Access Scheduling Research Articles

Schedules for detection, diagnosis and assessment of psychiatric disorders

Developmental Medicine & Child NeurologyVolume 43, Issue s90 p. 48-49 Free Access Schedules for detection, diagnosis and assessment of psychiatric disorders Yale-Brown Obsessive Compulsive Scale (YBOCS) First published: 12 November 2008 https://doi.org/10.1111/j.1469-8749.2001.tb12469.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume43, Issues90December 2001Pages 48-49 ReferencesRelatedInformation

Schedules for the detection, diagnosis, and assessment of autistic spectrum disorder

Developmental Medicine & Child NeurologyVolume 43, Issue s90 p. 5-6 Free Access Schedules for the detection, diagnosis, and assessment of autistic spectrum disorder Asperger Syndrome Screening Questionnaire (ASSQ) First published: 12 November 2008 https://doi.org/10.1111/j.1469-8749.2001.tb12426.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Ehlers S., Gillberg C. (1993) The epidemiology of Asperger syndrome: a total population study. Journal of Child Psychology and Psychiatry and Allied Disciplines 34: 1327– 50. 2 Ehlers S., Gillberg C., Wing L. (1999) A screening questionnaire for asperger syndrome and other high functioning autism spectrum disorders in school age children. Journal of Autism and Developmental Disorders 29: 129– 41. 3 Gillberg C., Nordin V., Ehlers S. (1996) Early detection of autism: diagnostic instruments for clinicians. European Journal of Child and Adolescent Psychiatry 5: 67– 74. 4 Gillberg IC, Gillberg C. (1989) Asperger syndrome: Some epidemiological considerations: a research note. Journal of Child Psychology and Psychiatry and Allied Disciplines 30: 631– 8. Citing Literature Volume43, Issues90December 2001Pages 5-6 ReferencesRelatedInformation

Schedules for detection, diagnosis and assessment of psychiatric disorders

Developmental Medicine & Child NeurologyVolume 43, Issue s90 p. 46-47 Free Access Schedules for detection, diagnosis and assessment of psychiatric disorders Schedule for Affective Disorders and Schizophrenia for School Age Children (K-SADS) First published: 12 November 2008 https://doi.org/10.1111/j.1469-8749.2001.tb12467.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Ambrosini PJ. (2000) Historical development and the present status of the Schedule for Affective Disorders and Schizophrenia for School Age Children. Journal of the American Academy of Child and Adolescent Psychiatry 39: 49– 58. 2 Kaufman J., Birmaher B., Brent D., Rao U., Flynn C., Moreci P., Williamson D., Ryan N. (1997) Schedule for Affective Disorders and Schizophrenia for School Age Children Present and Lifetime version (K-SADS-PL): Initial reliability and validity data. Journal of the American Academy of Child and Adolescent Psychiatry 36: 980– 8. Volume43, Issues90December 2001Pages 46-47 ReferencesRelatedInformation

Effects of Naltrexone and Ro 15‐4513 on a Multiple Schedule of Ethanol and Tang Self‐Administration

Both the opioid antagonist, naltrexone, and GABAA/benzodiazepine-site negative modulator, Ro 15-4513, decrease ethanol self-administration in rodents and nonhuman primates. However, the selectivity of these drugs for decreasing ethanol self-administration relative to reducing responding maintained by other reinforcers in primates is not clear. The present study used a multiple schedule self-administration procedure in cynomolgus monkeys to examine the selectivity of naltrexone and Ro 15-4513 for reducing ethanol self-administration relative to an orange flavored sugar-free sweetened solution (Sugar-free Tang). Six adult cynomolgus monkeys were trained to self-administer 4% (w/v) ethanol and 4% or 6% (w/v) Tang under a multiple schedule of liquid access. The effect of acute administration of naltrexone (0.1, 0.3, 1, 3 mg/kg) was examined. The effect of 15 days of chronic, 1 mg/kg naltrexone on ethanol and Tang self-administration was then examined in four monkeys. Acute administration of Ro 15-4513 (0.01, 0.03, 0.1, 0.3 mg/kg) as well as 15 days of chronic administration of 0.1 mg/kg Ro 15-4513 was also examined in four monkeys. Ethanol and Tang were self-administered at similar volumes and patterns under baseline conditions. Acute naltrexone administration significantly decreased total session ethanol and Tang intake as well as the number and volume of ethanol and Tang drinks. Chronic naltrexone also significantly decreased ethanol and Tang intake. Ethanol, but not Tang, drink volume was significantly decreased by chronic 1 mg/kg naltrexone pretreatment. The number of ethanol and Tang drinks and drink duration were not significantly decreased by chronic naltrexone. Acute Ro 15-4513 pretreatment significantly decreased ethanol and Tang intake, mean drinks and median drink duration. Chronic 0.1 mg/kg Ro 15-4513 pretreatment significantly decreased total ethanol intake only during the first week of pretreatment, but it significantly decreased Tang intake for all 3 pretreatment weeks. Similar to rodent studies, acute and chronic naltrexone and Ro 15-4513 reduced ethanol and Tang intake in cynomolgus monkeys. However, unlike rodent studies, neither drug showed selectivity for reducing ethanol intake compared with a comparison reinforcer. These differences highlight the need for testing putative ethanol abuse treatment drugs under diverse conditions and multiple species before undertaking human clinical trials.

