the PFH, which appears to mediate only the feeding-stimulatory actions of NPY.

Medial hypothalamic injections of 5-hydroxytryptamine (5-HT) or its agonists have been reported to inhibit feeding elicited by norepinephrine (NE), suggesting that these two transmitter systems interact antagonistically in the control of ingestive behavior. The present study was designed to directly test the hypothesis that 5-HT inhibits adrenergic feeding, specifically at the onset of the rat's nocturnal eating cycle. Free-feeding animals were injected with 5-HT (5-20 nmol) immediately before NE (20 nmol) and food intake was measured 1.5 h postinjection. In separate groups of rats, the serotonergic antagonist metergoline (MET) (2.5-20nmol) was injected into the paraventricular nucleus (PVN) immediately before 5-HT, or before combined injections of 5-HT and NE. The feeding-stimulant action of MET alone, injected IP (0.25-2 mg/kg) or centrally (2.5-40 nmol), was also examined. Results indicated that administration of 5-HT into the PVN suppressed dark onset feeding and dose-dependently blocked NE-stimulated eating. Pretreatment with MET attenuated the inhibitory action of 5-HT on feeding, and reversed the serotonergic blockade of the adrenergic eating response. Further, systemically injected MET significantly increased dark onset feeding, whereas PVN injections failed to alter food intake reliably. These findings provide the first direct evidence that serotonergic and adrenergic systems within the PVN interact in a competitive manner to modulate the natural high rates of feeding displayed by rats during the early dark period. Although MET effectively blocked the anorectic effect of 5-HT, the feeding-stimulant action of this compound alone does not appear to be mediated within the PVN.

The present study investigated the effects of neuropeptide Y (NPY) on food intake and body temperature (Tbo) in free-feeding unrestrained rats following injection into the medial hypothalamic paraventricular nucleus (PVN) or the lateral perifornical hypothalamus (PFH). NPY (78-235 pmol) or saline was infused unilaterally into the PVN or PFH in a volume of 0.4 microliter and simultaneous measures of food intake and Tbo were taken every 30 min for 3 h. Results indicated that NPY evoked changes in eating behavior and Tbo that were dependent upon the site of hypothalamic injection. Although PVN and PFH administration of NPY both increased food intake dose dependently within 30 min of treatment, PFH NPY-injected rats (n = 9) showed a stronger behavioral response compared to rats (n = 9) receiving NPY injections into the PVN. In PVN-treated rats, however, the increased eating was associated with a significant decline in Tbo evident within the first 30-min test interval. A mean maximal decline of 0.92 +/- 0.26 degree C occurred within 90 min of PVN treatment of the highest dose, which produced a reduction in Tbo that was maintained for 2.5 h. In contrast, NPY infusion into the PFH failed to reliably alter Tbo at any of the doses tested. These findings are consistent with evidence that NPY in the PVN and PFH may have distinct functions and suggest that although PFH NPY acts to stimulate a robust and relatively specific ingestive response, PVN NPY may participate in the complex integrative mechanisms responsible for the simultaneous regulation of feeding, thermoregulatory, and metabolic processes.

Previous research has shown that systemic injections of the nonselective serotonin (5-HT) antagonist metergoline (MET) can stimulate feeding in both rats and humans. Five experiments were conducted to determine if this drug would elicit feeding in otherwise satiated rats after direct injections into the brain. In experiment 1, intraventricular infusions of 100 nmol MET produced reliable enhancements of feeding for 1 h compared with control infusions of a 5% tartaric acid (vehicle) solution. In experiment 2, a dose-response study of 0, 50, 100, and 150 nmol MET intraventricularly revealed that both 100 and 150 nmol doses reliably enhanced 1-h feeding, whereas 50 nmol did not. In experiment 3, tests of 90-min locomotor activity and water intake in the absence of food revealed that 100 nmol MET intraventricularly did not modify either behavior compared with vehicle infusions, suggesting a degree of feeding specificity to this effect. In an attempt to determine the site of intraventricular MET effects on feeding, experiment 4 tested 1-h feeding responses after 0, 5, 10, 20, 40, or 60 nmol MET were infused unilaterally into the paraventricular nucleus (PVN) of the hypothalamus. No reliable feeding was induced at any of these drug doses, although injections of 30 nmol norepinephrine (NE) were effective in doubling food intake. Experiment 5 further showed that bilateral infusions of 50 nmol MET in each PVN (total dose, 100 nmol) were ineffective in altering 1-h feeding. This contrasted markedly to the high potency of 15 nmol NE per site (total dose, 30 nmol), which elicited fivefold greater feeding than control infusions.(ABSTRACT TRUNCATED AT 250 WORDS)

