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PubMed1984

Influence of naloxone on the effects of LSD in monkeys.

Three stump-tailed monkeys were trained in an appetitive behavioral task. Administration of 0.1 mg/kg of lysergic acid diethylamide (LSD) moderately disrupted performance acutely, and produced abnormal motor activity. With repeated administration of LSD, motor activity and task responding returned to normal. When 1.0 mg/kg of naloxone was administered prior to administration of LSD in a crossover design, appetitive responding was abolished acutely in all animals and behavior was substantially more disrupted than with LSD alone. Tolerance did not occur with repeated administration of this combination of drugs. Endorphins and/or opiate receptors may act to attenuate the effects of hallucinogenic agents, and may subserve the development of tolerance to these effects.

Animals↗

PubMed1985

A neural theory of circadian rhythms: split rhythms, after-effects and motivational interactions.

A neural theory of the circadian pacemaker within the hypothalamic suprachiasmatic nuclei (SCN) is used to explain parametric data about mammalian operant behavior. The intensity, duration, and patterning of ultradian activity-rest cycles and the duration of circadian periods due to parametric (LL) and nonparametric (LD) lighting regimes are simulated. Paradoxical data about split rhythms and after-effects are explained using homeostatic and nonhomeostatic neural mechanisms that modulate pacemaker activity. These modulatory mechanisms enable the pacemaker to adjust to pervasive changes in its lighting regime, as during the passage of seasons, and to ultradian changes in internal metabolic conditions. The model circadian mechanisms are homologous to mechanisms that model hypothalamically mediated appetitive behaviors, such as eating. The theory thus suggests that both circadian and appetitive hypothalamic circuits are constructed from similar neural components. Mechanisms of transmitter habituation, opponent feedback interactions between on-cells and off-cells, homeostatic negative feedback, and conditioning are used in both the circadian and the appetitive circuits. Output from the SCN circadian pacemaker is assumed to modulate the sensitivity of the appetitive circuits to external and internal signals by controlling their level of arousal. Both underarousal and overarousal can cause abnormal behavioral syndromes whose properties have been found in clinical data. A model pacemaker can also be realized as an intracellular system.

Animals↗

PubMed1998

Neurophysiological correlates of unconditioned and conditioned feeding behavior in the pond snail Lymnaea stagnalis.

We used a behavioral appetitive learning paradigm followed by electrophysiological analysis to investigate the neuronal expression of appetitive conditioning in Lymnaea. We first established the levels of unconditioned and conditioned feeding responses in intact animals. We then demonstrated that neuronal correlates of both unconditioned responses to touch and food and a conditioned response to touch could be found in semi-intact preparations of the same animals that had been subjected to behavioral tests and conditioning trials. In the conditioning experiments, the experimental animals received 15 trials in which touch to the lips, the conditioned stimulus (CS), was paired with sucrose, the unconditioned food stimulus (US). Control animals received 15 presentations of either CS or US, or both, applied in a random manner. After training, a strong conditioned response to touch was established in the experimental but not in the control groups. For subsequent electrophysiological analysis of posttraining neuronal responses to the touch CS, semi-intact preparations were set up from the same animals that had been behaviorally conditioned or subjected to control procedures. Intracellular recordings, made from previously identified motoneurons of the feeding system, allowed the fictive feeding response to the CS to be monitored. In experimental preparations, touch applied to the lips evoked significantly more fictive feeding cycles than in controls, and this demonstrated the existence of a neurophysiological correlate of the appetitively conditioned response observed in the whole animals.

Animals↗

PubMed1983

Behavior induced by periodic food delivery: The effects of interfood interval.

Pigeons were exposed to fixed-time schedules of food presentation ranging from five to 300 seconds. Although consistent, stereotyped response patterns developed during interfood intervals on all schedules, there were distinct differences in the behavior observed on schedules with short, as opposed to long, intervals. During the shorter intervals, responses were performed quite vigorously, a feeder-directed terminal response was observed, and most activities were localized near the feeder. On the longer schedules, no feeder-directed terminal response developed, although the birds were usually near the feeder at the end of intervals. The predominant response involved moving about the chamber, often pacing along one of the walls. Performance during short intervals is accounted for quite well by the antagonistic-motivational state hypothesis suggested by Staddon (1977); however, performance during longer intervals is not. Behavior during interfood intervals may more accurately be classified as reflecting a single (food) motivational state and described simply in terms of Craig's (1918) appetitive behavior.

