Effects of alcohol and polyphenols from beer on atherosclerotic biomarkers in high cardiovascular risk men: a randomized feeding trial.

BACKGROUND AND AIMS: Moderate alcohol consumption exerts a cardioprotective effect, but no studies have evaluated the alcohol-independent cardiovascular effects of the non-alcoholic components of beer. We aimed to evaluate the effects of ethanol and the phenolic compounds of beer on classical and novel cardiovascular risk factors. METHODS AND RESULTS: Thirty-three high risk male volunteers were included in a randomized, crossover feeding trial. After a washout period, all subjects received beer (30 g alcohol/d, 660 mL), the equivalent amount of polyphenols as non-alcoholic beer (990 mL), and gin (30 g alcohol/d, 100 mL) for 4 weeks. All outcomes were evaluated before and after each intervention period. Moderate alcohol consumption increased serum HDL-cholesterol (∼5%), ApoA-I (∼6%), ApoA-II (∼7%) and adiponectin (∼7%), and decreased serum fibrinogen (∼8%), and interleukin (IL)-5 (∼14%) concentrations, whereas the non-alcoholic fraction of beer (mainly polyphenols) increased the receptor antagonist of IL-1 (∼24%), and decreased lymphocyte expression of lymphocyte function-associated antigen-1 (∼11%), lymphocyte and monocyte expression of Sialil-Lewis X (∼16%) and monocyte expression of CCR2 (∼31%), and tumor necrosis factor (TNF)-ß (∼14%) and IL-15 (∼22%) plasma concentrations. No changes were observed in glucose metabolism parameters or in body weight and adiposity parameters. CONCLUSION: The phenolic content of beer reduces leukocyte adhesion molecules and inflammatory biomarkers, whereas alcohol mainly improves the lipid profile and reduces some plasma inflammatory biomarkers related to atherosclerosis.

Eyelash loss in frontal fibrosing alopecia: Microscopic features of two cases.

BACKGROUND: To report two cases of eyelash loss in Frontal Fibrosing Alopecia, providing microscopic description of the eyelashes and possible association with Demodex folliculorum. CASE PRESENTATION: We present two cases of postmenopausal women diagnosed with frontal fibrosing alopecia who consulted the ophthalmology department for eyelid itching and eyelash loss. On examination, there were no signs of blepharitis, but loss of lashes was observed, and the remaining eyelashes detached easily from the eyelid. The eyelashes were examined microscopically. The bulbs were small and narrow, and the caliber of the lashes was irregular, with thinner and thicker areas. The pigment distribution was irregular; there were portions with greater or lesser accumulation. In the second case, clusters of Demodex folliculorum were observed near the eyelash root. CONCLUSION: This is the first microscopic description of eyelash loss in frontal fibrosing alopecia in the published literature. We describe small, narrow bulbs, irregular caliber of the eyelashes and irregular pigment distribution. In the second case, in which we found Demodex folliculorum infestation, there was eyelash loss even though the disease was not very advanced. We suggest that there might be an association whereby Demodex infestation might accelerate autoimmune inflammation, leading to premature eyelash loss.

[Bilateral hip fracture in a patient with Down syndrome]. / Fractura bilateral de cadera en un paciente con síndrome de Down.

There are few published data available about simultaneous bilateral hip fractures. We present the case of a 56-year-old man with Down syndrome and Alzheimer-like dementia with simultaneous bilateral hip fracture. A bilateral partial hip cemented arthroplasty was performed on this patient. The aim was to avoid the partial burden that could be caused by ostheosynthesis, due to the patient's lack of cooperation arising from his mental deterioration and his problems realizing everyday activities. He was able to walk unaided with complete autonomy until his death fourth years later. In our experience, one stage surgery for bilateral hip prosthesis is safe and provides good results in patients with severe mental impairment.

Underweight rats have enhanced dopamine release and blunted acetylcholine response in the nucleus accumbens while bingeing on sucrose.