The 5-hydroxytryptamine (5-HT)1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) has been shown to elicit dose-dependent feeding in satiated rats when injected into the midbrain raphe nuclei. Because the feeding-stimulatory effects of this compound are associated with reduced 5-HT release in forebrain, and because recent evidence suggests that medial hypothalamic norepinephrine (NE) and 5-HT may function antagonistically in the control of feeding, the present study sought to determine whether 8-OH-DPAT would enhance feeding induced by infusing NE into the medial hypothalamus. All experiments were conducted using ad libitum-fed adult male rats with two indwelling cannulas, one aimed at the paraventricular nucleus (PVN), the other at either the dorsal or median raphe. In the first series of experiments rats received a fixed dose of 8-OH-DPAT (0.8 nmol) microinjected into the dorsal or median raphe, as well as NE (0, 10, 20 nmol) administered into the PVN. In the second series, rats received varying doses of raphe 8-OH-DPAT (0, 0.4, 0.8 nmol) coinjected with a single dose of PVN NE (20 nmol). Results indicated that 8-OH-DPAT and NE both elicited reliable increases in 1-h food intake, although their effects did not interact. In the final series, rats were injected with subthreshold doses of both compounds. While combined injections of 8-OH-DPAT and NE modestly increased feeding compared with saline control, this increase was not significantly greater than intake found after injection of 8-OH-DPAT or NE alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Past research has suggested that the paraventricular nucleus (PVN) of the hypothalamus is an important brain site mediating changes in feeding induced by drugs that modify 5-hydroxytryptamine (5-HT; serotonin) neurotransmission. To test this possibility, several experiments examined the impact of lesions of the PVN on both decreases and increases in feeding following treatment with 5-HT-acting drugs. Rats with free access to standard lab chow were given access also to a wet mash diet for 1 h each day. When intakes of this diet had stabilised, rats were divided into two groups: one group received bilateral radiofrequency lesions of the PVN, the other served as a sham-operated control group. The PVN-lesioned group consumed more lab chow and gained significantly more weight over a 10-week period than the control group. Clonidine stimulated feeding in the sham-operated group, but did not do so in the lesioned group. These findings confirmed that the PVN lesions disrupted the control of food intake, as well as body weight regulation. The indirect 5-HT agonists D-fenfluramine (0.63, 1.25 and 2.5 mg/kg) and fluoxetine (2.5, 5 and 10 mg/kg), and the 5-HT1 agonist 1-(m-trifluoromethylphenyl)piperazine (TFMPP, 0.63, 1.25 and 2.5 mg/kg) dose dependently reduced the intake of the wet mash diet in sham-operated animals. This action was not modified by the PVN lesions. The highest doses of D-fenfluramine and fluoxetine also suppressed intake of chow over the 23-h period subsequent to the wet mash presentations, but the magnitude of this effect was similar in sham-operated and PVN-lesioned animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous work has shown that injection of the 5-hydroxytryptamine (5-HT)1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) into the midbrain raphe nuclei activates somatodendritic 5-HT autoreceptors leading to decreased 5-HT synthesis and release in terminal forebrain regions and an increase in feeding behaviour. Since 5-HT is believed to function antagonistically with norepinephrine (NE) in the hypothalamic paraventricular nucleus (PVN) to control feeding, it has been proposed that 8-OH-DPAT elicits food intake by removing the inhibitory influence of 5-HT over PVN alpha 2-adrenergic feeding mechanisms. This hypothesis was tested by examining the ability of PVN injection of the alpha 2-adrenoceptor antagonist idazoxan (IDAZ) to attenuate the feeding stimulant action induced by raphe injection of 8-OH-DPAT. In the first series of experiments the dose-response effects of dorsal and median raphe injection of 8-OH-DPAT in addition to PVN NE on feeding were examined. Injection of NE (5-40 nmol) and 8-OH-DPAT (0.4-1.6 nmol) both elicited reliable dose-dependent increases in 1 h food intake compared to saline control. Similar doses of 8-OH-DPAT injected into the PVN failed to alter baseline feeding. A second series of experiments examined the effects of IDAZ on 8-OH-DPAT and NE-stimulated food intake in rats implanted with dorsal or median raphe cannulae as well as cannulae aimed at the PVN.(ABSTRACT TRUNCATED AT 250 WORDS)