Journal Article↗

PubMed1977

Hunger in humans induced by 2-deoxy-D-glucose: glucoprivic control of taste preference and food intake.

Intracellular glucopenia induced by 2-deoxy-D-glucose (2DG) administration in man produces increased hunger ratings and magnitude estimates of pleasantness for sucrose solutions. Augmented food intake substantiates these changes in affective behavior and relieves experimentally induced hunger. Intracellular glucopenia activates counterregulatory mechanisms to raise plasma glucose concentrations. Inducing hunger experimentally with 2DG provides a useful method for studying appetitive behavior in humans. The neurohumoral control of pituitary hormone release and other hypothalamic functions may be examined after 2DG infusion.

Adult↗

PubMed1994

An animal model for measuring behavioral responses to anxiogenic and anxiolytic manipulations.

A method for measuring behavioral responses of rats to both anxiolytic and anxiogenic manipulations, the open field drink test (OFDT), is described. This method utilizes the concept that in the open field, appetitive behavior is reduced because of the ambient level of fear experienced in such an environment. For the OFDT, rats were given restricted access to water for 1 h per day for 3 days, and then their behavior was assessed in an open field that contained a water spout at its center. Use of the open field permitted a number of measures to be taken; of these, "time spent drinking" was most sensitive in detecting differences. Three experiments showed that the OFDT: a) permitted dissociation between behavioral responses to an anxiolytic (diazepam) and an anxiogenic (FG7142) drug, b) detected a dose-response relationship for an anxiolytic drug (diazepam), and c) detected behavioral responses to environmental manipulations designed to increase fear (presence of an olfactory cue from rats that had received foot shock). Advantages of this test over previously described methods are outlined, and several guidelines are provided to aid investigators in using this behavioral test.

Animals↗

PubMed1997

Testosterone, preoptic dopamine, and copulation in male rats.

Steroid hormones prime neural circuits for sexual behavior, in part by regulating enzymes, receptors, or other proteins affecting neurotransmitter function. Dopamine facilitates male sexual behavior in numerous species and is released before and/or during copulation in three integrative neural systems. The nigrostriatal system enhances readiness to respond; the mesolimbic system promotes many appetitive behaviors; the medial preoptic area (MPOA) contributes to sexual motivation, genital reflexes, and copulation. We have reported a consistent relationship between precopulatory dopamine release in the MPOA, when an estrous female was behind a perforated barrier, and the ability to copulate after the barrier was removed. Recent, but not concurrent, testosterone was necessary for the precopulatory dopamine response and copulation. The deficit in MPOA dopamine release in castrates was observed in basal conditions as well as the sexual context. However, dopamine in tissue punches from castrates was higher than in intact males. Because tissue levels represent primarily stored neurotransmitter, dopamine appeared to have been synthesized normally, but was not being released. Amphetamine induced greater dopamine release in castrates, again suggesting excessive dopamine storage. The decreased release may result from decreased activity of nitric oxide synthase in the MPOA of castrates. A marker for this enzyme showed lower activity in castrates than in intact males. Finally, blocking nitric oxide synthase in intact males blocked the copulation-induced release of dopamine in the MPOA. Therefore, one means by which testosterone may promote copulation is by upregulating nitric oxide synthesis in the MPOA, which in turn enhances dopamine release.

Animals↗

PubMedDate not supplied

Effects of nerve growth factor on behavioral recovery following caudate nucleus lesions in rats.

Rats with bilateral lesions of the caudate nucleus received intracaudate injections of either nerve growth factor protein (NGF) on inert buffer immediately following surgery. NGF-treated animals demonstrated a faster recovery of normal appetitive behavior and perseverated less than their buffer-treated counterparts on a spatial reversal task, but both groups were impaired relative to sham controls on acquisition of an active avoidance response. Glia to neuron ratios were significantly increased in both lesion groups when compared with sham controls. However, this increase was less in the NGF-treated animals than in the buffer-treated animals. NGF treatment had no effect on steady-state caudate dopamine levels, measured six months after surgery.