The present study tested whether rats release more accumbens dopamine (DA) during a sugar binge when they are underweight vs. normal weight. Since acetylcholine (ACh) in the nucleus accumbens (NAc) normally increases as a meal progresses and satiety ensues, we also tested whether ACh release is altered when an animal has lost weight. Rats were maintained on daily 8-h access to chow, with 10% sucrose solution available for the first 2 h. Microdialysis performed on day 21, at normal body weight, revealed an increase in extracellular DA to 122% of baseline in response to drinking sucrose. Extracellular ACh peaked at the end of the meal. Next, the rats were food and sucrose restricted so that by day 28 they were at 85% body weight. When retested, these animals released significantly more DA when drinking sucrose (179%), but ACh release failed to rise. A control group was tested in the same manner but given sugar only on days 1, 21 and 28. At normal body weight, control animals showed a non-significant rise in DA when drinking sucrose on day 21. On day 28, at 85% body weight, the controls showed a small increase (124%) in DA release; however, this was significantly lower than the 179% observed in the underweight rats with daily sugar access. These findings suggest that when an animal binges on sugar and then loses weight, the binge releases significantly more DA and less ACh than when animals are at a normal body weight.

Micellar electrokinetic chromatography with laser induced fluorescence detection shows increase of putrescine in erythrocytes of Parkinson's disease patients.

A highly sensitive method was developed to measure putrescine by micellar electrokinetic chromatography with laser induced fluorescence detection with excellent linearity in the 1 nM to 3 µM range. The technique was tested on a drop of blood from Parkinson's disease patients obtained by finger prick. The results showed a statistically significant increase of putrescine in the erythrocytes compared to controls and a non-significant increase in plasma. This high level of putrescine does not constitute by itself proof that putrescine and polyamines are directly related to Parkinson's disease. However, the present results and several others addressed in the discussion suggest that these compounds might be causally involved in the pathophysiology of Parkinson's disease. In addition, the analytical method reported here may help to find new biomarkers for many diseases including Parkinson's disease.

Feeding and systemic D-amphetamine increase extracellular acetylcholine in the medial thalamus: a possible reward enabling function.

Acetylcholine neurons that project forward from the midbrain are known to enable dopaminergic reward functions in the ventral tegmental area. The question is whether acetylcholine might also be released in the mediodorsal thalamus for the same general purposes. Rats with a microdialysis probe lodged in the mediodorsal thalamus were allowed to eat chow for 20 min after 16-h food deprivation or were given varying doses of D-amphetamine when fed ad libitum. The result in both cases was a significant increase in extracellular acetylcholine. During feeding, acetylcholine increased to 177% of baseline. In response to d-amphetamine (2.5 mg/kg), acetylcholine increased to 184%, and with a higher dose (5 mg/kg) to 400% of baseline. It is concluded that midbrain projections to limbic portions of the thalamus provide acetylcholine for behavioral activation. This cholinergic function theoretically plays a role in enabling the limbic circuits that pass through the thalamus for reinforcement of feeding and psychostimulant abuse.

Behavioral depression in the swim test causes a biphasic, long-lasting change in accumbens acetylcholine release, with partial compensation by acetylcholinesterase and muscarinic-1 receptors.

The nucleus accumbens may play a role in acquisition and expression of behavioral depression as measured using the inescapable swim test. Previous work shows that a local injection of a cholinergic muscarinic-1 receptor agonist increases immobility and a specific muscarinic-1 antagonist acts as an antidepressant-like drug by increasing swimming escape efforts. The present study used microdialysis to monitor extracellular acetylcholine levels in the accumbens, fluorescent labeled toxins to monitor changes in acetylcholinesterase and muscarinic-1 receptors, and semiquantitative-polymerase chain reaction to detect changes in gene expression for the muscarinic-1 receptor. Microdialysis showed that acetylcholine levels did not change while an animal was swimming; however, a significant transient decrease occurred when the rat was returned to the dialysis cage, followed by a long-lasting increase that reached a maximum three hours after the test. Acetylcholine levels stayed high even 24 h after the initial test as evidenced by a significant elevation in basal level prior to the second swim. This increase in neurotransmitter may have been partially compensated by a significant increase in the degradative enzyme, acetylcholinesterase, and by a decrease in muscarinic-1 receptors and their gene expression. These results further demonstrate the importance of accumbens cholinergic function in the appearance of a depression-like state.

Sucrose sham feeding on a binge schedule releases accumbens dopamine repeatedly and eliminates the acetylcholine satiety response.