Food access schedule and diet composition alter rhythmicity of serum melatonin and pineal NAT activity

This study investigated the effect of dietary composition and food access schedule on the rhythmicity of serum melatonin and pineal N-acetyltransferase (NAT) activity. Wistar rats maintained on a 12:12 h light–dark cycle were assigned to two dietary groups: a group fed rat chow and a group fed a choice between a protein-rich and a carbohydrate-rich diet. Each dietary group was further divided based on feeding schedule, with food available between 0800 and 1600 h or ad lib access to food. Regardless of dietary condition, total food and carbohydrate intake of rats having free access to food was higher than under the restricted food access schedule. Protein intake of rats fed the dietary choice was lower with the restricted access than in the free access. In rats fed the dietary choice, melatonin levels and NAT activity were significantly decreased with restricted access compared to free access. Such results were not found in rats offered restricted chow. This study suggests that the rhythms of melatonin secretion and NAT activity can be altered by dietary composition.

Long-term effects of alcohol drinking on cerebral glucose utilization in alcohol-preferring rats

The 2-[ 14C]deoxyglucose (2-DG) quantitative autoradiography technique was used to determine rates of local cerebral glucose utilization (LCGU) in discrete brain regions in alcohol-chronic (A-C), alcohol-deprived (A-D) and alcohol-naı̈ve (A-N) adult, male alcohol-preferring (P) rats. The hypothesis to be tested is that neuronal alterations occur as a result of chronic alcohol drinking and some of these alterations persist for long periods in the absence of alcohol. Following 6 weeks of daily 4-h scheduled access sessions to 15% (v/v) ethanol and water, group A-D received only water during the sessions over the next 2 weeks, whereas groups A-C and A-N continued to receive ethanol–water and water–water, respectively. On the 14th day of the deprivation interval, LCGU rates were measured 1 h prior to the scheduled access period. Mean ethanol intake for the A-D and A-C groups was 1.5±0.1 g ethanol/kg body weight per 4 h. LCGU rates were significantly decreased in 49 of 57 regions or subregions examined in the A-C group compared to the A-N group, including subregions of the cerebral cortex, hippocampus and structures in the mesocorticolimbic and nigrostriatal systems. Following alcohol deprivation, LCGU values in the A-D group were partially or completely returned to A-N levels in many, but not all, regions. In several limbic regions (e.g., ventral tegmental area, olfactory tubercle, medial prefrontal cortex, ventral pallidum and lateral septum), no recovery of LCGU rates was observed after 2 weeks of alcohol deprivation. This study demonstrates that chronic alcohol consumption produces significant reductions in functional neuronal activity in P rats, some of which persist in the absence of ethanol. The extent to which LCGU rates returned to normal levels following 2 weeks of alcohol deprivation varied among brain regions, suggesting that there are imbalanced interactions among and within several CNS sites, which do not reflect either the alcohol-naı̈ve or chronic alcohol-exposed state. Such neuronal imbalances may underlie relapse of alcohol drinking following prolonged abstinence.

Page access scheduling in join processing

The join relational operation is one of the most expensive among database operations. In this study, we consider the problem of scheduling page accesses in join processing. This raises two interesting problems: (1) determining a page access sequence that uses the minimum number of buffer pages without any page reaccesses, and (2) determining a page access sequence that minimizes the number of page reaccesses for a given buffer size. We use a graph model to represent the pages from the relations that contain tuples to be joined, and present new heuristics for the two problems. Our experimental results show that the new heuristic performs well.