Animals↗

PubMedDate not supplied

[Parameters of searching activity in the structure of feeding, defensive, and drinking behavior (comparative analysis)].

Searching activity (SA) is the way to satisfy the need of overcoming and the mechanism of development of all forms of behavior under conditions of deficit of pragmatic information. SA is temporarily incorporated into the structure of the initial phase of all behavioral forms. The SA has energy and cognitive components that can be measured using Grigoriev's technique and his problem box. Quantitative and qualitative characteristics of SA are of prior significance in the structure of appetitive behavior and minimal significance in the structure of drinking behavior. Under described experimental conditions, in the structure of defensive behavior the values of the SA indices are mean.

Animals↗

PubMed1979

Ontogeny of feeding controls in suckling and weanling rats.

To rationalize conflicting data in the literature, the latency of attachment of fed and fasted rat pups to the nipples of their anesthetized mother has been studied at various postnatal ages. At 10 and 14 days of age, the mode of fasting had a critical effect on the results: pups fasted in a 30 degrees C incubator had shorter attachment latencies than fed pups, whereas when pups were fasted in a 34 degrees C incubator or with a nonlactating foster mother at room temperature, their latencies were no different from those of fed pups. Thus maternal deprivation has an important influence on attachment latencies, unless other steps are taken to maintain the body temperature of fasted pups. When this variable is controlled, it is apparent that at 10 and 14 days of age, the feeding behavior of rat pups is not related to nutritional status. In contrast, from 17 days onward, latencies of fed pups were significantly longer than those of faster pups, regardless of the mode of fasting. This appearance of appetitive behavior during the 3rd postnatal wk was shown to have a temporal correlation with the beginning of weaning, as measured by the appearance of chow in the stomachs.

Animal Population Groups↗

PubMed2005

A cocaine-and-amphetamine-regulated-transcript peptide projection from the lateral hypothalamus to the ventral tegmental area.

Cocaine-and-amphetamine-regulated-transcript peptides play a role in the modulation of feeding and psychomotor stimulant-like behaviors. The ventral tegmental area and the lateral hypothalamus are likely structures where cocaine-and-amphetamine-regulated-transcript peptides mediate both of these functions. Although lateral hypothalamus inputs to the ventral tegmental area have long been known, the chemical nature of this pathway remains poorly understood. To address this issue, we tested the possibility that cocaine-and-amphetamine-regulated-transcript peptide-containing neurons in the lateral hypothalamus project to the ventral tegmental area using the retrograde transport of cholera toxin subunit B combined with cocaine-and-amphetamine-regulated-transcript peptide immunostaining. The largest density of retrogradely-labeled neurons in the hypothalamus after cholera toxin subunit B injection in the ventral tegmental area was found, ipsi- and contralaterally, in the lateral hypothalamus/perifornical area, although substantial numbers of retrogradely-labeled cells were also found in the medial preoptic area, lateral preoptic area, paraventricular nucleus, dorsomedial hypothalamus and ventromedial hypothalamus. More than 80% of the retrogradely-labeled cocaine-and-amphetamine-regulated-transcript peptide-immunoreactive neurons in the hypothalamus were found in the lateral hypothalamus/perifornical area both ipsilateral and contralateral to the injection sites. Although retrogradely-labeled neurons were seen in the amygdala, locus coeruleus, and raphe nucleus, none of them displayed cocaine-and-amphetamine-regulated-transcript peptide immunoreactivity. Therefore, the hypothalamic projection to the ventral tegmental area provides a substrate whereby cocaine-and-amphetamine-regulated-transcript peptides could mediate the rewarding aspects of feeding and psychomotor stimulant-like behaviors. These findings, combined with the fact that the lateral hypothalamus receives strong inputs from the shell of the nucleus accumbens and ventral pallidum, suggest that these structures are part of integrative functional loops that control reward and appetitive behaviors.

Animals↗

PubMed1998

Life without neuropeptide Y.

