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Attenuation of antipredator defensive behavior in rats following chronic treatment with imipramine.

The anxiety/defense test battery has been developed to assess defensive reactions in rats to situations associated with a natural predator, the domestic cat. This comprises three paradigms designed to study the effects of cat exposure on general activity and location with respect to the cat (proxemic avoidance), the effects of cat exposure on non-defensive consummatory behavior, and the behavioral response to cat odor. In the present study subjects were exposed to 21 days pretreatment with imipramine (0, 5, and 15 mg/kg), before being assessed in the three experimental paradigms (carried out over a total period of 7 days). Imipramine treatment was maintained on a daily basis during the 7 days taken to complete the series of tests. The data indicated a behaviorally specific profile consistent with anxiety/fear reduction, but not with sedation, in three different paradigms, following treatment with 15 mg/kg imipramine. These behavioral changes included a reduction in freezing, proxemic avoidance and a disinhibition of suppressed feeding in response to cat presentation. Similarly, imipramine treatment (15 mg/kg) significantly reduced behaviors associated with risk assessment (e.g. flat back approach, stretch attend) during presentation of a cat odor stimulus. This behavioral profile suggests that chronic pretreatment with imipramine produces an attenuation of antipredator defensive behavior.

Aggression↗

Firing of nucleus accumbens neurons during the consummatory phase of a discriminative stimulus task depends on previous reward predictive cues.

The nucleus accumbens (NAc) plays an important role in both appetitive and consummatory behavior. To examine how NAc neurons encode information during reward consumption, we recorded the firing activity of rat NAc neurons during the performance of a discriminative stimulus task. In this task, the animal must make an operant response to an intermittently presented cue to obtain a sucrose reward delivered in a reward receptacle. Uncued entries to the receptacle were not rewarded. Both excitations and inhibitions during reward consumption were observed, but substantially more neurons were inhibited than excited. These excitations and inhibitions began when the animal entered the reward receptacle and ended when the animal exited the receptacle. Both excitations and inhibitions were much smaller or nonexistent when the animal made uncued entries into the reward receptacle. In one set of experiments, we randomly withheld the reward in some cued trials that would otherwise have been rewarded. Excitations and inhibitions were of similar magnitude whether or not the reward was delivered. This indicates that the sensory stimulus of reward does not drive these phasic responses; instead, the reward-associated responses may be driven by the conditioned stimuli associated with reward, or they may encode information about consummatory motor activity. Another population of NAc neurons was excited on exit from the reward receptacle. Many of these excitations persisted for tens of seconds after the receptacle exit and showed a significant inverse correlation with the rate of uncued operant responding. These findings are consistent with a contribution of NAc neurons to both reward consummatory and reward seeking behavior.

Action Potentials↗

A descriptive analysis of the structure and temporal pattern of voluntary ethanol intake within an acquisition paradigm.

OBJECTIVE: The present experiment examined the microstructure and temporal pattern of consummatory behavior to provide insight into the behavioral processes that regulate the acquisition of voluntary oral ethanol intake. METHOD: A microcomputer-controlled data acquisition system was used to dynamically monitor food, water and ethanol intake in Long Evans rats across acquisition of ethanol drinking initiated through the presentation of a sequence of increasing concentrations of ethanol solutions in a free choice with water. RESULTS: The results showed a biphasic pattern of ethanol intake as a function of presentation of increasing concentrations of ethanol. Total ethanol intake decreased as the ethanol concentration was increased from 2% to 6%, while, inversely, ethanol intake was significantly increased as the concentration went from 6% to 10%. The initial decrease in ethanol intake, across 2% to 6% ethanol, was a function of decreases in both frequency and size of ethanol bouts. The increase in ethanol intake observed following presentation of higher ethanol presentations was solely a function of increased size of ethanol bouts. The increased size of ethanol bouts was paralleled by an increase in the rate of intake which was not evident across presentation of concentrations below 6%. The pattern of intake across the 23-hour daily sessions exhibited no differences across the dark/light cycle in ethanol or water intake as the concentrations of ethanol were increased. The results indicated, however, that food intake was characterized by increases in consumption during the first hour following the presentation of fluids and the night portion of the dark/light cycle. CONCLUSIONS: The present study revealed, for the first time, the involvement of differential, concentration dependent, behavioral processes in the mediation of the acquisition of voluntary ethanol intake.

Alcohol Drinking↗

Conditioned taste aversion is a confound in behavioral studies that report a reduction in the reinforcing effects of drugs.