Drinking a sugar solution on an intermittent schedule can promote sugar bingeing and cause signs of dependence while releasing dopamine repeatedly like a drug of abuse. It is hypothesized that sweet taste alone is sufficient for this effect in sucrose bingeing rats. On the theory that acetylcholine in the nucleus accumbens plays a role in satiety, it is further hypothesized that purging the stomach contents will delay acetylcholine release. Rats with gastric fistulas and nucleus accumbens guide shafts for microdialysis were fed 12 h each day. During the first hour, fistulas were open for the sham-feeding group and closed for the real-feeding group, and 10% sucrose was the only food source. For the remaining 11 h, liquid rodent diet was available as well as the 10% sucrose to provide a balanced diet. In microdialysis tests during the first sugar meal on days 1, 2 and 21, extracellular dopamine increased at least 30% each day in both groups. Acetylcholine also increased during the sugar meals for the real-feeding animals, but not during sham feeding. In conclusion, the taste of sugar can increase extracellular dopamine in the nucleus accumbens without fail in animals on a dietary regimen that causes bingeing and sugar dependency. During sham feeding, the acetylcholine satiation signal is eliminated, and the animals drink more. These findings support the hypothesis that dopamine is released repeatedly in response to taste when bingeing on sweet food, and the acetylcholine satiety effect is greatly reduced by purging; this may be relevant to bulimia nervosa in humans.

[Rivaroxaban versus standard of care in venous thromboembolism prevention following hip or knee arthroplasty in daily clinical practice (Spanish data from the international study XAMOS)]. / Rivaroxaban frente al tratamiento estándar en la prevención del tromboembolismo venoso tras artroplastia de cadera o rodilla en la práctica clínica diaria (datos de España del estudio internacional XAMOS).

OBJECTIVE: To analyse the effectiveness and safety of rivaroxaban vs. standard treatment (ST) in the prevention of venous thromboembolism after hip or knee replacement in daily clinical practice in Spain. MATERIAL AND METHOD: A sub-analysis of the Spanish data in the XAMOS international observational study that included patients>18 years who received 10mg o.d. rivaroxaban or ST. FOLLOW-UP: up to 3 months after surgery. PRIMARY OUTCOMES: incidence of symptomatic/asymptomatic thromboembolic events, bleeding, mortality, and other adverse events; SECONDARY OUTCOMES: use of health resources and satisfaction after hospital discharge. RESULTS: Of the total 801 patients included, 410 received rivaroxaban and 391 ST (64.7% heparin, 24.0% fondaparinux, 11% dabigatran). The incidence of symptomatic thromboembolic events and major bleeding was similar in both groups (0.2% vs. 0.8% wit ST and 0.7% vs. 1.3% with ST [EMA criteria]/0.0% vs. 0.3% with ST [RECORD criteria]). The adverse events incidence associated with the drug was significantly higher rivaroxaban (overall: 4.4% vs. 0.8% with ST, P=.001; serious: 1.5% vs. 0.0% with ST, P=.03). The rivaroxaban used less health resources after discharge, and the majority considered the tolerability as «very good« and the treatment as «very comfortable¼. DISCUSSION: Rivaroxaban is at least as effective as ST in the prevention of venous thromboembolism prevention in daily clinical practice, with a similar incidence of haemorrhages. It provides greater satisfaction/comfort, and less health resources after discharge. These results should be interpreted taking into account the limitations inherent in observational studies.

Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell.

Most drugs of abuse increase dopamine (DA) in the nucleus accumbens (NAc), and do so every time as a pharmacological response. Palatable food also releases accumbens-shell DA, but in naïve rats the effect can wane during a long meal and disappears with repetition. Under select dietary circumstances, sugar can have effects similar to a drug of abuse. Rats show signs of DA sensitization and opioid dependence when given intermittent access to sucrose, such as alterations in DA and mu-opioid receptors, cross-sensitization with amphetamine and alcohol, and behavioral and neurochemical signs of naloxone-precipitated withdrawal. The present experiment asks whether sucrose-dependent rats release DA each time they binge. We also predict that acetylcholine (ACh), which rises as the end of a meal, will be delayed in rats with intermittent access to sucrose. To create dependency, the experimental group (Daily Intermittent Sucrose) was maintained on a diet of 12-h food deprivation that extended 4 h into the dark, followed by 12-h access to a 10% sucrose solution and chow, daily, for 21 days. As the main result, these rats gradually increased their sucrose intake from 37 to 112 ml per day (from 13 to 20 ml in the first hour of access), and repeatedly increased extracellular DA to 130% of baseline as measured in the NAc shell by microdialysis during the first hour of sucrose access on day 1, day 2 and day 21. Three control groups failed to show a significant increase in extracellular DA on day 21: Sucrose only for 1 h on days 1 and 21 (Sucrose Twice), ad libitum access to sucrose and chow (Daily Ad libitum Sucrose), and intermittent chow instead of sucrose (Daily Intermittent Chow). Acetylcholine measured at the same time as DA, increased significantly toward the end and after each test meal in all groups. In the Daily Intermittent Sucrose group, the highest ACh levels (133%) occurred during the first sample after the sucrose meal ended. In summary, sucrose-dependent animals have a delayed ACh satiation response, drink more sucrose, and release more DA than sucrose- or binge-experienced, but non-dependent animals. These results suggest another neurochemical similarity between intermittent bingeing on sucrose and drugs of abuse: both can repeatedly increase extracellular DA in the NAc shell.