A Five-Phase Reservation Protocol (FPRP) for Mobile Ad Hoc Networks

A new single channel, time division multiple access (TDMA)-based broadcast scheduling protocol, termed the Five-Phase Reservation Protocol (FPRP), is presented for mobile ad hoc networks. The protocol jointly and simultaneously performs the tasks of channel access and node broadcast scheduling. The protocol allows nodes to make reservations within TDMA broadcast schedules. It employs a contention-based mechanism with which nodes compete with each other to acquire TDMA slots. The FPRP is free of the "hidden terminal" problem, and is designed such that reservations can be made quickly and efficiently with negligible probability of conflict. It is fully-distributed and parallel (a reservation is made through a localized conversation between nodes in a 2-hop neighborhood), and is thus scalable. A "multihop ALOHA" policy is developed to support the FPRP. This policy uses a multihop, pseudo-Bayesian algorithm to calculate contention probabilities and enable faster convergence of the reservation procedure. The performance of the protocol, measured in terms of scheduling quality, scheduling overhead and robustness in the presence of nodal mobility, has been studied via simulations. The results showed that the protocol works very well in all three aspects. Some future work and applications are also discussed.

Naltrexone and alcohol drinking in mice lacking β-endorphin by site-directed mutagenesis

Alcohol-induced activation of the opioid system may contribute to the reinforcing properties of alcohol. This study investigated whether elimination of β-endorphin (BE) synthesis via site-directed mutagenesis in embryonic stem cells would alter alcohol intake in mice. Both BE-deficient and wildtype (WT) mice generated from the targeted stem cells were backcrossed for nine generations onto a C57BL/6 background, and were maintained with ad libitum food and water. Mice had access to alcohol (10% v/v) under the following conditions: 24 h, scheduled access for 2 h/day, following acute (1 or 2 days) or chronic (5 weeks) alcohol deprivation, and scheduled access following six doses of naltrexone (0.125–16.0 mg/kg BW, ip) or saline treatment. Alcohol intake was similar in BE-deficient and WT mice given chronic access to alcohol, but greater in BE-deficient compared with WT mice during the first 10 days of scheduled access to alcohol, but not after more extensive experience with scheduled access. BE-deficient, but not WT mice, increased alcohol intake following 2 days, but not 1 day or 5 weeks, of deprivation. Naltrexone reduced alcohol drinking both in BE-deficient and WT mice, suggesting that drinking is mediated, in part, by activation of opioid receptors in both genotypes.

Effects of MDL 72222, a Serotonin3 Antagonist, on Operant Responding for Ethanol by Alcohol‐Preferring P Rats

Previous studies indicated that, under continuous access conditions, the 5-HT3 antagonist MDL 72222 (MDL) effectively reduced ethanol drinking of alcohol-preferring P rats. However, MDL was without effect when similar doses were tested under scheduled access conditions, unless the ethanol access period was randomly presented. This study examined the effects of MDL on operant responding for ethanol and water by adult male alcohol-preferring P rats. During the dark cycle, subjects in the first experiment were trained to respond concurrently for 15% ethanol and water on a fixed-ratio 5 (FR-5) and FR-1 schedule of reinforcement, respectively. Approximately 30 min before the 4-hr operant session, rats were injected subcutaneously (sc) with saline or MDL (1, 3, or 5 mg/kg). A second experiment tested the effects of 1 mg/kg MDL on operant responding for 15% ethanol in 1-hr sessions when operant access was given at a fixed time each day (fixed scheduled access, FSA group) or at variable time periods throughout the dark cycle (variable scheduled access, VSA group). In the first experiment, only the 5 mg/kg dose of MDL decreased responding for ethanol (approximately 20%) during the first 30 min of the 4-hr session. This dose also reduced total 4-hr responding for ethanol and water. In the second experiment, the 1 mg/kg dose of MDL had no effect on operant responding by the FSA group, but significantly reduced ethanol responding by the VSA group. These results suggest that 5-HT3 receptors may be involved in mediating the reinforcing effects of ethanol, and that temporal-environmental cues associated with the presentation of ethanol may be one factor involved in reducing the effectiveness of 5-HT3 antagonists to attenuate ethanol intake.