Pharmacologic agents with a potential to attenuate the reinforcing properties of drugs of abuse may have an important role in the treatment of drug addiction. The reduction of drug self-administration and sweet solution intake are two common animal models employed to screen for promising therapeutic agents. When these agents are effective in suppressing the behavior maintained by drugs of abuse, the cause is usually attributed to a neuronal mechanism such as the modification of neurotransmitters that subserve reinforcement. These experiments present data for an alternate interpretation which suggest that some of these agents produce a conditioned taste aversion (CTA) that acts as a confounding variable in the screening of potential therapeutic agents. Both carbamazepine and isradipine were shown to establish a CTA at doses reported to attenuate the reinforcing properties of drugs of abuse. It is concluded that CTA represents a potential experimental confound in studies of pharmacologic agents that appear to attenuate the reinforcing properties of drugs. These results suggest that screening for a CTA is necessary in any paradigm that measures the suppression of consummatory behavior in response to pharmacologic intervention.

Analgesics, Non-Narcotic↗

Tail pinch induced eating: psychogenetic comparison of Roman high- and low-avoidance rats.

Consummatory behavior elicited by mild tail pinch in the presence of solid food was studied in male Roman high-avoidance (RHA/Verh) and Roman low-avoidance (RLA/Verh) rats. RLA/Verh rats, characterized as the more emotional of the two rat lines, exhibited significantly shorter latencies to bite and eat solid food during tail pinch than the RHA/Verh rats. Treatment with 6, 12 and 24 mg/kg sodium pentobarbital prior to tail pinch failed to increase the elicited eating in either rat line.

Animals↗

RO15-4513 antagonizes the anxiolytic effects of ethanol in a nonshock conflict task at doses devoid of anxiogenic activity.

RO15-4513 is a partial benzodiazepine inverse agonist that has been reported to antagonize some of the biochemical and neurobehavioral actions of ethanol. However, whether this antagonistic action of RO15-4513 is dependent on the drug exerting its intrinsic (inverse agonist) properties is unclear at present. The purpose of the present study was to examine whether RO15-4513 was capable of antagonizing the anxiolytic effects of ethanol in a nonshock conflict task at doses that, by themselves, do not reveal the compound's intrinsic anxiogenic properties. The consummatory conflict task employed (negative contrast) involves quantifying how animals respond to an abrupt, unexpected reduction in reward (sucrose solution), and is particularly sensitive to the effects of anxiolytic agents, including ethanol. As previously demonstrated, depressed consummatory behavior engendered by reward reduction was significantly alleviated by ethanol (0.75 g/kg). This anxiolytic effect of ethanol, however, was antagonized dose dependently by RO15-4513 (0.1875-3.0 mg/kg). Only the highest dose of RO15-4513 (3.0 mg/kg) showed evidence of further response suppression. Lower doses of RO15-4513 tested did not exert an anxiogenic effect when given alone. Thus the antagonism of EtOH's anxiolytic (contrast-reducing) effects occurred at doses of RO15-4513 (0.375-1.5 mg/kg) that did not exhibit any intrinsic anxiogenic activity. As such, these results suggest that RO15-4513 interacts with the anxiolytic effects of ethanol in a nonadditive fashion in this test situation.

Animals↗

Temporal dynamics of corticosterone elevation in successive negative contrast.

A negative contrast effect in consummatory behavior that occurred when rats were shifted from 32% to 4% sucrose was accompanied by elevations in corticosterone that were measurable at 10 and 20 min but not at 40 min after the second postshift day. No corticosterone elevations were found to accompany contrast at 10 or 15 min after the first postshift day in these experiments nor immediately after the first postshift day in an earlier experiment. The present study also found an anticipatory elevation in plasma corticosterone in shifted animals just before their placement in the apparatus on the second postshift day. These results are discussed in terms of a multistage hypothesis of successive negative contrast. The anticipatory elevation is discussed in terms of uncontrollability and unpredictability of aversive events.

Animals↗

Effects of subfornical organ extracts of salt-water balance in the rat.