Central monoaminergic neurotransmitters have been implicated in the control of food intake in different animal species but it remains unclear whether these same neurochemical systems effectively regulate feeding behaviour in the genetically obese (ob/ob) mouse. Neuropharmacological studies have demonstrated, for example, that microinjection of norepinephrine can elicit a reliable feeding response in the rat, particularly at dark onset. The present study was therefore designed to examine the impact of central injection of norepinephrine (20-160 nmol) and clonidine (5-80 nmol), an alpha 2-adrenoceptor agonist, on food intake in ob/ob mice and lean (+/?) controls. Presatiated obese and lean mice were injected with norepinephrine or clonidine immediately prior to the onset of the dark cycle. Food intake (kcal) was measured 1 h postinjection. Obese mice ingested more food than lean mice under baseline saline conditions. Injection of norepinephrine and clonidine increased eating in both phenotypes, although the ob/ob showed an enhanced feeding response to norepinephrine and clonidine administration. Intracerebroventricular pretreatment with the alpha 2-adrenoceptor antagonist yohimbine (12.5-50 nmol) significantly attenuated the increase in food intake observed in response to central injection of norepinephrine (40 nmol) and clonidine (10 nmol). However, the alpha 1-adrenoceptor antagonist corynanthine (15-60 nmol) or the beta-adrenoceptor antagonist propranolol (25-100 nmol) failed to alter noradrenergic feeding. These results suggest that modification of central alpha 2-noradrenergic function can alter natural feeding in mice, and that the ob/ob is particularly sensitive to this effect.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of central injection of norepinephrine (NE), clonidine (CLON), and 5-hydroxytryptamine (5-HT) on feeding and macronutrient selection in genetically obese (C57B1/6J, ob/ob) and lean mice (C57B1/6J, +/?) were examined. Mice were adapted to single-energy source diets of carbohydrate, protein, and fat and then injected with NE (20-80 nmol) or CLON (5-20 nmol) immediately prior to dark onset (17h00). Measurements of nutrient intake were determined 2 h postinjection. In a separate study, obese and lean mice were deprived of food for 1 h (1700-1800) and subsequently treated with 5-HT (35-140 nmol). The results of this study demonstrate that the hyperphagic effect of NE and CLON and the anorectic effect of 5-HT are dose dependent and nutrient selective. Specifically, at the onset of the nocturnal cycle, obese and lean mice exhibit a shift in diet choice resulting in an increased preference for carbohydrate and a reduction in the proportional intake of protein and fat. At this time, central injection of NE or CLON potentiates an already enhanced preference for carbohydrate; whereas injection of 5-HT suppresses carbohydrate intake (kcal) in both phenotypes without altering fat or protein intake. However, in comparison to lean mice, obese mice showed significantly augmented hyperphagic responses to NE and CLON administration but decreased inhibition of feeding after 5-HT injection. This suggests that the stimulatory effect of alpha 2-noradrenergic mechanisms controlling feeding and carbohydrate ingestion is enhanced in obese mice, while the inhibitory influence of serotonergic mechanisms is attenuated.

Biochemical abnormalities in the hypothalamus of the genetically obese (C57B1/6J, ob/ob) mouse, including increased levels of endogenous norepinephrine (NE) in the paraventricular nucleus (PVN) and reduced medial hypothalamic NE metabolism, have been cited as evidence of a CNS defect contributing to altered caloric intake in this genetic strain. In the current study, the alpha 2-antagonist yohimbine (YOH) and the alpha 2-agonist clonidine (CLON) were administered systemically to 6-h meal-feeding obese and lean mice. Yohimbine (3-5 mg/kg, IP) significantly reduced total energy intake and intake of carbohydrate and fat, in both phenotypes, without altering protein intake. In contrast, CLON (25 micrograms/kg, IP) potentiated feeding, resulting in a shift in macronutrient selection toward a significant increase in the proportional intake of carbohydrate. Obese mice, however, showed an enhanced behavioral response to CLON injection. Pretreatment with 1 mg/kg YOH, a dose that alone did not significantly alter energy intake or diet selection, blocked CLON's stimulatory effect on feeding and carbohydrate preference. These results are consistent with a role for alpha 2-noradrenergic receptors in appetite regulation of ob/ob and lean mice and suggest that disturbances in this system may be involved in the development of genetic obesity.

Hypothalamic noradrenergic mechanisms contribute to altered caloric intake in genetically obese (C57BL/6J, ob/ob) mice. Noradrenergic mechanisms, principally in the paraventricular hypothalamus and of the alpha 2 subtype, have also been implicated in the macronutrient intake regulation of nonpathological models. Accordingly, this study assessed the extent to which clonidine, an alpha 2 agonist, altered macronutrient intake in genetically obese (ob/ob) and lean (C57BL/6J, +/?) mice. Following adaptation to a 6-h feeding regimen, mice were injected intraperitoneally with either clonidine (0.1, 0.5 mg/kg) or 0.15 M NaCl (Experiment 1) or 0.025 mg/kg clonidine or saline (Experiment 2) 30 min prior to simultaneous access to separate sources of carbohydrate, fat, and protein. Clonidine doses of 0.1 mg/kg or greater reduced total energy intake and intake of carbohydrate and fat (p less than 0.005) in all mice (Experiment 1). However, 0.025 mg/kg clonidine selectively increased ingestion of carbohydrate in obese mice by 212% of vehicle-injected values (p less than 0.001) without altering intake in lean mice (Experiment 2). These results implicate an alpha 2 receptor mechanism in genetic obesity.