NAALADase inhibition reduces alcohol consumption in the alcohol‐preferring (P) line of rats

N-acetyl-aspartyl-glutamate (NAAG) is a major peptide component of the brain, with millimolar tissue levels of 0.1-5 nmol/mg wet weight. NAAG is hydrolyzed by the enzyme N-acetylated alpha-linked acidic dipeptidase (NAALADase; glutamate carboxypeptidase II; EC no. 3.4.17.21) to N-acetyl-aspartate (NAA) and glutamate. Recently, a potent and selective NAALADase inhibitor termed 2-(phosphonomethyl)pentanedioic acid (2-PMPA) was identified that has a 300 pM Ki for NAALADase inhibition. Given the accumulating evidence indicating an important role of the glutamate system in alcoholism and dependence, the objective of this study was to evaluate the effects of systemic administration of 2-PMPA (50, 100 and 200 mg/kg; i.p.) upon the ethanol intakes of alcohol-preferring (P) rats. Female P rats (n = 8) received daily 1-hour scheduled access to a 10% (v/v) ethanol. In a within-subjects design, 2-PMPA treatments were tested once a week. Baseline ethanol drinking consisted of the mean of the 3 days prior to testing in which saline injections were given. Results indicated that, whereas the 200 mg/kg dose of 2-PMPA had no effect on ethanol intake, both the 50 and 100 mg/kg doses significantly reduced ethanol consumption by approximately 25% (p < 0.05) during the 1-hour access period. Body weights and 24-hour water intakes were not altered at any of the doses. These data suggest that the NAAG/NAALADase system may be involved in neuronal systems regulating alcohol-drinking behavior.

Reverse Microdialysis of a Dopamine Uptake Inhibitor in the Nucleus Accumbens of Alcohol‐Preferring Rats: Effects on Dialysate Dopamine Levels and Ethanol Intake

The mesolimbic dopamine (DA) system has been implicated in mediating the reinforcing actions of ethanol (EtOH). This study examines the effects of local perfusion of the DA uptake inhibitor GBR12909 (GBR) on (1) DA levels in the nucleus accumbens (NAc) and (2) EtOH drinking in alcohol-preferring rats. Stable drinking of a 15% (v/v) EtOH solution (minimum of 0.75 g/kg body weight) was established in daily 1 hr limited access sessions. Rats were then implanted with bilateral guide cannulae aimed 4 mm above the NAc. After recovery from surgery, concentric microdialysis probes (2 mm dialysis membrane surface) were inserted into the NAc. Most placements were in the shell or overlapping both shell and core. Two days later, the probes were perfused at 1.0 microl/min with artificial cerebral spinal fluid (aCSF) for at least a 90 min washout period followed by collection of five basal samples over 150 min. Rats were then perfused with either aCSF alone or 10, 25, 100, or 200 microM of GBR for 240 min on the first day of microdialysis. During the last 60 min of the drug treatment phase, rats were given their scheduled access to 15% EtOH. All rats were then perfused with aCSF for the last 90 min of the experiment. The following day, the procedure was repeated, but animals that received aCSF on the first day were given a dose of GBR and rats given GBR on the first day received only aCSF. GBR perfusion increased extracellular NAc DA levels dose dependently to more than 800% of basal levels at 100 to 200 microM but failed to alter EtOH intake (p > 0.05, paired t test) at any concentration tested. Moreover, after 100 microM of GBR perfusion had terminated, the extracellular levels of DA in the NAc remained elevated for approximately 24 hr (790% of day 1 basal; p < 0.05). The increase in dialysate DA levels observed during GBR perfusion with 100 microM was significantly greater for EtOH-experienced rats than for EtOH-naïve rats [F(7,59) = 14.85, p < 0.0001, analysis of variance, Student-Newman-Keuls post hoc test]. The results suggest (1) that EtOH drinking experience induces neuroadaptations that increase DA release in the NAc, and (2) that additional elevation in synaptic levels of DA in the NAc does not influence the maintenance of ongoing alcohol drinking under scheduled access conditions in alcohol-preferring animals.

Reverse Microdialysis of a Dopamine Uptake Inhibitor in the Nucleus Accumbens of Alcohol-Preferring Rats: Effects on Dialysate Dopamine Levels and Ethanol Intake

