Conditions Of Food Deprivation Research Articles

Feeding behaviour after injection of α-adrenergic receptor agonists into the median raphe nucleus of food-deprived rats

This study investigated the participation of median raphe nucleus (MnR) α1-adrenergic receptors in the control of feeding behaviour. The α1-adrenergic agonist phenylephrine (PHE) and α2-adrenergic agonist clonidine (CLON) (at equimolar doses of 0, 6 and 20nmol) were injected into the MnR of: a) rats submitted to overnight fasting (18h); or b) rats maintained with 15g of lab chow/day for 7days. Immediately after the drug injections, the animals were placed in the feeding chamber and feeding and non-ingestive behaviours such as grooming, rearing, resting, sniffing and locomotion were recorded for 30min. The results showed that both doses of PHE injected into the MnR of overnight fasted animals decreased food intake accompanied by an increase in the latency to start feeding. A reduction in feeding duration was observed only after treatment of the MnR with the 20nmol dose of PHE. Both locomotion duration and sniffing frequency increased after injection with the highest dose PHE into the MnR. Feeding frequency and the other non-ingestive behaviours remained unchanged after PHE treatment in the MnR. Both doses of PHE injected into the MnR of food-restricted rats decreased food intake. This hypophagic response was accompanied by a decrease in feeding duration only after treatment of the MnR with the highest dose of PHE. The latency to start feeding and feeding frequency were not affected by injection of either dose of PHE into the MnR. While both doses of PHE increased sniffing duration, the highest dose of PHE increased resting duration and resting frequency. Treatment with CLON into the MnR did not affect feeding behaviour in either of the food deprivation conditions. The present results indicate the inhibitory functional role of α1-adrenergic receptors within the MnR on feeding behaviour.

Endocannabinoids Gate State-Dependent Plasticity of Synaptic Inhibition in Feeding Circuits

Changes in food availability alter the output of hypothalamic nuclei that underlie energy homeostasis. Here, we asked whether food deprivation impacts the ability of GABA synapses in the dorsomedial hypothalamus (DMH), an important integrator of satiety signals, to undergo activity-dependent changes. GABA synapses in DMH slices from satiated rats exhibit endocannabinoid-mediated long-term depression (LTD(GABA)) in response to high-frequency stimulation of afferents. When CB1Rs are blocked, however, the same stimulation elicits long-term potentiation (LTP(GABA)), which manifests presynaptically and requires heterosynaptic recruitment of NMDARs and nitric oxide (NO). Interestingly, NO signaling is required for eCB-mediated LTD(GABA). Twenty-four hour food deprivation results in a CORT-mediated loss of CB1R signaling and, consequently, GABA synapses only exhibit LTP(GABA). These observations indicate that CB1R signaling promotes LTD(GABA) and gates LTP(GABA). Furthermore, the satiety state of an animal, through regulation of eCB signaling, determines the polarity of activity-dependent plasticity at GABA synapses in the DMH.

Differences between the anorexic actions of amphetamine and fenfluramine--possible effects on hunger and satiety.

The inhition of feeding in rats brought about by amphetamine and fenfluramine was continuously monitored for periods of up to 24 h using a pellet detecting eatometer. For rats tested under conditions of food deprivation the two drugs gave rise to distinctive anorexic profiles: amphetamine delayed the onset of eating whereas fenfluramine allowed eating to commence normally but brought about an early termination of the initial bout of feeding. When the drugs were administrated to rats with free access to food, analysis of the meal pattern showed that amphetamine gave rise to a small increase in the inter-meal interval while fenfluramine brought about a clear reduction tion in meal size. It is suggested that the contrasting modes of action of these drugs represent an effect of amphetamine upon hunger and an action of fenfluramine on satiety. This suggestion is in keeping with the proposed mechanisms of action of these drugs, amphetamine acting upon a hpothalamic motivational system and fenfluramine acting by means of a postulated serotoninergic satiety system. Use of the continuous monitoring technique has pointed pointed to certain limitations in the assessment of anorexic drug action by means of discrete food sampling periods.

