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PubMed1985

Neural mediation of conditioned food aversions.

The above discussion is only a brief review of what is known about the neural mediation of conditioned food aversions. Although several other approaches were not mentioned (e.g. biochemical studies), one can still appreciate the value of the aversion paradigm for providing important information about neural mechanisms in learning and memory. A theoretical approach that may be valuable in understanding brain function in conditioned food aversion data is Hughlings Jackson's hierarchical notions of nervous organization. Hedonic responses to food stimuli appear to be brainstem reflexes. On top of these are rostral brain structures that add greater complexity to the consummatory behavior of the organism. An important aspect of this complexity is reflected in an animal's ability to form conditioned food aversions, a process undoubtedly tied intimately to particular neural mechanisms.

Afferent Pathways↗
PubMed1992

Neural mechanisms of drug reinforcement.

The brain substrates involved in the effect of cocaine on brain stimulation reward, in the psychomotor activation associated with cocaine, and in cocaine self-administration appear to be focused on the medial forebrain bundle and its connections with the basal forebrain, notably the nucleus accumbens. Chronic access to cocaine produces a withdrawal state as reflected in increases in brain stimulation reward thresholds, and this change in reward threshold appears to be opposite to the actions of the drug administered acutely. These effects are thought to reflect a change in the activity of reward elements in the medial forebrain bundle and may be responsible for the negative reinforcing state associated with the anhedonia of cocaine withdrawal. Opiate receptors particularly sensitive to the reinforcing effects of heroin also appear to be located in the region of the nucleus accumbens and the ventral tegmental area. There is good evidence for both dopamine-dependent and dopamine-independent opioid interactions in the ventral tegmental-nucleus accumbens connection. In addition, the opiate receptors in the region of the nucleus accumbens may become sensitized during the course of opiate withdrawal and thus become responsible for the aversive stimulus effects of opiate dependence. Reliable measures of the acute reinforcing effects of ethanol have been established in rat models, and substantial evidence exists to show that non-deprived rats will orally self-administer pharmacologically relevant amounts of ethanol in lever-press choice situations. Neuropharmacological studies of ethanol reinforcement in non-dependent rats suggest important roles for serotonin, GABA and dopamine. A role for opioid peptides in ethanol reinforcement may reflect more general actions of opioid peptides in consummatory behavior. Studies of ethanol dependence have implicated brain GABAergic and CRF systems in the more motivational aspects of withdrawal. Future studies will need to focus on the common neurobiologic changes associated with all these drugs, particularly regarding their hedonic and motivational properties.

Animals↗
PubMed2003

Human urocortin II, a selective agonist for the type 2 corticotropin-releasing factor receptor, decreases feeding and drinking in the rat.

Corticotropin-releasing factor (CRF) has been hypothesized to modulate consummatory behavior through the Type 2 CRF (CRF(2)) receptor. However, behavioral functions subserved by the CRF(2) receptor remain poorly understood. Recently, human urocortin II (hUcn II), a selective CRF(2) receptor agonist, was identified. To study the effects of this neuropeptide on ingestive behavior, we examined the effects of centrally infused hUcn II (i.c.v. 0, 0.01, 0.1, 1.0, 10.0 micro g) on the microstructure of nose-poke responding for food and water in nondeprived, male rats. Malaise-inducing properties of the peptide were monitored using conditioned taste aversion (CTA) testing. To identify potential sites of action, central induction of Fos protein expression was examined. hUcn II dose dependently reduced the quantity and duration of responding for food and water at doses lower (0.01-1.0 micro g) than that forming a CTA (10 micro g). Effects were most evident during hours 4 to 6 of the dark cycle. Meal pattern analysis showed that hUcn II potently (0.1 micro g) increased the satiating value of food. Rats ate and drank smaller and shorter meals without changing meal frequency. Rats also ate more slowly. hUcn II induced Fos in regions involved in visceral sensory processing and autonomic/neuroendocrine regulation and resembling those activated by appetite suppressants. hUcn II is a promising neuropeptide for investigating the role of the CRF(2) receptor in ingestive behavior.