The subfornical organ (SFO) is regarded as a neurosecretory structure but no information is available on the nature or biological effects of the secretory products(s). Supernatants of water homogenates of rat SFO were lyophilized and reconsittuted in artificial cerebrospinal fluid (CSF). Intracerebroventricular (IVT), but not subcutaneous, administration of this material to rats produced diuresis, natriuresis and kaliuresis in the following 8 h daylight period. During the overnight cycle, consummatory behavior and excretion of sodium and potassium were reduced. Similar responses were obtained after IVT administration of cerebellar cortex (CB) or large amounts of plasma. SFO, CB and cerebral cortex (CC) were incubated in potassium-enriched CSF to enhance release of secretory products. Urine volume was increased 8 h after IVT injection of SFO media; in the overnight cycle, food consumption, absolute urinary sodium and potassium, and [Na+-a1 were reduced. These effects were not produced by IVT injection of CC or CB media, or equal amounts of plasma proteins. Additional experiments demonstrated that choroid plexi and SFO effects were similar and that the active SFO material was dialyzable and thermal stable. These data suggest that SFO contains a water-soluble substance which is released into a posassium-enriched medium. The material is heat stable, has a relatively low molecular weight, and alters salt-water balance after injection into ventricular cerebrospinal fluid.

Animals↗

Effect of p-chlorophenylalanine and tryptophan on sleep, EEG and motor activity in the rat.

The effects of a single injection of parachlorophenylalanine (PCPA, 300 mg/kg i.p.) on sleep, motor activity and consummatory behavior were investigated in unrestrained rats which were continuously recorded with telemetric techniques on two control days and six drug days. Slow wave sleep (SWS) was defined as the non-REM sleep (NREMS) fraction with a low predominant EEG frequency. In the 24 h following PCPA administration, motor activity and food intake were reduced and sleep was increased. SWS was massively enhanced, while REM sleep (REMS) was depressed. The initial phase of sedation was followed by a phase of partial insomnia lasting 1-2 days. SWS and REMS were particularly depressed. A rebound phenomenon was observed at the end of recovery period when some of the SWS and REMS values exceeded the control level. The administration of tryptophan (Trp, 150 mg/kg i.p.) 28 h after PCPA pretreatment, causing a significant rise in the brain serotonin (5-HT) concentration, produced a temporary increase in SWS and REMS, and a reduction of motor activity. The experiments show that the depression of SWS and REMS, and the hyperactivity 1-2 days after PCPA administration, are a consequence of the reduced 5-HT level, whereas the involvement of serotonergic mechanisms in the initial sedative phase and in the recovery phase is less clear. The persistence of the daily distribution of sleep and activity, and of the specific pattern of SWS and REMS, indicates that the circadian sleep organization is little affected by 5-HT depletion.

Animals↗

Neurokinin type-3 receptor stimulation impairs ethanol-associated appetitive behavior in Wistar rats.

OBJECTIVES: Stimulating central neurokinin type-3 (NK-3) receptors decreases ethanol intake in rats. Although paraventricular nucleus of the hypothalamus (PVN) has a high density of NK-3 receptors, their influence on ethanol reinforcement has not been examined. This study's purpose was to assess the effects of intra-PVN infusion of senktide, a NK-3 receptor agonist, on ethanol self-administration. In a follow-up study, senktide's effects on ethanol self-administration after intracerebroventricular (ICV) infusion were examined. METHODS: Male Wistar rats were trained to self-administer 10% ethanol (10E) in the "Sipper Tube" model described by Samson and colleagues, Guide cannula were then aimed bilaterally at the PVN or unilaterally at the lateral cerebral ventricle. Intra-PVN (5-100 ng/side) or ICV (30-500 ng/rat) effects of senktide on 10E self-administration were also examined as a preliminary test of senktide's selectivity. RESULTS: Intra-PVN and ICV infusion of senktide reduced the average number of consecutive lever presses and increased the time taken to complete the lever press requirement when 10E served as the reinforcer. Increased duration of the lever-pressing component was observed when senktide was administered prior to 2S self-administration sessions. Neither PVN nor ICV senktide administration significantly altered 10E or 2S consumption. CONCLUSIONS: These data suggest that stimulation of central neurokinin typ-3 receptors in the Wistar rat reduces appetitive behavior while having little or no impact on consummatory behavior. Ethanol "seeking" appeared more sensitive to disruption by senktide than sucrose "seeking." However, further studies assessing the senktide's effects on sucrose-maintained behavior are needed to verify this hypothesis. Lastly, it is hypothesized that lack of effect of senktide on intake is in part related to the use of outbred Wistar rats in these studies instead of selectively bred rats.

Animals↗

Extracellular adenosine levels in neostriatum and hippocampus during rest and activity periods of rats.