Galanin and alcohol dependence: neurobehavioral research.

It is known that microinjection of galanin (GAL) intraventricularly or in specific hypothalamic sites increases food consumption and, conversely, the intake of food increases the expression of GAL in hypothalamic sites. Ethanol (EtOH) is a calorie-rich food as well as a drug of abuse. The research reviewed here shows that GAL may play a similar role in alcohol intake. First, experiments in which GAL was microinjected into the third ventricle or the paraventricular nucleus (PVN) showed increases in EtOH consumption. The increase in EtOH consumption occurred during both the light and dark cycles after GAL injection in the third ventricle in rats with limited EtOH access. Injection of GAL did not increase food intake in rats that had been chronically drinking alcohol. GAL receptor blockade reversed these increases. Microinjection of GAL directly into the PVN also increased ad libitum EtOH intake and blockade of these receptors in the PVN inhibited ad libitum EtOH consumption. Secondly, rats administered EtOH showed increases in GAL in the PVN and related hypothalamic sites. EtOH injection and voluntary intake, both ad libitum and limited access, increased GAL gene and peptide expression in the PVN consistently across administration procedures. These experiments show that GAL injection increases alcohol intake and that the intake of alcohol increases GAL, suggesting a positive feedback relationship between alcohol intake and specific hypothalamic GAL systems. Such a relationship may contribute to the motivation to consume excessive alcoholic beverages and the development of alcohol dependence.

Validity of magnetic resonance arthrography as a diagnostic tool in femoroacetabular impingement syndrome.

INTRODUCTION: Femoroacetabular impingement (FAI) is one of the main causes of hip pain in young adult and a contributory factor for development of early primary osteoarthritis. An accurate clinical diagnosis, supported by imaging studies, is important to determine the best treatment for the patient. The aim of this study is to determine the diagnostic correlation between direct magnetic resonance imaging (MRI) arthrography and the arthroscopic findings. MATERIALS AND METHOD: A review was performed on a series of 36 patients diagnosed with FAI, and who underwent hip arthroscopy surgery between 2009 and 2012. All of them had a direct MRI arthrography performed in our hospital. The presence of labral lesions, CAM deformity, and acetabular and femoral cartilage damage, were evaluated in both imaging techniques. RESULT: After analysing the results and taking the hip arthroscopy as 'gold standard', a sensitivity of 87% and a specificity of 77% were obtained, with a PPV of 87% for the diagnosis of labral lesions by direct MR arthrography. The specificity for CAM deformity was 100%, with a sensitivity of 79% and PPV of 100%. For chondral disorders lower values were found for both acetabulum and femoral head. For acetabular lesions the sensitivity was 78.5%, and specificity was 82% with a PPV of 73% and NPV of 80%. For femoral lesions, there was a sensitivity of 71.5%, a specificity of 73%, with a PPV of 62.5% and NPV of 80%. CONCLUSIONS: Due to the high sensitivity for the detection of labral lesions and the high specificity to detect CAM deformity, hip MR arthrography is a useful diagnostic tool for femoroacetabular impingement.

Clinical and radiological short-term complications after single-stage bilateral uncemented total hip arthroplasty.