Background: The mesolimbic dopamine (DA) system has been implicated in mediating the reinforcing actions of ethanol (EtOH). This study examines the effects of local perfusion of the DA uptake inhibitor GBR12909 (GBR) on (1) DA levels in the nucleus accumbens (NAc) and (2) EtOH drinking in alcohol-preferring rats. Methods: Stable drinking of a 15% (v/v) EtOH solution (minimum of 0.75 g/kg body weight) was established in daily 1 hr limited access sessions. Rats were then implanted with bilateral guide cannulae aimed 4 mm above the NAc. After recovery from surgery, concentric microdialysis probes (2 mm dialysis membrane surface) were inserted into the NAc. Most placements were in the shell or overlapping both shell and core. Two days later, the probes were perfused at 1.0 μl/min with artificial cerebral spinal fluid (aCSF) for at least a 90 min washout period followed by collection of five basal samples over 150 min. Rats were then perfused with either aCSF alone or 10, 25, 100, or 200 μM of GBR for 240 min on the first day of microdialysis. During the last 60 min of the drug treatment phase, rats were given their scheduled access to 15% EtOH. All rats were then perfused with aCSF for the last 90 min of the experiment. The following day, the procedure was repeated, but animals that received aCSF on the first day were given a dose of GBR and rats given GBR on the first day received only aCSF. Results: GBR perfusion increased extracellular NAc DA levels dose dependently to more than 800% of basal levels at 100 to 200 μM but failed to alter EtOH intake (p > 0.05, paired t test) at any concentration tested. Moreover, after 100 μM of GBR perfusion had terminated, the extracellular levels of DA in the NAc remained elevated for approximately 24 hr (790% of day 1 basal;p < 0.05). The increase in dialysate DA levels observed during GBR perfusion with 100 μM was significantly greater for EtOH-experienced rats than for EtOH-naïve rats [F (7,59) = 14.85, p < 0.0001, analysis of variance, Student-Newman-Keuls post hoc test]. Conclusions: The results suggest (1) that EtOH drinking experience induces neuroadaptations that increase DA release in the NAc, and (2) that additional elevation in synaptic levels of DA in the NAc does not influence the maintenance of ongoing alcohol drinking under scheduled access conditions in alcohol-preferring animals.

Memory access scheduling

The bandwidth and latency of a memory system are strongly dependent on the manner in which accesses interact with the “3-D” structure of banks, rows, and columns characteristic of contemporary DRAM chips. There is nearly an order of magnitude difference in bandwidth between successive references to different columns within a row and different rows within a bank. This paper introduces memory access scheduling, a technique that improves the performance of a memory system by reordering memory references to exploit locality within the 3-D memory structure. Conservative reordering, in which the first ready reference in a sequence is performed, improves bandwidth by 40% for traces from five media benchmarks. Aggressive reordering, in which operations are scheduled to optimize memory bandwidth, improves bandwidth by 93% for the same set of applications. Memory access scheduling is particularly important for media processors where it enables the processor to make the most efficient use of scarce memory bandwidth.

Differences in the Consumption of Ethanol and Flavored Solutions in Three Strains of Rats

Several studies have shown a correlation between ethanol consumption and the intake of flavored solutions in rats, particularly sweet solutions. This observation, however, has not been shown in all strains of rats. The present study examined whether the intake of ethanol and that of flavored solutions would be related in Lewis (LEW), Wistar (WIS), and Wistar Kyoto (WKY) rats. During phase I, all rats were presented with water and a flavored solution following a continuous access paradigm as developed by Overstreet et al.: quinine (0.25% wt/vol), saccharin (0.1% wt/vol), ethanol (ETOH) (10% vol/vol), and saccharin-quinine (SQ) solutions (0.4% wt/vol–0.04% wt/vol). During phase II, fluid presentations were reduced to a 10-min limited access schedule and were presented in the same order. Results showed strain differences in intake and preference for ETOH and SQ during both phases, but not in quinine or saccharin intake. ETOH and saccharin intake were only correlated in the LEW strain during limited access drinking, while ETOH and SQ intake were correlated in the LEW strain as well as when all strains were collapsed during continuous drinking. These findings suggested that any association between ETOH and sweet intake may not be generalizable to all rat strains. The animals used in this study may have differed in taste sensitivity, as low ETOH-consuming LEW rats were sensitive to the bitter taste of quinine alone, as well as when mixed with saccharin. Sensitivity to bitter tastes may be an important predictor of low ETOH consumption and/or preference. These data provide further evidence for the role of taste factors in the mediation of voluntary ETOH consumption in rats.

Delta modulation based prediction for access control in integrated voice/data CDMA systems

In this paper, we propose access control protocols for integrated voice/data code division multiple access (CDMA) systems that are based on estimating the residual capacity available for data users. The data model considered in the analysis is suitable for non-transparent services (e.g., e-mail, file transfer, store-and-forward facsimile, etc.). The residual capacity is derived from the feasibility condition for power control using an adaptive prediction technique based on delta modulation. The analysis is extended for the case of imperfect power control. Two access control protocols are considered: modified delta modulation with scheduled access (MDM-S) and modified delta modulation with random access (MDM-R). Comparisons with earlier proposed protocols reveal a better performance in terms of average throughput for data for a given system capacity and outage probability.