Adenosine is an inhibitory modulator in the mammalian brain with a possible role in sleep regulation, which is mainly indicated by pharmacological studies showing that adenosine or its analogs can induce sedation and sleep, whereas adenosine antagonists, like caffeine and theophylline, are potent behavioral and neuronal stimulants. In contrast to these pharmacological findings, data on endogenous adenosine in relation to sleep and waking are sparse. Therefore, we have now used in vivo microdialysis to investigate the extracellular levels of adenosine in the neostriatum and hippocampus of freely moving rats. Adenosine was monitored over a time course of 24 h, during which the animals were exposed to a 12 h day/night rhythm with lights-off from 19.00 to 07.00. In this lights-off period, i.e. the rats' active period, the maximal levels of neostriatal and hippocampal extracellular adenosine were higher than during the lights-on period. In contrast to the neostriatum, extracellular levels of hippocampal adenosine tended to increase towards the end of the lights-off period, reaching its maximal level at 07.00, and decreasing again within the following hour. The changes of hippocampal adenosine levels were related to behavior, since significant increases in "sleep-like" behavior, as well as decreases in overall movements and consummatory behavior, were observed when adenosine levels had reached their maxima in the hippocampus; no such relationship was found with respect to the neostriatum. These results are in keeping with a role of endogenous adenosine in the regulation of sleep and wakefulness, and point to a specific role of adenosine in the hippocampus. They also raise the possibility that adenosine may be involved in different behavioral processes dependent on the area of the brain, as well as the type of adenosine receptor involved. Finally, given the known evidence for neuroprotective actions of adenosine, its accumulation in the hippocampus as a function of behavioral activity may serve to prevent or repair the neural degenerative consequences of such activity. It is proposed that adenosine's sleep-promoting effects result from its signalling to cease behavioral activity in order to prevent excessive activity-related changes, and thus allow other restorative sleep-related processes to take over.

Adenosine↗

The GABA(A) receptor alpha1 subtype in the ventral pallidum regulates alcohol-seeking behaviors.

We investigated the potential role of the alpha1-containing GABA(A) receptor in regulating the reinforcing properties of alcohol. To accomplish this, we developed 3-propoxy-beta-carboline hydrochloride (3-PBC), a mixed agonist-antagonist benzodiazepine site ligand with binding selectivity at the alpha1 receptor. We then tested the capacity of 3-PBC to block alcohol-maintained responding in the ventral pallidum (VP), a novel alcohol reward substrate, which primarily expresses the alpha1-receptor isoform. Our results demonstrated that bilateral microinfusion of 3-PBC (0.5-40 microg) in the anterior and medial VP produced marked reductions in alcohol-maintained responding in a genetically selected rodent model of alcohol drinking. The VP infusions showed both neuroanatomical and reinforcer specificity because no effects were seen in sites dorsal to the VP (e.g., nucleus accumbens, caudate putamen). The saccharin-maintained responding was reduced only with the highest dose (40 microg). Parenteral injections of 3-PBC (1-20 mg/kg) also showed a similar selectivity on alcohol-maintained responding. Complementary in vitro studies revealed that 3-PBC exhibited a low partial agonist efficacy profile at recombinant diazepam-sensitive receptors (e.g., alpha1beta3gamma2, alpha2beta3gamma, and alpha3beta3gamma2). The selective suppression of 3-PBC on alcohol-maintained responding after central and parenteral administrations, together with its low-efficacy agonist profile, suggest that the reduction in alcohol-maintained behaviors was not attributable to a general suppression on consummatory behaviors. These results demonstrate that the alpha1-containing GABA(A) receptors in both the anterior and medial VP are important in regulating the reinforcing properties of alcohol. These receptors represent novel targets in the design and development of pharmacotherapies for alcohol-dependent subjects.

Alcoholism↗

Lesions of nucleus accumbens reduce instrumental but not consummatory negative contrast in rats.

In Experiment 1, rats provided with brief daily access to 4% sucrose which preceded brief access to 32% sucrose (4-32) suppressed licking the 4% solution relative to 4-4 controls. This anticipatory negative contrast (ANC) was diminished when the 32% solution was downshifted to 4%. Licking the second 4% solution in shifted rats (4-32-4) was lower than licking of the second 4% solution in 4-4 control rats - a successive negative contrast (SNC) effect. Neither SNC nor ANC or their recovery were influenced by electrolytic lesions of the nucleus accumbens (NAC). Latency to initiate licking followed a concentration function, with rats initiating licking faster for 32 than 4% sucrose, but was not affected by the lesion. In Experiment 2, rats showed clear SNC in consummatory behavior when shifted from 32 to 4% sucrose and also showed SNC in running speed when shifted from a 12- to 1-pellet reward in a straight runway. As in Experiment 1, consummatory SNC was not affected by the lesion. However, in the runway, lesioned animals showed contrast later (after more trials) than the sham-lesioned rats and did not show contrast in the goal section, when goal speed was averaged across the postshift period. Reward downshift also increased the animals' tendency to backtrack in the runway and backtracking was greater in the lesioned rats during both the preshift and postshift periods. These data suggest that the NAC is not a necessary structure for the generation of expectancies, the comparison of rewards or the modulation of ingestive behavior. However, the NAC may be involved in responding to unmet expectancies when the task involves approach or instrumental behavior.