PURPOSE: Economic crisis time gives to efficient procedures an important role in healthy system. Total hip replacement is a common bilateral orthopedic procedure, but there exists an important controversy to perform it in single or two stages. Our aim is to report our clinical and radiological short-term complications of bilateral uncemented total hip arthroplasty in a single time. MATERIALS AND METHODS: We have retrospectively reviewed the patients treated between 2000 and 2011 in our center by bilateral uncemented total hip replacement in a single time. We have reviewed the medical history and analyzed by age, diagnosis and ASA parameters related to the procedure, hospital stay, transfusion requirements and clinical complications. Radiological evaluation was made with anteroposterior hip radiograph evaluation (acetabular radiolucencies and stem migration). Functional assessment was carried out by the Merle D'Aubigné score. RESULTS: Seventeen patients with mean age of 47.4 (18-68) years were reviewed with a mean follow-up of 44.3 (6-172) months. ASA distribution: 29.4 % grade I; 52.9 % grade II and 17.6 % grade III. Merlé D'Aubigné score improved from 11.01 to 16.45. Hospital stay was 6 days. Transfusion requirements were two hematic concentrates for each patient. Two external popliteal sciatic nerve neurapraxias fully recovered at follow-up. Radiological results showed one case of axial migration. CONCLUSIONS: With proper patient selection and multidisciplinary team, the bilateral uncemented total hip arthroplasty in a single time has low complication rates. Our results could be used in the development of future randomized controlled trials or prospective cohort studies. LEVEL OF EVIDENCE: IV.

Systemic morphine simultaneously decreases extracellular acetylcholine and increases dopamine in the nucleus accumbens of freely moving rats.

Microdialysis was used to measure extracellular levels of acetylcholine (ACh) and dopamine (DA) simultaneously in the nucleus accumbens (NAC) of freely moving rats. Systemic injection of morphine (20 mg/kg) significantly decreased ACh (30%, p less than .01) while it increased DA (55%, p less than .01). The effects of morphine were eliminated by naloxone. The results confirm that morphine increases DA and in addition, demonstrate an inhibitory influence of this opiate on extracellular levels of ACh in the NAC.

Inescapable stress enhances extracellular acetylcholine in the rat hippocampus and prefrontal cortex but not the nucleus accumbens or amygdala.

A number of experimental results has pointed to a cholinergic involvement in the stress response. Recently, analytical techniques have become available to measure acetylcholine release in vivo during exposure to various stressors. In these experiments, microdialysis was used to monitor acetylcholine output every 15 min in the dorsal hippocampus, amygdala, nucleus accumbens and prefrontal cortex before, during and after 1 h of restraint, including a 15-min session of intermittent tail-shock (1/min, 1 mA, 1-s duration) in rats. In response to the stressful event, acetylcholine release was significantly increased in the prefrontal cortex (186%; p < 0.01) and hippocampus (168%; P < 0.01) but not in the amygdala or nucleus accumbens. The sole effects observed in the amygdala and nucleus accumbens occurred upon release from the restrainer, at which point acetylcholine levels were significantly elevated in both areas (amygdala: 150%; P < 0.05; nucleus accumbens: 13%; P < 0.05). An enhanced acetylcholine release was also evident during this sample period in the hippocampus and prefrontal cortex. These data demonstrate an enhancement of cholinergic activity in response to stress in two acetylcholine projection systems (hippocampus and prefrontal cortex) but not in the intrinsic acetylcholine system of the nucleus accumbens or the extrinsic innervation of the amygdala. Moreover, the data showed that relief from stress was accompanied by a more ubiquitous acetylcholine response that extended to each site tested.

Nucleus accumbens muscarinic receptors in the control of behavioral depression: antidepressant-like effects of local M1 antagonist in the Porsolt swim test.

Systemically administered cholinomimetics or cholinesterase inhibitors can depress behavior in humans and animals, whereas antimuscarinic agents reverse this effect or even produce euphoria. Although these effects have been well documented, the specific brain regions that mediate them remain largely unknown. In the present experiments, muscarinic agonists and antagonists were locally injected into the nucleus accumbens of female Sprague-Dawley rats to test for their effects on behavioral depression in the Porsolt swim test and locomotor activity. Local, microinjections of the drugs in the accumbens elicited behaviors that were similar to the systemic effects reported in other studies. Injection of the non-specific agonist arecoline (40 and 80 microg) dose-dependently inhibited swimming and escape behavior. This may be mediated in part by accumbens M1 receptors because blocking these receptors with the specific antagonist pirenzepine (17.5 and 35.0 microg) did the opposite by increasing swimming. Gallamine (0.13, 0.44, and 0.88 microg), an antagonist at M2 receptors, dose-dependently decreased swimming. Two-way microdialysis suggested that this was in part due to the release of ACh by blocking M2 autoreceptors. Scopolamine, a mixed M1/M2 receptor antagonist, also released ACh but did not decrease swimming, probably because the M1 receptors were blocked; the drug (1.0 microg) increased swimming time, much like pirenzepine. With the exception of arecoline, none of the drugs significantly affected locomotor activity in a photocell cage. Arecoline (40 microg), which had decreased swimming, reduced activity. The present study suggests that muscarinic receptors in the nucleus accumbens can control immobility in the Porsolt swim test. The onset of immobility may depend on the activation of post-synaptic M1 receptors.