Animals↗
PubMed1983

Insulin elicits ingestion in decerebrate rats.

Insulin administered to rats reliably elicits ingestion of food. To determine whether the neural mechanisms sufficient to control insulin-elicited ingestion are located in or caudal to the forebrain, decerebrate rats were treated with insulin and ingestive responses were measured. Insulin treatment produced hypoglycemia that was comparable, in magnitude and duration, in control and decerebrate rats. Decerebrate and control rats ingested significantly more sucrose solution while hypoglycemic than while normoglycemic. In contrast, insulin did not augment the water consumption of either group. These data indicate that neural systems caudal to the forebrain are sufficient to control ingestive consummatory behavior through the integration of metabolic signals generated by insulin treatment and taste afferent input from the oropharynx.

Animals↗
PubMed1989

Lateral cerebroventricular injection of neuropeptide Y stimulates feeding in sheep.

We compared the effects of neuropeptide Y (NPY) injected into the lateral ventricle (LV) and periphery (ip in rats; iv in sheep) on feed and water intake. In sated rats, a bolus injection of 1.18 or 2.35 nmol of NPY administered LV, but not ip, increased (P less than 0.05) feed intake on average of 809% within 30 min of injection. In sated sheep, an LV bolus injection of 2.35 nmol of NPY increased feed intake by 154% within 30 min. Similar doses of human pancreatic polypeptide and peptide YY were less orexigenic than NPY in sheep. After 24 h, cumulative feed intakes were similar among control and peptide treatments. Intravenous injection of 2.35 nmol NPY did not increase feed intake in sheep. Water intake was stimulated (P less than 0.05) by NPY (LV injection) in both the presence and absence of feed. We propose that NPY is involved in the central regulation of consummatory behavior in sheep.

Animals↗
PubMed1997

Central infusion of GLP-1, but not leptin, produces conditioned taste aversions in rats.

Leptin (ob protein) and glucagon-like peptide-1-(7-36) amide (GLP-1) are peptides recently proposed to be involved in the regulation of food intake. Although the ability of exogenous leptin and GLP-1 to modulate consummatory behavior is consistent with the suggestion that these peptides are endogenous regulatory agents, central administration of these peptides may have aversive side effects, which could explain the anorexia. In the present experiment, exposure to a saccharine taste was immediately followed by central administration of leptin or GLP-1 to determine if these drugs could produce a conditioned taste aversion (CTA) in rats. At doses equated for producing comparable reductions in short-term food intake, GLP-1, but not leptin, generated a robust CTA. Although leptin caused no aversion, this peptide was the only drug to cause relatively long-term reductions in food consumption (16 h) and body weight (24 h). Hence, the results indicate that central GLP-1 produces aversive side effects, and it is argued that these nonspecific effects may explain the anorectic actions of GLP-1.

Animals↗
PubMed2005

An in vitro model of hippocampal sharp waves: regional initiation and intracellular correlates.

During slow wave sleep and consummatory behaviors, electroencephalographic recordings from the rodent hippocampus reveal large amplitude potentials called sharp waves. The sharp waves originate from the CA3 circuitry and their generation is correlated with coherent discharges of CA3 pyramidal neurons and dependent on activities mediated by AMPA glutamate receptors. To model sharp waves in a relatively large hippocampal circuitry in vitro, we developed thick (1 mm) mouse hippocampal slices by separating the dentate gyrus from the CA2/CA1 areas while keeping the functional dentate gyrus-CA3-CA1 connections. We found that large amplitude (0.3-3 mV) sharp wave-like field potentials occurred spontaneously in the thick slices without extra ionic or pharmacological manipulation and they resemble closely electroencephalographic sharp waves with respect to waveform, regional initiation, pharmacological manipulations, and intracellular correlates. Through measuring tissue O2, K+, and synaptic and single cell activities, we verified that the sharp wave-like potentials are not a consequence of anoxia, nonspecific elevation of extracellular K+ and dissection-related tissue damage. Our data suggest that a subtle but crucial increase in the CA3 glutamatergic activity effectively recruits a population of neurons thus responsible for the generation of the sharp wave-like spontaneous field potentials in isolated hippocampal circuitry.