The selfish brain: Competition for energy resources

Obesity and type 2 diabetes have become the major health problems in many industrialized countries. Here, I present the unconventional concept that a healthy organism maintains its systemic homeostasis by a "competent brain-pull", i.e., the brain's ability to properly demand glucose from the body, and that the underlying cause of obesity is "incompetent brain-pull." I describe the energy fluxes from the environment, through the body, toward the brain as the final consumer in a "supply chain" model. There is data-based support for the hypothesis, which states that under conditions of food abundance incompetent brain-pull will lead to build ups in the supply chain culminating in obesity and type 2 diabetes. There is also support for the related hypothesis, which states that under conditions of food deprivation, a competent brain-pull mechanism is indispensable for the continuation of the brain's high energy level. To experimentally determine how the competent brain-pull functions to demand for cerebral energy, healthy young men undergoing psychosocial stress were studied. It was found that the brain under stressful conditions demands for energy from the body by using a brain-pull mechanism, which is referred to as "cerebral insulin suppression" and in so doing it can satisfy its excessive needs during stress. This article gives an overview about the recent work on the "Selfish Brain" theory dealing with the maintenance of the cerebral and peripheral energy homeostasis.

External incentives and internal states guide goal-directed behavior via the differential recruitment of the nucleus accumbens and the medial prefrontal cortex

Goal-directed behavior is governed by internal physiological states and external incentives present in the environment (e.g. hunger and food). While the role of the mesocorticolimbic dopamine (DA) system in behavior guided by environmental incentives has been well studied, the effect of relevant physiological states on the function of this system is less understood. The current study examined the role of the medial prefrontal cortex (mPFC) and the nucleus accumbens (NAcc) in the kind of food-reinforced behaviors known to be sensitive to the internal state produced by food deprivation conditions. Operant lever-press reinforced on fixed ratio 1 (FR1) and progressive ratio (PR) schedules was tested after temporary inactivation of, or DA receptor blockade in, the prelimbic mPFC or NAcc core of rats with differing levels of food deprivation (0, 12 and 36-h). Food deprivation increased PR breakpoints, as well as the number of lever-presses emitted on the FR1 schedule. Both temporary inactivation and DA blockade of NAcc reduced breakpoints across deprivation conditions, while temporary inactivation and DA blockade of mPFC reduced breakpoints only in food-deprived rats. Neither manipulation of mPFC and NAcc had any effect on behavior reinforced on the FR1 schedule. Thus, mPFC and NAcc were differentially relevant to the behaviors tested–NAcc was recruited when the behavioral cost per reinforcer was rising or high regardless of food deprivation conditions, while mPFC was recruited when food-deprived animals behaved through periods of sparse reinforcement density in order to maximize available gain.

The Anorexigenic Neuropeptide, Nesfatin-1, Is Indispensable for Normal Puberty Onset in the Female Rat

The hypothalamic peptide, nesfatin-1, derived from the precursor NEFA/nucleobindin 2 (NUCB2), was recently identified as anorexigenic signal, acting in a leptin-independent manner. Yet its participation in the regulation of other biological functions gated by body energy status remains unexplored. We show herein that NUCB2/nesfatin-1 is involved in the control of female puberty. NUCB2/nesfatin mRNA and protein were detected at the hypothalamus of pubertal female rats, with prominent signals at lateral hypothalamus (LHA), paraventricular (PVN), and supraoptic (SON) nuclei. Hypothalamic NUCB2 expression raised along pubertal transition, with detectable elevations of its mRNA levels at LHA, PVN, and SON, and threefold increase of its total protein content between late-infantile and peripubertal periods. Conditions of negative energy balance, such as 48 h fasting or sustained subnutrition, decreased hypothalamic NUCB2 mRNA and/or protein levels in pubertal females. At this age, central administration of nesfatin-1 induced modest but significant elevations of circulating gonadotropins, whose magnitude was notably augmented in conditions of food deprivation. Continuous intracerebroventricular infusion of antisense morpholino oligonucleotides (as-MONs) against NUCB2 along pubertal maturation, which markedly reduced hypothalamic NUCB2 protein content, delayed vaginal opening and decreased ovarian weights and serum luteinizing hormone (LH) levels. In contrast, in adult female rats, intracerebroventricular injection of nesfatin did not stimulate LH or follicle-stimulating hormone secretion; neither did central as-MON infusion alter preovulatory gonadotropin surges, despite suppression of hypothalamic NUCB2. In sum, our data are the first to disclose the indispensable role of NUCB2/nesfatin-1 in the central networks driving puberty onset, a function that may contribute to its functional coupling to energy homeostasis.