Animals↗

The effects of scopolamine on extinction and spontaneous recovery.

The effects of scopolamine hydrobromide on baseline extinction levels and spontaneous recovery were assessed. Rats were trained on one of four reinforcement schedules (CRF, FR 10, FR 20, FR 40) with either food or water reinforcement. Scopolamine increased response rates in extinction and spontaneous recovery following training on all four schedules when the reinforcer was water, but had no effect on responding previously maintained by food. The results are discussed in terms of the limitations of a general theory of a cholinergic system mediating all suppressed behavior and the effects of anticholinergic drugs on central thirst mechanisms and consummatory behavior.

Animals↗

Preferential effects of the metabotropic glutamate 2/3 receptor agonist LY379268 on conditioned reinstatement versus primary reinforcement: comparison between cocaine and a potent conventional reinforcer.

Metabotropic glutamate receptors (mGluRs) have been implicated in regulating anxiety, stress responses, and the neurobehavioral effects of psychostimulants. The present study sought to determine whether group II mGluR activation by the potent mGlu2/3 receptor agonist, (-)-2-oxa-4-aminobicylco hexane-4,6-dicarboxylic acid (LY379268), antagonizes reinstatement of cocaine-seeking induced by cocaine-related stimuli and whether this effect extends to behavior induced by stimuli conditioned to a potent conventional reinforcer, sweetened condensed milk (SCM). Also, we tested whether the suppressant effects of LY379268 on conditioned reinstatement extend to the primary reinforcing effects of cocaine or SCM. Rats were trained to associate discriminative stimuli (S(D)) with the availability of cocaine or SCM versus non-reward and then subjected to repeated extinction sessions during which the respective reinforcers and S(D) were withheld. Subsequent reexposure to the cocaine or SCM S(D), but not the non-reward S(D), produced recovery of responding at the previously active lever. LY379268 (0.3-3.0 mg/kg, s.c.) dose-dependently attenuated recovery of cocaine seeking but reduced conditioned reinstatement by the SCM S(D) only at the highest dose. LY379268 did not alter responding reinforced directly by SCM, and only the highest LY379268 dose reduced cocaine self-administration. The results suggest that the effects of LY379268 are selective for behavior maintained by cocaine as opposed to palatable conventional reinforcers. More importantly, the results show that LY379268 suppresses behavior motivated by stimuli conditioned to cocaine or SCM more effectively than consummatory behavior maintained by the unconditioned effects of these substances. As such, the results identify group II mGluRs as a pharmacotherapeutic target for craving and relapse prevention associated with cocaine cue exposure.

Amino Acids↗

Long-lasting potentiation of GABAergic synapses in dopamine neurons after a single in vivo ethanol exposure.

The mesolimbic dopamine (DA) system originating in the ventral tegmental area (VTA) is involved in many drug-related behaviors, including ethanol self-administration. In particular, VTA activity regulating ethanol consummatory behavior appears to be modulated through GABA(A) receptors. Previous exposure to ethanol enhances ethanol self-administration, but the mechanisms underlying this phenomenon are not well understood. In this study, we examined changes occurring at GABA synapses onto VTA DA neurons after a single in vivo exposure to ethanol. We observed that evoked GABA(A) IPSCs in DA neurons of ethanol-treated animals exhibited paired-pulse depression (PPD) compared with saline-treated animals, which exhibited paired-pulse facilitation (PPF). Furthermore, PPD was still present 1 week after the single exposure to ethanol. An increase in frequency of spontaneous miniature GABA(A) IPSCs (mIPSCs) was also observed in the ethanol-treated animals. Additionally, the GABA(B) receptor antagonist (3-aminopropyl)(diethoxymethyl) phosphinic acid shifted PPD to PPF, indicating that presynaptic GABA(B) receptor activation, likely attributable to GABA spillover, might play a role in mediating PPD in the ethanol-treated mice. The activation of adenylyl cyclase by forskolin increased the amplitude of GABA(A) IPSCs and the frequency of mIPSCs in the saline- but not in the ethanol-treated animals. Conversely, the protein kinase A (PKA) inhibitor N-[z-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide significantly decreased both the frequency of spontaneous mIPSCs and the amplitude of GABA(A) IPSCs in the ethanol-treated mice but not in the saline controls. The present results indicate that potentiation of GABAergic synapses, via a PKA-dependent mechanism, occurs in the VTA after a single in vivo exposure to ethanol, and such potentiation might be a key synaptic modification underlying increased ethanol intake.