Analysis of Variance↗
PubMed2006

Conditional rhythmicity and synchrony in a bilateral pair of bursting motor neurons in Aplysia.

This investigation examined the activity of a bilateral pair of motor neurons (B67) in the feeding system of Aplysia californica. In isolated ganglia, B67 firing exhibited a highly stereotyped bursting pattern that could be attributed to an underlying TTX-resistant driver potential (DP). Under control conditions, this bursting in the two B67 neurons was infrequent, irregular, and asynchronous. However, bath application of the neuromodulator dopamine (DA) increased the duration, frequency, rhythmicity, and synchrony of B67 bursts. In the absence of DA, depolarization of B67 with injected current produced rhythmic bursting. Such depolarization-induced rhythmic burst activity in one B67, however, did not entrain its contralateral counterpart. Moreover, when both B67s were depolarized to potentials that produced rhythmic bursting, their synchrony was significantly lower than that produced by DA. In TTX, dopamine increased the DP duration, enhanced the amplitude of slow signaling between the two B67s, and increased DP synchrony. A potential source of dopaminergic signaling to B67 was identified as B65, an influential interneuron with bilateral buccal projections. Firing B65 produced bursts in the ipsilateral and contralateral B67s. Under conditions that attenuated polysynaptic activity, firing B65 evoked rapid excitatory postsynaptic potentials in B67 that were blocked by sulpiride, an antagonist of synaptic DA receptors in this system. Finally, firing a single B65 was capable of producing a prolonged period of rhythmic synchronous bursting of the paired B67s. It is proposed that modulatory dopaminergic signaling originating from B65 during consummatory behaviors can promote rhythmicity and bilateral synchrony in the paired B67 motor neurons.

Action Potentials↗
PubMed1983

Eating, drinking and urine output after prolonged cerebroventricular vasopressin infusions in rats.

Prior studies suggested that centrally administered single doses of vasopressin (VP) do not affect consummatory behavior or peripheral hydration. To reduce uncertainties related to factors of unknown distribution, concentration and duration, we infused VP (0.5 or 50 ng/h) continuously for 5 h or 5 days into a lateral cerebroventricle of conscious male rats. Eating and drinking behavior, as well as urine volume and sodium and potassium output, were unaffected by these treatments. The results suggest that VP, at sites reached from cerebrospinal fluid, does not alter peripheral hydration of rats.

Animals↗
PubMed1986

Prolactin release and milk ejection in rats suckling underfed pups.

Mother rats chronically exposed to underfed pups (obtained daily from nonlactating mothers) show increased milk production which is associated with increased consumption of food and water. The purpose of the present study was 2-fold: to examine whether the magnitude of maternal PRL discharge is related to the nutritional state of the pups and to differentiate between the role of the mother and that of the pups themselves in the regulation of milk intake. PRL release in response to reunion with pups (preceded by 4-h separation from pups) was measured between days 12 and 14 postpartum; each mother was tested twice, once with hungry pups (deprived of food for 24 h) and once with satiated (normally fed) pups. The magnitude of PRL discharge elicited by hungry pups in lactating as well as in thelectomized rats was twice as large as the discharge elicited by satiated pups. For each type of stimulus pups, the magnitude of PRL release was smallest in thelectomized rats, largest in rats that had nursed normally fed pups before testing, and intermediate in rats that had nursed underfed pups. The frequency of milk ejection was considerably reduced in mothers that were chronically exposed to underfed pups compared with mothers that had nursed normally fed pups. Regardless of the mother's previous history, and independent of the milk ejection frequency or maternal food and water intake, hungry pups ingested more milk than did satiated pups over the same suckling period even when both types of pups were suckled simultaneously by the same female. Milk ingestion in satiated pups was not enhanced by the vigorous sucking exerted by hungry littermates. It is suggested that hungry pups are able to meet their increased nutritional demands both directly, by withdrawing a larger portion of the milk available in the mammary glands, and indirectly, by enhancing maternal PRL secretion which in turn may promote maternal consummatory behavior and milk production.

