Comparison of Direct and Indirect Detection of Toxoplasma gondii in Ovine Using Real-Time PCR, Serological and Histological Techniques.

Toxoplasma gondii is a zoonotic pathogen and the ingestion of tissue cysts by consumption of lamb or mutton has been identified as a possible cause of infection in humans. Many serological surveys in sheep have been performed, showing relevant serological rates; however, while the detection of antibodies indicates an exposure to T. gondii, this does not necessarily imply the presence of tissue cysts in edible tissue. The current study aims to provide further understanding on the occurrence of T. gondii in sheep muscles and the strength of correlation between serological positivity and presence of the parasite in sheep. From 349 sheep, samples (i.e., blood, heart and diaphragm) were collected and subjected to ELISA tests, real-time PCR and histological tests. Despite the high seroprevalence, T. gondii DNA was detected in the heart and/or the diaphragm from 13 out of the 349 tested sheep (3.7%); all were adults (13/191). Furthermore, the histological tests did not reveal the presence of T. gondii tissue cysts in any of the examined portions of interventricular septum. It should be considered that the likelihood of detecting genetic material of the parasite is probably influenced by the uneven distribution of the tissue cysts in the carcass as well as the methodology applied. The findings of this study support the importance of describing the uncertainty associated with the data used for risk assessment to reduce inaccurate estimation or risk overestimation.

Toxoplasma gondii in sheep: Serological occurrence at slaughterhouse level in Italy and environmental risk factors.

Toxoplasmosis is a parasitic disease affecting a wide range of species, including humans, and can be responsible for important clinical manifestations such as abortion and neurological signs. Sheep show a remarkable susceptibility to its causative agent, Toxoplasma gondii, and zoonotic transmission may occur in case of consumption of undercooked meat obtained from infected animals. Toxoplasma gondii seroprevalence in sheep can significantly vary on a geographical basis, as shown by numerous surveys conducted worldwide. To investigate environmental and climate conditions that may affect the likelihood of ovine infection, 405 serum samples from selected sheep raised in 91 farms were collected from two abattoirs, with each abattoir receiving animals from two regions (1/Tuscany-Latium and 2/Campania-Basilicata). The seroprevalence of infection in all examined animals was 53.8%. Young animals (n = 165) had a lower likelihood of being T. gondii positive compared to the adults (OR = 0.21), and the seropositive rate of animals slaughtered in abattoir 2 was significantly higher than that of animals slaughtered in abattoir 1 (60.5 vs. 43.2%, p < 0.01). The significant bioclimatic variables (p < 0.05) associated with the presence of T. gondii antibodies were related to areas with a lower range of temperature and higher precipitation. In conclusion, this study expands on the interpretation of serological data, with the inclusion of environmental and climatic variables, as possible risk factors in the spread of toxoplasmosis in the study area. These findings provide novel insights to support public health measures, such as risk-based control plan, and contribute to a "One Health" approach, taking into account the environmental and climatic perspectives.

Prevalence of prothrombotic polymorphisms in a selected cohort of cryptogenic and noncryptogenic ischemic stroke patients.

Ischemic stroke is a complex multifactorial disease and approximately 30%, especially in the young, are cryptogenic. In some of the patients with cryptogenic ischemic stroke the underlying risk factor may be a prothrombotic state. We studied 101 patients with ischemic stroke under 55 years of age. All the patients underwent an extensive diagnostic evaluation to determine the cause of stroke. Common variations in the genes encoding factor V, prothrombin, 5,10-methylenetetrahydrofolate reductase, plasminogen activator inhibitor-1, and human platelet alloantigens-1 were evaluated. Of the 101 patients with ischemic stroke, 28 patients had cryptogenic ischemic stroke. At least one of the different genetic polymorphisms investigated was present in 44% patients in the total group and in 48% of patients with cryptogenic ischemic stroke. In this study population under 55 years of age there was no significant difference in the prevalence of various genetic polymorphisms, factor V, prothrombin, 5,10-methylenetetrahydrofolate reductase, plasminogen activator inhibitor-1, and human platelet alloantigens) in patients with cryptogenic ischemic stroke and in patients with ischemic stroke of determined cause.