A logarithmic lower bound for time-spread multiple-access (TSMA) protocols

TimedSpread MultipledAccess lTSMAr protocols are scheduled access protocols for mobile multidhop radio networks that guarantee deterministic access to the shared channel regardless of the possibility of radio interference. In scheduled access methods, time is considered to be slotted and time slots are cyclically organized into frames. In general, the shorter the frame, the more efficient the protocol. An O(loglog n) lower bound is known on the minimum length of the frame of TSMA protocols in networks with n nodes. In this note we improve that lower bound by characterizing the multiple access to the radio channel as a combinatorial problem. The proposed characterization allows us to prove that no TSMA protocols can successfully schedule the transmissions of the nodes of a multidhop radio network in frames with less than log n time slots.

Naloxone retards the expression of a genetic predisposition toward alcohol drinking.

This study examined whether repeated daily treatment with naloxone prevents expression of a genetic predisposition toward high alcohol drinking in rats selectively bred for alcohol preference (P line). In phase 1, alcohol-naive male rats were given food and water ad libitum and were pretreated with naloxone (2.5, 5.0, or 10.0 mg/kg, IP) or saline prior to scheduled access to alcohol (2 h/day) for 30 days. In phase 2, naloxone treatment was suspended for 30 days while rats continued to receive food and water ad libitum and scheduled access to alcohol. In phase 3, alcohol access was suspended for 14 days while rats continued to receive food and water ad libitum. In phase 4, daily pretreatment with naloxone or saline, followed by scheduled access to alcohol, was reinstated for an additional 30 days. Naloxone dose-dependently retarded acquisition of alcohol drinking. Following discontinuation of naloxone treatment, alcohol intake increased to levels comparable to those seen in the saline-treated group. Naloxone dose-dependently suppressed reinstatement of alcohol drinking (relapse) after a period of imposed abstinence. The results suggest that naloxone retards the acquisition of alcohol drinking and suppresses reinstatement of alcohol drinking in rats genetically predisposed toward high alcohol intake.

Gut vagal afferent lesions increase meal size but do not block gastric preload-induced feeding suppression.

Subdiaphragmatic vagal afferent (SVA) signals arising from gut sites may provide critical feedback for the control of food intake within a meal. To evaluate the role of SVAs in both spontaneous and scheduled meals, food intake was assessed in two paradigms in male Sprague-Dawley rats. In the first study, control (Con) rats (n = 6) and rats with subdiaphragmatic vagal deafferentation (SDA) (n = 7) had 12-h nightly access to Ensure liquid diet (1 kcal/ml). SDA rats had larger and fewer meals and maintained initial rapid rates of licking, yet total numbers of licks were unaffected. In the second study, Con (n = 8) and SDA (n = 7) rats had scheduled access to 12. 5% liquid glucose after overnight food deprivation. Glucose intake was assessed after 5-ml gastric preloads of 0.9% saline or glucose, peptone, and Intralipid solutions at three concentrations (0.5, 1, and 2 kcal/ml). Glucose and peptone preloads suppressed intake similarly in Con and SDA rats, whereas Intralipid was ineffective. These results suggest that meal-related SVA signals 1) are not critical in determining preload-induced feeding suppression after deprivation, yet 2) contribute to satiety during spontaneous meals.

Meal-synchronized CEA in rats: effects of meal size, intragastric feeding, and subdiaphragmatic vagotomy.

Within a feeding schedule of intermittent food access, large meals have the ability to induce activity at the same time the next day [circadian ensuing activity (CEA)]. In these experiments, we evaluated the minimum meal size necessary to induce CEA and whether oral-pharyngeal factors and afferent vagal activity played necessary roles in the induction of the underlying process. In experiment 1, every 33 h rats were given two meals separated by a 2-h interval. The size of the first meal was varied, while total intake every feeding cycle was held constant. When the initial meal was <10 g (34 kcal) CEA occurred later, indicating that such a meal size was subthreshold for inducing CEA. In experiment 2, rats were given intragastric (IG) meals every 33 h, before and after complete subdiaphragmatic vagotomy. IG nutrient meals induced CEA, indicating that extensive oral-pharyngeal experience was not necessary for CEA induction. CEA occurred in vagotomized rats but, compared with intact rats, appeared to occur later relative to nutrient infusion, indicating that afferent vagal activity may be sufficient but not necessary to induce CEA.