Glutamate release in the nucleus accumbens is involved in behavioral depression during the PORSOLT swim test.

An abnormality in glutamate function has been implicated in the neural substrate of depressive disorders. To investigate this in rats, the Porsolt swim test was used to assess the role of glutamate in the nucleus accumbens. Glutamate injected into the nucleus accumbens dose-dependently decreased swimming time on the test day (day 2), whereas N-methyl-D-aspartate antagonists dizocilpine and 2-amino-5-phosphonovalerate increased swimming, like an antidepressant. Dizocilpine injected before the conditioning trial (day 1) did not modify the swimming times during the first day but abolished behavioral depression on day 2. Microdialysis coupled to capillary-zone electrophoresis was then used to determine in vivo changes in glutamate release in 1-min samples during the swim test. On day 1, glutamate increased significantly and reached a maximum of 222% after 3 min of swimming. On day 2, baseline glutamate levels were back to normal, but when the animal was placed in the water, glutamate increased to 419% during the first minute, and the animals swam significantly less. For comparison, tail pinch on consecutive days was used as a nonspecific, repeated stressor while accumbens glutamate levels were measured. Tail pinch on the first day increased glutamate similar to the effect obtained during the first day of swimming; however, a second day of tail pinch decreased glutamate levels, instead of the potentiated response observed during the second day of swimming. These results show that accumbens glutamate plays a role in causing the behavioral aspects of depressed behavior as modeled in the swim test. The accumbens may be a potential site of action for drugs that alter behavioral depression.

Effects of nicotine and mecamylamine-induced withdrawal on extracellular dopamine and acetylcholine in the rat nucleus accumbens.

RATIONALE: Prior research suggests that high levels of acetylcholine (ACh) in the nucleus accumbens (NAc) are associated with aversive states such as morphine withdrawal, but this has not been tested for nicotine withdrawal. OBJECTIVES: The goal was to test the hypothesis that acute nicotine decreases extracellular ACh and increases extracellular dopamine (DA) in the NAc, while withdrawal from nicotine causes an opposite neurochemical imbalance with high extracellular ACh and low DA. METHODS: Rats were prepared with a microdialysis probe in the NAc (primarily the shell region). They received one injection of nicotine (0.5 mg/kg, s.c.) or chronic nicotine (9 mg/kg per day via osmotic minipump). RESULTS: Naive animals receiving acute nicotine showed a mild, significant increase in both ACh (122% of baseline) and DA (124%). After chronic nicotine administration for 7 days, the nicotinic antagonist mecamylamine (1.0 mg/kg, s.c.) precipitated withdrawal with the appearance of somatic signs (teeth chattering and shakes/tremors) and a significant increase in extracellular ACh to 125% of baseline, while extracellular DA decreased to 65%. Control groups receiving saline in place of nicotine or mecamylamine did not show these effects. CONCLUSIONS: Earlier work suggests that the observed release of accumbens ACh and DA in response to acute nicotine administration may be a factor in nicotine-induced suppression of appetite. ACh release during withdrawal, coupled with the decrease in extracellular DA may play a role in the aversive aspects of nicotine withdrawal that contribute to dependency.

Excessive sugar intake alters binding to dopamine and mu-opioid receptors in the brain.

Palatable food stimulates neural systems implicated in drug dependence; thus sugar might have effects like a drug of abuse. Rats were given 25% glucose solution with chow for 12 h followed by 12 h of food deprivation each day. They doubled their glucose intake in 10 days and developed a pattern of excessive intake in the first hour of daily access. After 30 days, receptor binding was compared to chow-fed controls. Dopamine D-1 receptor binding increased significantly in the accumbens core and shell. In contrast, D-2 binding decreased in the dorsal striatum. Binding to dopamine transporter increased in the midbrain. Opioid mu-1 receptor binding increased significantly in the cingulate cortex, hippocampus, locus coeruleus and accumbens shell. Thus, intermittent, excessive sugar intake sensitized D-1 and mu-1 receptors much like some drugs of abuse.