Primary Gliosarcoma of the Cerebellum in a Young Pregnant Woman: Management Challenges and Immunohistochemical Features.

BACKGROUND: Gliosarcoma (GS) represents a rare, high-grade (WHO Grade IV), central nervous system neoplasm, characterized by a very poor prognosis. Similar to other high-grade gliomas, GS affects mainly adults in the 5th-7th decade of life and presents a higher incidence in males. The most reported locations of GS are the temporal lobe and the frontal lobe, while only eight cases of GS originating from the posterior cranial fossa are reported in the literature. CASE DESCRIPTION: We report the first case occurring during pregnancy in a 33-year-old patient. Diagnosis was obtained on the 15th week of gestation when patient presented with signs and symptoms of life-threatening raised intracranial pressure. Surgical excision was followed by early recurrence and eventually disease progression because the patient refused adjuvant treatment to save her fetus. CONCLUSIONS: GS should be considered in the differential diagnosis of posterior cranial fossa tumors with radiological features of meningioma or glioblastoma, even in young patients. To this regard, sarcomas, solitary fibrous tumors, and even metastases should be considered, especially in light of the tendency of GS to give rise to extracranial localizations. Whenever an aggressive management with radical excision and adjuvant treatment is not safely achievable, disease progression is likely to be unavoidable.

Long-term evolution of EEG in Unverricht-Lundborg disease.

PURPOSE: Unverricht-Lundborg disease (ULD) is a progressive myoclonus epilepsy characterized by myoclonus, epilepsy, and ataxia, without major cognitive decline. There is no systematic study on the long-term evolution of EEG in this condition. PATIENTS AND METHODS: Twenty-five patients with ULD who came to our observation before 1995 and periodically followed in our Epilepsy Centres were included. All waking EEG traces were visually reviewed for the characterization background activity, with particular regard to the frequency of the posterior dominant rhythm (PR), and for the occurrence of spontaneous generalized spike or polyspike and wave discharges (GSWD) and photoparoxysmal response (PPR). Sleep recordings were analyzed with particular regard to the preservation of the physiological sleep patterns and the occurrence of GSWD and other epileptic abnormalities. RESULTS: PR was normal in 68% of patients at the beginning of the disease and kept stable over the years. GSWD were present in 92% of patients at the onset of the disease and gradually disappeared during the follow-up with a significant difference (p<0.001) after the 15th year of disease. PPR was present in 88% of patients at the disease onset and gradually disappeared with a significant difference (p<0.001) after the 10th year of disease. A gradual reduction of GSWD and a progressive disappearance of physiological sleep patterns were observed in sleep EEGs. CONCLUSION: In patients with ULD followed for an extended period of time, EEG shows no relevant deterioration of BA while a gradual reduction of GSWD and PPR is observed over time, well correlating with the good seizure outcome in this condition.

The neuroanatomical plates of Guido da Vigevano.

Guido da Vigevano was an Italian physician and engineer who lived in the 13th and 14th centuries. He was the first scientist who used pictures to illustrate his anatomical descriptions, developing for the first time a close relationship between anatomical studies and artistic drawings. This was further developed in the Renaissance. In his textbook Anathomia are displayed six plates showing for the first time neuroanatomical structures and techniques: dissection of the head by means of trephination, and depictions of the meninges, cerebrum, and spinal cord. On the surface of the brain painting it is possible to recognize a vague patterning of cortical convolutions. Ventricles are also described and shown. This book constituted the first attempt in the history of neuroscience to illustrate an anatomical description with schematic pictures to achieve a better understanding of such complex structures.