Local Agouti Signaling Protein/Melanocortin Signaling System that Possibly Regulates Lipid Metabolism in Adipose Tissues of Chickens

The agouti signaling protein (ASIP)/melanocortin signaling system regulates lipid metabolism in humans but not in mice. To examine whether the system is present in adipose tissues in chickens, we performed reverse transcription-polymerase chain reaction (RT-PCR) analysis using mRNAs extracted from subcutaneous and visceral adipose tissues. This revealed that mRNAs for melanocortin 1 receptor (MC1R), MC5R, ASIP, pro-opiomelanocortin (POMC), prohormone convertase 1 (PC1) and PC2 were expressed in both adipose tissues, suggesting the presence of a local ASIP/melanocortin signaling system in these tissues in chickens. To investigate the potential biological role of this system, the adipose tissue mRNA expression of ASIP and POMC was examined under food-deprived conditions. Forty-eight-hour fasting significantly decreased body weight and reduced the cell size in adipose tissues. In addition, the plasma levels of free fatty acids were increased while those of glucose, triacylglycerols and insulin were decreased, suggesting the activation of lipolysis and gluconeogenesis in the fasted chickens. Under this condition, the mRNA expression of ASIP and POMC was decreased and increased, respectively, in subcutaneous and visceral adipose tissues. ASIP and melanocortins are lipogenic and lipolytic hormones, respectively. Therefore, these findings suggest that lipid metabolism in the adipose tissues is regulated by a local ASIP/melanocortin signaling system in chickens. This is the first report demonstrating changes in the expression of ASIP mRNA in adipose tissues in the negative-energy state in vertebrates.

Selfish Brain and the field of research on ingestive behaviour

Event Abstract Back to Event Selfish Brain and the field of research on ingestive behaviour Achim Peters1* 1 University of Luebeck, Medical Clinic 1, Germany Obesity and type 2 diabetes have become the major health problems in many industrialized countries. A few theoretical frameworks have been set up to derive the possible determinative cause of obesity. One concept views that food availability determines food intake, i.e. that obesity is the result of an external energy “push” into the body. Another one views that the energy milieu within the human organism determines food intake, i.e. that obesity is due to an excessive “pull” from inside the organism. Here we present the unconventional concept that a healthy organism is maintained by a “competent brain-pull” which serves systemic homeostasis, and that the underlying cause of obesity is “incompetent brain-pull”, i.e. that the brain is unable to properly demand glucose from the body. We describe the energy fluxes from the environment, through the body, towards the brain with a mathematical “supply chain” model and test whether its predictions fit medical and experimental data sets from our and other research groups. In this way, we show data-based support of our hypothesis, which states that under conditions of food abundance incompetent brain-pull will lead to build-ups in the supply chain culminating in obesity and type 2 diabetes. In the same way, we demonstrate support of the related hypothesis, which states that under conditions of food deprivation a competent brain-pull mechanism is indispensable for the continuance of the brain´s high energy level. To experimentally determine how the competent brain-pull functions to demand for cerebral energy, 40 healthy young men undergoing psychosocial stress were studied. We found that stress increased carbohydrate intake from a rich buffet by 34.3 gram. While these stress-extra carbohydrates increased blood glucose concentrations, they did not increase serum insulin concentrations. The ability to suppress insulin secretion was found to be linked to the sympatho-adrenal stress-response. Thus, exogenous energy supply was shown to counteract a neuroglycopenic state that developed during exposure to stress. In this way, the brain under stressful conditions demands for energy from the body by using a brain-pull mechanism, which we refer to as ‘cerebral insulin suppression’ and in so doing it can satisfy its excessive needs during stress. In conclusion, we took the viewpoint of integrative physiology and provided evidence how brain-pull functions and that its proper functioning is necessary for the benefit of health. Along these lines, our work supports recent molecular findings from the field of neuroenergetics and continues the work on the “Selfish Brain” theory dealing with the maintenance of the cerebral and peripheral energy homeostasis. Conference: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour, 23554 Luebeck, Germany, 27 May - 28 May, 2010. Presentation Type: Oral Presentation Topic: Talks Citation: Peters A (2010). Selfish Brain and the field of research on ingestive behaviour. Front. Neurosci. Conference Abstract: 2nd Selfish Brain Conference New research on the neurobiology of ingestive behaviour. doi: 10.3389/conf.fnins.2010.08.00001 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 12 Apr 2010; Published Online: 12 Apr 2010. * Correspondence: Achim Peters, University of Luebeck, Medical Clinic 1, Luebeck, Germany, Achim.peters@uksh.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Achim Peters Google Achim Peters Google Scholar Achim Peters PubMed Achim Peters Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

