Patterns of feeding behavior in the pigeon.
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: Nucleus accumbens dopamine has been shown to play a role in the processing of behaviorally relevant stimuli and to mediate ethanol-reinforced responding. Previous research that used a fixed-ratio schedule of responding maintained by the presentation of small dippers (0.1 ml) of ethanol demonstrated that the dopamine D2 antagonist, raclopride, decreased total responding for ethanol by both delaying the onset of responding and causing the early termination of lever-press behavior. Because these studies required animals to continuously respond to obtain access to small amounts of ethanol over a period of self-administration, this procedure assessed a combination of appetitive (seeking) and consummatory (drinking) behavior. The paradigm used in the present study separated the appetitive or seeking response from the consummatory response to assess the effects of raclopride on both types of ethanol-related behaviors. METHODS: Male Long-Evans rats were trained to emit a fixed number of lever-press responses that resulted in access to a drinking tube that contained 10% ethanol for 20 min, once each day. We measured the effects of microinjections of raclopride (1.0, 3.0, and 10.0 microg/subject) into the nucleus accumbens, before the sessions, on appetitive and consummatory responding. RESULTS: Raclopride delayed the onset of ethanol-seeking (appetitive responding) at all doses and decreased the number of responses made at the low and high doses. The rate of responding, however, was unaffected. Raclopride had no effect on the latency to begin consuming ethanol or on any of the characteristics of the initial bout of ethanol intake at all doses tested. Total ethanol intake was decreased, after an initially "normal" pattern of self-administration, following only the highest dose of raclopride. Mean ethanol intake (g/kg) was 0.54 (+/-0.03) after no injection, 0.51 (+/-0.04) after sham treatment, and 0.38 (+/-0.05) after 10 microg of raclopride. CONCLUSIONS: The procedural separation of the seeking and intake responses used in this experiment allowed us to assess the effects of dopamine receptor antagonism in the nucleus accumbens on these two different behaviors. Overall, appetitive responding that preceded the delivery of an ethanol solution was more sensitive to raclopride treatment than was consummatory responding. These findings are consistent with a stimulus-processing function of the mesolimbic dopamine system.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rats shifted from 4% to 32% sucrose displayed successive negative contrast by initiating significantly fewer bouts of licking than control rats maintained on 4% sucrose. No significant increase in dopamine (DA) efflux in the nucleus accumbens (NAc) was observed during consumption of 4% sucrose by rats shifted from 32%. In contrast, consumption of 4% sucrose by control rats was accompanied by a significant increase in DA efflux in the NAc, which remained elevated 10 min postconsumption. These data are consistent with the hypothesis that DA efflux in the NAc reflects the current incentive valence of sucrose reward and its influence on initiation of individual bouts of sucrose consumption.
To investigate the role of opioids in the mediation of sucrose intake in the preweanling rat pup, we measured the effect of naloxone on intake of pups licking 10% sucrose from the floor of a beaker (independent ingestion test) and of pups ingesting 10% sucrose that was continuously infused through an anterior, sublingual oral catheter (oral catheter test). Pups were tested only once to eliminate the possible effect of test experience. Pups were tested in the second postnatal week (PN7, 9, 10, 11, and 14 days) with naloxone (1 mg/kg) or vehicle controls. Fourteen-day-old pups were also tested with 0.1 and 0.5 mg/kg. Naloxone began to be efficacious for inhibiting intake on PN10 in the oral catheter test and on PN11 in the independent ingestion test. On PN14, the inhibition of intake was dose related and naloxone was more potent for inhibiting intake in independent ingestion tests than in oral catheter tests. Naloxone not only decreased intake, it also decreased the incidence of licking, increased mouthing and resting, and had no significant effect on locomotion. The site of the inhibitory effect of naloxone on intake was in the central nervous system, presumably in the brain, because naloxonemethiodide, an analogue of naloxone that does not cross the blood-brain barrier, did not inhibit sucrose in either test. These results demonstrate that the intake of 10% sucrose depends on endogenous opioids as early as PN10 and that this opioid mechanism operates when pups have not had prior test experience and in a test (oral catheter test) where intake is not dependent on appetitive behaviors.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Cats with pontile or frontal neocortical lesions display a tactually elicited dissociation of appetitive and consummatory grooming behaviors. Systemic administration of glucocorticoids abolished the abnormal grooming behavior in cats with lesions, even when the stimulatory effect of glucocorticoids on serotonin metabolism was blocked by administration of p-chlorophenylalanine (PCPA). Microinjections of glucocorticoids into the superior colliculi also significantly decreased the abnormal grooming behavior. Adrenalectomized cats did not display the abnormal grooming behavior, but the abnormal behavior did occur in PCPA-treated adrenalectomized cats. Administration of either glucorticoids or 5-hydroxytryptophan abolished the abnormal behavior in PCPA-treated adrenalectomized cats. Thus, it appears that the pontile and frontal neocortical lesions produce deficits in both glucocorticoids and serotonin, and these deficits are necessary and sufficient conditions for inducing the abnormal grooming behavior.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The exposure of humans and animals to high doses of psychostimulant drugs, followed by their withdrawal, leads to a number of aversive psychological symptoms. These symptoms include increased anxiety and anhedonia, and may be manifested behaviorally as a decreased interest in normally rewarding stimuli. In the present study, we determine the effects of withdrawal from an escalating-dose schedule of D-amphetamine on the consumption of a 4% sucrose solution under normal conditions, and after an incentive downshift. The downshift was induced by subjecting animals to a consumatory negative contrast paradigm, by switching them from a familiar 32% sucrose solution to a novel 4% solution. In unshifted animals, there was no effect of D-amphetamine withdrawal on consumption of the 4% solution. In contrast, drug-withdrawn animals displayed an exaggerated negative contrast effect, primarily reflected as a delayed recovery from the downshift lasting for at least 60 h. This effect is interpreted as a consequence of the increased emotionality of withdrawn animals, and may be related to disruption of normal search behaviors.
Explore the source record for details and available documents.
Developmental and seasonal changes in the production of androgens, estrogens, and progestins seem to control sex-specific differentiation and seasonal changes in appetitive and consummatory sexual behaviors of birds. This results in profound sex differences in the quality (sex-specific) or quantity (sex-typical) of behaviors such as courtship, territoriality, or copulation. Steroids affect the brain by binding to intracellularly located receptors. The same brain areas express androgen, estrogen, and progesterone receptors in male and female brains. Sex differences in these genetically determined patterns occur in the size of neuron populations that intrinsically express sex steroid receptors. Further permanent sex differences are subsequent to degenerative fates of receptor expressing neuron populations during ontogeny. Transient sex differences in receptor expression appear to be due to area-specific up- and down-regulation of receptor levels, reflecting transient changes in the level of circulating steroids, changes in environmental conditions, or in the physiological status of the individuals. In particular, intrinsic sex differences in the expression pattern of sex steroid receptors and steroid-independent regulation of the expression level of these receptors in the brain are limiting mechanisms for gonad-dependent sexual development and activities.
Explore the source record for details and available documents.
Explore the source record for details and available documents.