Baclofen-induced suppression of alcohol deprivation effect in Sardinian alcohol-preferring (sP) rats exposed to different alcohol concentrations.

This study investigated the effect of the gamma-aminobutyric acid(B) (GABA(B)) receptor agonist, baclofen, on alcohol deprivation effect (the transient increase in alcohol intake occurring after a period of alcohol abstinence) in Sardinian alcohol-preferring (sP) rats exposed to 4 bottles containing water and 10%, 20%, and 30% (v/v) alcohol, respectively. Acute administration of baclofen (1 mg/kg, i.p.) suppressed both aspects of alcohol deprivation effect: the extra-intake of alcohol and the selection of the highest concentrated alcohol solution. These results suggest that the GABA(B) receptor is part of the neural substrate mediating alcohol deprivation in sP rats.

First-ever stroke incidence and 30-day case fatality in the Sicilian Aeolian archipelago, Italy.

BACKGROUND AND PURPOSE: Not many data on stroke epidemiology come from studies on islands. This is the first report on a Mediterranean archipelago population. METHODS: Using recommended criteria, from July 1, 1999, to June 30, 2002, information was collected on first-ever stroke and 30-day case fatality in Aeolian island residents (13,431). RESULTS: The overall crude incidence rate was 154 of 100,000 (95% CI, 118 to 197; 128 in men and 180 in women) or 180, 154, and 87, if adjusted to the Italian, European, and world populations, respectively. The 30-day case fatality rate was 24.2% (95% CI, 14.22 to 36.75). CONCLUSIONS: Besides genetic or dietary factors, our results may reflect local, limited possibilities of diagnosis and management for stroke patients.

Effect of the combination of naltrexone and baclofen, on acquisition of alcohol drinking behavior in alcohol-preferring rats.

Recent surveys suggest that positive outcomes in the pharmacotherapy of alcoholism may be obtained through drug combinations. The present study evaluated the effect of the combination of the opioid receptor antagonist, naltrexone, with the GABA(B) receptor agonist, baclofen, on the acquisition of alcohol drinking behavior in Sardinian alcohol-preferring (sP) rats. Rats were treated with either saline, 0.5 mg/kg naltrexone, 1mg/kg baclofen, or 0.5 mg/kg naltrexone plus 1mg/kg baclofen once a day for 10 days. Alcohol was offered immediately after the first drug injection under the 2-bottle regimen. Alcohol intake in saline-treated rats rose to 5-6 g/kg/day within a few days, indicative of a rapid acquisition of alcohol drinking behavior. Neither naltrexone nor baclofen, when given alone, affected alcohol drinking behavior. In contrast, the drug combination resulted in a significant reduction in daily alcohol intake and retardation in the acquisition of alcohol drinking behavior. These results suggest that combination of naltrexone plus baclofen may result in a synergistic reduction in alcohol intake in sP rats. These results are discussed in terms of naltrexone and baclofen exerting a concomitant and reciprocally potentiating inhibitory action on alcohol-induced activation of mesolimbic dopamine transmission.

Endocannabinoid system and alcohol addiction: pharmacological studies.

The present paper describes the results of recent pharmacological studies implicating the cannabinoid CB1 receptor in the neural circuitry regulating alcohol consumption and motivation to consume alcohol. Cannabinoid CB1 receptor agonists have been found to specifically stimulate alcohol intake and alcohol's motivational properties in rats. Conversely, the cannabinoid CB1 receptor antagonist, SR 141716, has been reported to specifically suppress acquisition and maintenance of alcohol drinking behavior, relapse-like drinking and alcohol's motivational properties in rats. More recent data indicate that opioid receptor antagonists a) blocked the stimulatory effect of cannabinoids on alcohol intake, and b) synergistically potentiated the suppressing effect of SR 141716 on alcohol intake and alcohol's motivational properties. Consistently, SR 141716 blocked the stimulatory effect of morphine on alcohol intake. These results suggest a) the existence of a functional link between the cannabinoid and opioid receptor systems in the control of alcohol intake and motivation to consume alcohol, and b) that novel and potentially effective therapeutic strategies for alcoholism may come from the combination of cannabinoid and opioid receptor antagonists.