In VivoRole of a Potassium Channel-Binding Protein in Regulating Neuronal Excitability and Behavior

Molecular details of ion channel interactions with modulatory subunits have been investigated widely in transfected cells, but the physiological roles of ion channel modulatory protein complexes in native neurons remain largely unexplored. The Drosophila large-conductance calcium-activated potassium channel (dSlo) binds to and is modulated by its binding partner Slob. We have constructed flies in which Slob expression is manipulated by P-element mutagenesis, or by transgenic expression of Slob protein or Slob-RNAi. In vivo recordings of both macroscopic and single dSlo channel currents in identified neurosecretory neurons in the pars intercerebralis (PI) region of the Drosophila brain reveal that whole-cell potassium current and properties of single dSlo channels are modulated by Slob expression level. Furthermore, Slob genotype influences action potential duration in vivo. This unprecedented combination of current-clamp, macroscopic-current, and single-channel recordings from neurons in brains of living flies defines a critical role for an ion channel modulatory protein complex in the control of neuronal excitability. We show further that Slob-null flies exhibit significantly longer lifespan than controls under conditions of complete food deprivation. Crosses with deficiency lines demonstrate that this enhanced resistance to starvation-induced death maps close to the slob locus. Together, these results indicate that Slob may serve a novel regulatory function in feeding behavior, possibly by influencing the excitability of the PI neurons.

Expression of brush border enzymes and transporters in the intestine of European sea bass ( Dicentrarchus labrax) following food deprivation

Studies on aquacultured fish nutrition have focused solely on performance and the activity of the brush-border enzymes, while the molecular aspects have barely been addressed. Nevertheless, the expression of genes encoding enzymes and transporters of the brush-border membrane is crucial for the final stages of digestion and absorption of nutrients through the epithelial luminal membrane of the intestine. To establish a molecular tool for such studies, primers for the European sea bass intestinal genes were designed utilizing evolutionarily conserved DNA sequences for the following intestinal enzymes and transporters: maltase, APN, PepT1 and Na +/K +-ATPase. The derived European sea bass cDNA fragments showed 64–92% homology to other animal species and enabled us to study the differences in their expression. The mRNA expression of these genes in pyloric caeca and the upper and lower intestinal sections were compared in fed fish vs conditions of food deprivation for 3, 7, 14 and 21 days. The mRNA expression examined using real time PCR of APN, maltase and PepT1 in all the intestinal tract sections, was the highest after 7 days of food deprivation. Na +/K +-ATPase showed a different pattern of expression in each section of the intestine. Significant positive linear correlations between APN, maltase and PepT1 mRNA expression were detected in all but day 3 post food deprivation. The cDNA fragments isolated in this study provide a novel molecular tool for revealing new aspects in fish nutrition and can provide additional information regarding the pattern of expression of intestinal genes following long-term fasting in fish.

Build-ups in the supply chain of the brain: on the neuroenergetic cause of obesity and type 2 diabetes mellitus.