Neuropeptide Y (NPY), a 36 amino acid neuromodulator that is secreted by neurons throughout the peripheral and central nervous system, has been implicated in the control of many physiological processes. We have begun to examine its role in regulation of appetite, behavior, and excitotoxicity by examining mice that are unable to produce NPY as a consequence of gene inactivation. These mutant mice are remarkably normal when reared under standard vivarium conditions. Despite considerable evidence that NPY plays a central role in stimulating appetite, NPY-deficient mice eat normally, grow normally, and refeed after a fast normally. Furthermore, all of their endocrine responses to fasting are normal. The response of NPY-null mice to diet-induced obesity, chemically induced obesity (monosodium glutamate and gold thioglucose), and genetic-based obesity (lethal yellow agouti, Ay; uncoupling protein-diphtheria toxin transgenics, UCP-DT) were all normal. However, NPY deficiency does partially ameliorate the obesity and all of the adverse endocrine effects of leptin deficiency in ob/ob mice. NPY-null mice as well as mice deficient in both NPY and leptin are more sensitive to leptin, suggesting that NPY may normally have a tonic inhibitory action on leptin-mediated satiety signals. NPY-null mice display the normal voracious feeding response to injected NPY. Thus, the only condition where we have observed a role for NPY in body-weight regulation is in the context of complete leptin deficiency--where absence of NPY is beneficial. The activity and general behavior of NPY-null mice are normal. They appear to have normal spatial and contextual learning ability; however, they manifest more anxiety under some conditions. NPY-null mice occasionally display spontaneous, seizure-like events. They also are less able to terminate seizures induced by GABA receptor antagonists or glutamate receptor agonists. These observations are consistent with previous data suggesting that NPY plays an important role in dampening excitotoxicity.

Animals↗

PubMed2006

Hypocretins: the timing of sleep and waking.

The appropriate time and place for sleep and waking are important factors for survival. Sleep and waking, rest and activity, flight and fight, feeding, and reproduction are all organized in relation to the day and night. A biological clock, the suprachiasmatic nucleus (SCN), synchronized by photic influences and other environmental cues, provides an endogenous timing signal that entrains circadian body rhythms and is complemented by a homeostatic sleep pressure factor. Cholinergic, catecholaminergic, serotonergic, and histaminergic nuclei control wakefulness and mutually interact with the SCN as well as sleep- and wake-promoting neurons in the hypothalamus to form a bistable switch that controls the timing of behavioral state transitions. Hypocretin neurons integrate circadian-photic and nutritional-metabolic influences and act as a conductor in the aminergic orchestra. Their loss causes narcolepsy, a disease conferring the inability to separate sleep and waking. Their role in appetitive behavior, stress, and memory functions is important to our understanding of addiction and compulsion.

Behavior↗

PubMed1984

Compulsive polydipsia presenting as diabetes insipidus: a behavioral approach.

Although compulsive polydipsia or self-induced water intoxication is known to occur with a relatively high frequency in psychiatric patients, much of the literature has focused on medication treatment and interactions; little has been written describing alternative methods of intervention. This paper describes an inpatient treatment using both EMG biofeedback and response prevention. The relationship between compulsive appetitive behaviors and more classic presentations is discussed. Because the patient was treated on the endocrine service, the importance of adequately training non-psychiatric staff is emphasized. It is suggested that this may be a model for the behavioral management of psychiatric problems on medical/surgical wards.

Adult↗

PubMed1998

Neuroendocrine interactions between galanin, opioids, and neuropeptide Y in the control of reproduction and appetite.

Galanin is a pleiotropic neuroendocrine signal produced in discrete subpopulations of neurons distributed in several sites in the hypothalamus. Neuropeptide Y and beta-endorphin also display pleiotropism, but they are produced by subpopulations of neurons located only in the arcuate nucleus of the hypothalamus. Each of these neuropeptides exerts a regulatory influence on reproduction and appetitive behavior. Experimental and morphologic evidence from our laboratory show direct contacts and interplay among these diverse signals. Seemingly, an interconnected network composed of these three neuropeptide-producing neurons provides precision and site specificity in the relay of information necessary to govern reproduction and appetite. Disruptions in this interplay are likely to manifest in untoward consequences such as infertility and obesity.

Animals↗

PubMed2003

Reduced sodium appetite and increased oxytocin gene expression in mutant mice lacking beta-endorphin.