Administration, Oral↗

Tiagabine reduces ethanol reward in C57BL/6 mice under acute and chronic administration regimens.

Three experiments conducted on male C57BL/6 (B6) mice examined the effects of subcutaneous injections of the GABA uptake inhibitor, tiagabine, on appetitive (lever responding) and consummatory behavior (fountain contacts) of food restricted B6 mice for 12% ethanol and water rewards (Exp-1), and for food reward (Exp-2) delivered on a fixed ratio 4 schedule of reinforcement. Effects of acute injections (1,3,6,9 mgkg) and chronic administration (6,9 mg/kg) was examined. Exp-3 examined tiagabine effects on the voluntary consumption of continuously available 12% ethanol, and on the interactive effects of tiagabine and ethanol on motor activity of non-food restricted B6 mice. Results of Exp-1 and Exp-2 indicated that tiagabine can reduce appetitive behavior for ethanol reward with no evidence of tolerance upon chronic exposure. Tiagabine doses that reduced ethanol reward had less effect on behavior maintained by either water or food, and had no effect on motor activity. In contrast to the absence of tolerance to its effect on appetitive behavior for ethanol, mice rapidly developed tolerance to tiagabine's initial reduction of the consummatory response for ethanol (Exp-1), and the intake of freely available ethanol exceeded pre-tiagabine levels after several daily injections (Exp-3). Importantly, mice developed tolerance to tiagabine's sedative effect after three daily injections and its sedation was not enhanced when combined with ethanol, an effect consistent with the lack of a tiagabine + ethanol interaction previously reported for humans. The results of the experiments suggest that in addition to reducing alcohol withdrawal symptoms, tiagabine might also reduce the potency of ethanol-conditioned cues that drive appetitive behavior for ethanol.

Alcohol Drinking↗

Initiation of ethanol self-administration in the rat using sucrose substitution in a sipper-tube procedure.

RATIONALE: The concepts of appetitive and consummatory behaviors provide a framework for examining ethanol-drinking behavior. However, traditional studies of ethanol self-administration using dipper procedures make separating the appetitive from the consummatory components difficult. OBJECTIVE: This study compared the ability to initiate ethanol self-administration using a new sipper-tube self-administration procedure with the older established sucrose-substitution initiation model that employed dipper presented reinforcement. The new model was developed to allow for an assessment of the appetitive and consummatory components in ethanol self-administration. METHODS: For the sipper-tube procedure, the rats were initiated to self-administer ethanol using a sucrose-substitution procedure that provided limited access to a sipper tube containing ethanol. This procedure required the completion of a fixed ratio requirement (FR4) in order to gain access to a sipper tube for 20 min. Initially, a 20% sucrose solution with no ethanol was provided in the sipper tube. Over sessions, the concentration of sucrose was reduced and the ethanol concentration increased, until 10% ethanol in water was the solution presented. A second group of animals was initiated to self-administer ethanol using the dipper-presentation procedure employed in our laboratory for many years. This group was used for comparison of the effectiveness of initiation in the sipper-tube procedure. RESULTS: Following initiation, the sipper-tube rats self-administered 10% ethanol in water with intakes averaging 0.75 g/kg during the 20-min drinking period. Increasing the ethanol concentrations as high as 20%, increased intakes as high as 1.5 g/kg. The ethanol intakes observed were similar to those obtained with the dipper initiation procedure but occurred in one-third of the time. CONCLUSIONS: The sipper-tube procedure employed here results in similar ethanol self-administration behavior as has been found with a dipper presentation procedure. More importantly, however, it allows for a separation of the appetitive and consummatory components of ethanol self-administration. This separation may prove useful for examining the strength of ethanol-seeking behaviors without the confound of increasing levels of ethanol interacting with the appetitive seeking behaviors.

Alcohol Drinking↗