Obesity and type 2 diabetes have become the major health problems in many industrialized countries. A few theoretical frameworks have been set up to derive the possible determinative cause of obesity. One concept views that food availability determines food intake, i.e. that obesity is the result of an external energy “push” into the body. Another one views that the energy milieu within the human organism determines food intake, i.e. that obesity is due to an excessive “pull” from inside the organism. Here we present the unconventional concept that a healthy organism is maintained by a “competent brain-pull” which serves systemic homeostasis, and that the underlying cause of obesity is “incompetent brain-pull”, i.e. that the brain is unable to properly demand glucose from the body. We describe the energy fluxes from the environment, through the body, towards the brain with a mathematical “supply chain” model and test whether its predictions fit medical and experimental data sets from our and other research groups. In this way, we show data-based support of our hypothesis, which states that under conditions of food abundance incompetent brain-pull will lead to build-ups in the supply chain culminating in obesity and type 2 diabetes. In the same way, we demonstrate support of the related hypothesis, which states that under conditions of food deprivation a competent brain-pull mechanism is indispensable for the continuance of the brain´s high energy level. In conclusion, we took the viewpoint of integrative physiology and provided evidence for the necessity of brain-pull mechanisms for the benefit of health. Along these lines, our work supports recent molecular findings from the field of neuroenergetics and continues the work on the “Selfish Brain” theory dealing with the maintenance of the cerebral and peripheral energy homeostasis.

Endogenous nociceptin modulates diet preference independent of motivation and reward

Previous studies show that the opioid peptide nociceptin stimulates food intake. Here, we studied nociceptin receptor knockout (NOP KO) mice in various behavioral paradigms designed to differentiate psychological and physiological loci at which endogenous nociceptin might control feeding. When presented a choice under food restriction, NOP KO mice displayed reduced preference for high sucrose diet, but lower intake of high fat diet under no-choice conditions. These responses were absent under ad libitum feeding conditions. Conditioned place preference to high fat diet under food-deprived conditions was unaltered in NOP KO mice, suggesting no difference in reward responses. Furthermore, operant food self-administration under a variety of conditions showed no genotype-dependent differences, suggesting no differences in the motivational properties of food. Taste reactivity to sucrose was unchanged in NOP KO mice, though NOP KO mice had altered aversive reactions to quinine solutions under ad libitum feeding, suggesting minor differences in the affective impact of palatable and unpalatable tastants. Although NOP KO mice re-fed following food-deprivation showed normal increases in plasma glucose and insulin, multidimensional scaling analysis showed that the relationship between these measures, body weight and plasma leptin was substantially disrupted in NOP KO, particularly in fasted mice. Additionally, the typical positive relationship between body weight and plasma leptin was considerably weaker in NOP KO mice. Together, these findings suggest that endogenous nociceptin differentially modulates diet preference depending on macronutrient content and homeostatic state, independently of the motivating, rewarding or orosensory properties of food, but may involve metabolic or postingestive processes.

Nutritional benefits of filial cannibalism in three-spined sticklebacks (Gasterosteus aculeatus)

Although filial cannibalism (eating one's own offspring) occurs in numerous species, including several teleost fishes, its adaptive value is still not well understood. One often-discussed explanation is that individuals enhance their mass and body condition by consuming part of their eggs. However, evidence for this assumption is scarce thus far. In this study, male three-spined sticklebacks (Gasterosteus aculeatus), a species with paternal care, were allowed to care for a batch of eggs or for an empty nest under food-deprived conditions. All brood-caring males cannibalised at least part of their eggs and thus preserved their initial mass and body condition. Furthermore, mass as well as body condition was significant positively correlated with the number of cannibalised eggs. In contrast, empty-nest males that had no possibility to cannibalise eggs significantly lost mass and body condition. This is, to our knowledge, the first experimentally documented evidence that mass as well as body condition were preserved by filial cannibalism.

NaCl preference and water intake effects of food availability in median eminence polydipsia

Lesions in the median eminence (ME) produce a well-known neurological model of polydipsia and polyuria in rats. The effect of food availability ( ad lib/deprivation) on the polydipsic/polyuric behaviour of animals was tested. As expected, all lesioned rats developed strong polyuria and polydipsia during the first postoperative 24 h. This effect was maintained during day 2 when food was available ad lib (experiment A), but both polyuria and polydipsia were abolished when animals were deprived of food during the next 24 h (day 3). Animals deprived of food from the first post-operative day (experiment B) showed a significant reduction in the initial polyuria and polydipsia (day 1) on day 2, but these effects were again observed on day 3 when food was available ad lib. Finally, when food-deprived animals were able to choose between a 1.5% sodium chloride solution and water (experiment C), they preferentially chose (82% of total liquid consumed) the hypertonic saline solution (day 1); during the next 24 h (day 2), when only water was available, the polyuric/polydipsic effect was abolished but returned when food became available ad lib on day 3. Hence, the polyuria/polydipsia effect produced by ME lesions appears to be consistent during the first 24 h but might later be related to the availability of standard food and is completely abolished under food deprivation conditions. Preference for the hypertonic solution supports the volemic component of this syndrome and demonstrates the need for appropriate amounts of hypertonic nutrients to be consumed during the first 24 h.