Central opioid and oxytocinergic systems have been involved in the regulatory control of sodium appetite. In addition, previous studies support the existence of a functional interaction between opioid peptides and oxytocinergic pathways, and suggest that beta-endorphin neurons would modulate the activity of central oxytocinergic pathways, its pituitary secretion and sodium appetite. To investigate the role of this opioid peptide in the control of oxytocin (OT) synthesis and sodium appetite regulation we used mice with gene dosage-dependent variations in brain beta-endorphin content, expressing either 100%, 50%, or 0% of normal beta-endorphin content. Our results show that beta-endorphin knockout (KO) and heterozygous (HT) mutant mice consume approximately a 50% less 2% NaCl solution compared with wild type mice (WT), after furosemide and low sodium diet treatment. These data suggest that beta-endorphin may facilitate induced sodium appetite, giving new evidence about the role of beta-endorphin on sodium appetite behavior. Our data also indicate that OT mRNA levels evaluated by in situ hybridization significantly increased within the hypothalamic paraventricular nucleus of WT animals after induced sodium ingestion, giving support to former evidence indicating an inhibitory role for central OT in the control of sodium appetite. Moreover, beta-endorphin mutated mice have similar higher levels of OT mRNA expression after the different conditions analyzed: basal, control or experimental, compared with WT mice. Both control HT and KO mice showed higher OT mRNA expression levels than control WT group and these levels did not change after induced sodium intake. Taken together, our data suggest that the reduced sodium ingestion observed in beta-endorphin deficient mice could be due to a higher expression of the OT gene. This conclusion would support the hypothesis that OT inhibits sodium intake and provides new evidence about beta-endorphin modulation of OT synthesis and sodium appetite.

Animals↗

PubMed1985

Effects of peripherally injected vasopressin and des-glycinamide vasopressin on the extinction of a spatial learning task in rats.

An elevated eight-arm radial maze was employed to study the effects of neuropeptide administration on the spatial learning abilities of food-deprived rats. Following 18 days of reinforced training, each animal was briefly exposed to the maze with no food available in any of the eight food-cups. Immediately after this preliminary trial, animals were injected with a single subcutaneous dose of either saline, arginine vasopressin (AVP: 1.0 or 5.0 micrograms/kg), or an AVP analog with only weak endocrinological activity, des-gly-arginine vasopressin (DG-AVP: 1.0, 5.0 or 10.0 micrograms/kg). Additional extinction trials were conducted at 2, 4, 6 and 8 h post-injection. These tests consisted of individually placing an animal on the empty maze and recording the number of arms chosen in a 5-min period. In this situation, animals learn that food is no longer present in the maze and, consequently, extinguish responding. Vasopressin potentiated this radial maze extinction behavior while DG-AVP produced behavioral results directionally opposite to those predicted by a memory facilitation hypothesis. In a subsequent experiment, vasopressin had no effects on unconditioned locomotor activity measured 2 and 4 h post-injection. These results suggest that: vasopressin improved the learning that occurred during extinction of conditioned appetitive behaviors, these vasopressin effects on conditioned behavior were independent of any unconditioned, sedative or non-specific actions of the peptide, and peripheral endocrinological responses may be necessary to demonstrate memory-enhancing effects following peripherally administered AVP.

Animals↗

PubMed2001

Distinguishing BIS-mediated and BAS-mediated disinhibition mechanisms: a comparison of disinhibition models of Gray (1981, 1987) and of Patterson and Newman (1993).

The theoretical framework developed by J. A. Gray (1981, 1987a, 1987b) was used to study disinhibitory behavior. Using a point-scoring reaction time procedure, 4 different experiments were conducted to differentiate 2 disinhibitory mechanisms associated with the behavioral activation system (BAS) and the behavioral inhibition system (BIS). Consistent with the work of C. M. Patterson and J. P. Newman (1993), the BAS-mediated mechanism was related to a lack of inhibition in reward-directed behavior after introducing an occasional aversive contingency and to deficits in learning from aversive cues when responding for reward (Experiments 1-3). The BIS-mediated mechanism was related to a higher ability to extinguish aversive associations (Experiment 1), a lower aversive generalization gradient (Experiment 3), and a lower interference with appetitive behavior in the presence of aversive stimuli (Experiment 4).

Adult↗