Animal Population Groups↗
PubMed1999

p-Chloroamphetamine (PCA) suppresses ingestive behavior in male rats.

Ingestive behavior was activated in male rats by intraoral intake and intake from a bottle of 1-M solution of sucrose. Intraperitoneal injection of p-chloroamphetamine (PCA), releasing central 5-hydroxytryptamine (5-HT) from serotonergic nerve terminals, inhibited ingestion of the sucrose solution. Significant inhibition of sucrose intake by PCA was observed at 1.25 and 2.5 mg/kg dose in a bottle intake test, and at 5.0 mg/kg dose in an intraoral intake test. These findings suggested that 1.25 and 5.0 mg/kg of PCA suppressed appetitive ingestive behavior and consummatory ingestive behavior in male rats, respectively.

Administration, Oral↗
PubMed1977

Stimulus- and response-reinforcer contingencies in autoshaping, operant, classical, and omission training procedures in rats.

Separate groups of rats received 500 trials of lever-press training under autoshaping (food delivery followed 10-second lever presentations, or occurred immediately following a response); operant conditioning (responding was necessary for food delivery); and classical conditioning (food followed lever presentations regardless of responding). Each group then received 500 trials on an omission procedure in which food was omitted on trials with a response. Another group received 1000 trials on the omission procedure, and a fifth group, random control, received 1000 uncorrelated presentations of lever and food. The autoshaping, operant, and classical groups reached high response levels by the end of initial training. Acquisition was fastest in the autoshaping group. Responding remained consistently low in the control group. The omission group responded at a level between the control group and the other three groups. During omission training, responding in these three groups declined to the omission-group level. During omission training, the rats continued contacting the lever frequently after lever pressing had declined. Response maintenance under omission training seems not to require topographic similarity between the response and reinforcer-elicited consummatory behaviors.

Journal Article↗
PubMed2003

The monoamine hypothesis for the pathophysiology of paraphilic disorders: an update.

A monoamine hypothesis for the pathophysiology of paraphilic disorders was first articulated in 1997 by Kafka. This hypothesis was based on four converging lines of empirical evidence. First, the monoamine neurotransmitters, dopamine, norepinephrine, and serotonin serve a modulatory role in human and mammalian sexual motivation, appetitive, and consummatory behavior. Second, the sexual effects of pharmacological agents that affect monoamine neurotransmitters can have both significant facilitative and inhibitory effects on sexual behavior. Third, paraphilic disorders appear to have Axis I comorbid associations with nonsexual psychopathologies that are associated with monoaminergic dysregulation. Last, pharmacological agents that enhance central serotonergic function in particular, have been reported to ameliorate paraphilic sexual arousal and behavior. Contemporary data supporting or refuting a monoaminergic hypothesis as a biological component associated with paraphilic sex offending behaviors will be reviewed. Particular attention will be given to pharmacological-metabolic probe studies, reports of Axis I comorbidity, the proposed role of disinhibited sexual motivation or sexual appetitive behavior, and cumulative pharmacological treatment data sets.

Dopamine↗
PubMed2003

The affinity for sweet substances and cigarette smoking in chronic alcoholism.

The purpose of the present study was to examine the possible relationship between the consumption of alcohol and the smoking of cigarettes and the intake of sweet tasting substances in a group of in-patient chronic alcoholics residing in the Israeli governmental treatment center. Patients were interviewed regarding their alcohol intake, cigarette use and consumption of sweetened substances prior to entry to the center. No relationship between alcohol consumption and intake of sweetened substances or between alcohol intake and cigarette smoking was observed for the total sample. However, high alcohol consumption did have a significant correlation with cigarette smoking but not with the consumption of sweets. In contrast, low alcohol consumption had a significant relationship with consumption of sweets but not with cigarette smoking. In addition, a sub-group with an apparent family history of alcoholism had a significant correlation between alcohol intake and smoking but not sweets consumption. The data argue against a common central substrate mediating all three consummatory behaviors. The phenomena examined in the present study seem to be behavioral and motivational in nature rather than reflecting the effects of a direct biological mechanism.

Adult↗