Leptin receptor deficiency is associated with upregulation of cannabinoid 1 receptors in limbic brain regions

Leptin receptor dysfunction results in overeating and obesity. Leptin regulates hypothalamic signaling that underlies the motivation to hyperphagia, but the interaction between leptin and cannabinoid signaling is poorly understood. We evaluated the role of cannabinoid 1 receptors (CB(1)R) in overeating and the effects of food deprivation on CB(1)R in the brain. One-month-old Zucker rats were divided into unrestricted and restricted (fed 70% of unrestricted rats) diet groups and maintained until adulthood (4 months). Levels of relative binding sites of CB(1)R (CB(1)R binding levels) were assessed using [(3)H] SR141716A in vitro autoradiography. These levels were higher (except cerebellum and hypothalamus) at 4 months than at 1 month of age. One month CB(1)R binding levels for most brain regions did not differ between Ob and Lean (Le) rats (except in frontal and cingulate cortices in Le and in the hypothalamus in Ob). Four month Ob rats had higher CB(1)R binding levels than Le in most brain regions and food restriction was associated with higher CB(1)R levels in all brain regions in Ob, but not in Le rats. CB(1)R binding levels increased between adolescence and young adulthood which we believe was influenced by leptin and food availability. The high levels of CB(1)R in Ob rats suggest that leptin's inhibition of food-intake is in part mediated by downregulation of CB(1)R and that leptin interferes with CB(1)R upregulation under food-deprivation conditions. These results are consistent with prior findings showing increased levels of endogenous cannabinoids in the Ob rats corroborating the regulation of cannabinoid signaling by leptin.

The effect of food deprivation on cigarette smoking in females

Food deprivation is associated with increased self-administration of nicotine and other substances in laboratory animals, although little is known about the effects of food deprivation on substance use in humans. A within-subjects design was utilized to test the primary hypotheses that smoking rate and expired carbon monoxide (CO) levels would be greater among 15 female participants following a 24-hour fasting period than when participants were not food-deprived. Food-deprived participants were also expected to endorse greater negative mood, smoking urges, and pleasure from smoking, as well as less positive mood. Analyses indicated that CO levels were significantly greater in the food-deprived condition than in the non-deprived condition ( p = .05), although no differences were found in the number of cigarettes smoked during the laboratory session. Participants reported significantly lower Vigor–Activity in the food-deprived condition ( p = .02). No differences were found between conditions in urges to smoke or pleasure from smoking. Findings suggest that nicotine intake may increase among females during acute food deprivation.

Oral THC produces minimal behavioral alterations in preadolescent rats

Although the oral route has traditionally been used for THC administration during the perinatal period in the rat, most studies administering THC during the postnatal period utilize intraperitoneal (ip) administration. In an effort to utilize the same route of administration in both prenatal and postnatal studies, we administered Δ-9-tetrahydrocannabinol (THC) in sesame oil by gavage during postnatal days 22–40 (equivalent to childhood to early adolescence) to male and female rats. We quantified behavior 40 min after administration in the Accuscan activity monitor on days 22, 29 and 40. In addition, we examined active and passive avoidance behaviors in treated adults. Acutely, THC had subtle effects on activity when measured during the period of drug administration and minimal effects on avoidance behaviors examined up to 140 days of age. Since several groups have found that lower doses of THC administered intraperitoneally to periadolescent rats do produce behavioral alterations, we suspect that the inordinately slow absorption of the drug via the oral route may be responsible for the paucity of significant findings in our study. Therefore, oral administration of THC, particularly under conditions of mild food deprivation, may lead to sub-psychoactive concentrations of the drug within the brain.

Food Deprivation Attenuates Seizures through CaMKII and EAG K+ Channels

Accumulated research has demonstrated the beneficial effects of dietary restriction on extending lifespan and increasing cellular stress resistance. However, reducing nutrient intake has also been shown to direct animal behaviors toward food acquisition. Under food-limiting conditions, behavioral changes suggest that neuronal and muscle activities in circuits that are not involved in nutrient acquisition are down-regulated. These dietary-regulated mechanisms, if understood better, might provide an approach to compensate for defects in molecules that regulate cell excitability. We previously reported that a neuromuscular circuit used in Caenorhabditis elegans male mating behavior is attenuated under food-limiting conditions. During periods between matings, sex-specific muscles that control movements of the male's copulatory spicules are kept inactive by UNC-103 ether-a-go-go–related gene (ERG)–like K+ channels. Deletion of unc-103 causes ∼30%–40% of virgin males to display sex-muscle seizures; however, when food is deprived from males, the incidence of spontaneous muscle contractions drops to 9%–11%. In this work, we used genetics and pharmacology to address the mechanisms that act parallel with UNC-103 to suppress muscle seizures in males that lack ERG-like K+ channel function. We identify calcium/calmodulin-dependent protein kinase II as a regulator that uses different mechanisms in food and nonfood conditions to compensate for reduced ERG-like K+ channel activity. We found that in food-deprived conditions, calcium/calmodulin-dependent protein kinase II acts cell-autonomously with ether-a-go-go K+ channels to inhibit spontaneous muscle contractions. Our work suggests that upregulating mechanisms used by food deprivation can suppress muscle seizures.

Effect of Biotic and Abiotic Factors on In Vitro Proliferation, Encystment, and Excystment of Pfiesteria piscicida

Pfiesteria spp. are mixotrophic armored dinoflagellates populating the Atlantic coastal waters of the United States. They have been a focus of intense research due to their reported association with several fish mortality events. We have now used a clonal culture of Pfiesteria piscicida and several new environmental isolates to describe growth characteristics, feeding, and factors contributing to the encystment and germination of the organism in both laboratory and environmental samples. We also discuss applied methods of detection of the different morphological forms of Pfiesteria in environmental samples. In summary, Pfiesteria, when grown with its algal prey, Rhodomonas sp., presents a typical growth curve with lag, exponential, and stationary phases, followed by encystment. The doubling time in exponential phase is about 12 h. The profiles of proliferation under a standard light cycle and in the dark were similar, although the peak cell densities were markedly lower when cells were grown in the dark. The addition of urea, chicken manure, and soil extracts did not enhance Pfiesteria proliferation, but crude unfiltered spent aquarium water did. Under conditions of food deprivation or cold (4 degrees C), Pfiesteria readily formed harvestable cysts that were further analyzed by PCR and scanning electron microscopy. The germination of Pfiesteria cysts in environmental sediment was enhanced by the presence of live fish: dinospores could be detected 13 to 15 days earlier and reached 5- to 10-times-higher peak cell densities with live fish than with artificial seawater or f/2 medium alone. The addition of ammonia, urea, nitrate, phosphate, or surprisingly, spent fish aquarium water had no effect.

Honest begging in the blue-footed booby: signaling food deprivation and body condition

To determine whether solicitation by blue-footed booby chicks accurately encodes their need for food, we independently manipulated the body condition and recent food ingestion of singleton chicks and recorded three measures of begging. Variations in the three measures of begging covaried only partially, but in general, chicks begged more intensely when they were in poor body condition and also when suffering recent food deprivation. Effects of body condition and recent food deprivation on begging were broadly additive, although deprived chicks in poor condition failed to beg more intensely than those in good condition. Protracted short-term deprivation may create such a high level of need that the body condition component of need becomes temporarily unimportant. Parents more frequently fed chicks that begged more intensely, chicks in poor condition, and chicks suffering food deprivation. Deprived chicks in poor condition received more food than deprived chicks in normal condition even though they did not beg more intensely, possibly because parents responded not only to current begging but also to begging earlier in the day, or to other cues to body condition. These results support the hypothesis that begging of boobies represents honest signaling of need.