Baclofen-induced reduction of alcohol reinforcement in alcohol-preferring rats.

Recent studies have demonstrated that treatment with the gamma-aminobutyric acid (GABA(B)) receptor agonist, baclofen, reduces alcohol intake in selectively bred Sardinian alcohol-preferring rats tested under the homecage two-bottle "alcohol versus water" choice regimen. This study was designed to investigate whether baclofen also reduces alcohol-reinforcing effects in Sardinian alcohol-preferring rats. To this aim, sP rats were trained to lever press for oral alcohol (15%, vol/vol) or sucrose (0.3%, wt/vol; included as alternative reinforcer to evaluate the specificity of baclofen effect on alcohol reinforcement) under a fixed ratio schedule of 4. Once steady levels of alcohol or sucrose self-administration behavior were established, the effects of acutely administered baclofen (0, 1.7, and 3 mg/kg, intraperitoneal [ip]) and naloxone (0, 1, and 3 mg/kg, ip; included as reference compound) on alcohol- or sucrose-reinforced responding were evaluated. Baclofen administration dose dependently, although not specifically, reduced alcohol-reinforced responding to an extent comparable to that of naloxone. Baclofen also produced a dose-dependent and specific delay in the onset of alcohol-reinforced responding, suggesting that it suppressed the rats' motivation to start drinking alcohol. These data are discussed in terms of adding further support to the hypothesized involvement of the GABA(B) receptor in the neural system mediating alcohol reinforcement. These data are also in agreement with the results of recent preliminary clinical studies suggesting that baclofen may have therapeutic efficacy in the treatment of alcohol dependence.

Baclofen suppresses motivation to consume alcohol in rats.

RATIONALE: Recent studies demonstrated that treatment with the gamma-aminobutyric acid (GABA)(B) receptor agonist baclofen reduced alcohol intake in selectively bred Sardinian alcohol-preferring (sP) rats tested under the home-cage, two-bottle choice regimen. OBJECTIVES: The present study investigated the effect of baclofen on the appetitive, rather than consummatory, aspects of alcohol ingestion in sP rats. METHODS: Rats were trained to lever-press for oral alcohol (10%, v/v) or sucrose (3%, w/v) under a fixed-ratio schedule of 4. Once self-administration behavior was established, alcohol intake averaged approximately 0.7 g/kg over the 30-min session. Subsequently, the effect of the acute administration of baclofen (0, 1, 2 and 3 mg/kg, i.p.) on the extinction responding for alcohol and sucrose (defined as the maximal number of lever responses reached in the absence of reinforcement and used as index of motivation to consume alcohol and sucrose) was evaluated. RESULTS. All doses of baclofen produced a marked suppression of extinction responding for alcohol. Conversely, only the 3-mg/kg baclofen dose significantly affected extinction responding for sucrose. A separate open-field test indicated that baclofen (0, 1, 2 and 3 mg/kg, i.p.) did not affect spontaneous motor activity in sP rats. CONCLUSIONS: These results suggest that baclofen may specifically reduce the motivational properties of alcohol; further, these results are in agreement with the recently reported anti-craving potential of baclofen in alcoholics.

Suppression of GABA(B) receptor function in vivo by disulfide reducing agent, DL-dithiothreitol (DTT).

RATIONALE: A recent in-vitro study demonstrated that the potent disulfide reducing agent, DL-dithiothreitol (DTT), may alter the structural stability of the GABA(B) receptor, probably inactivating the disulfide bonds between four cysteine residues located in the GABA(B1(a)) receptor structure. OBJECTIVES: The present study was designed to evaluate whether DTT treatment was capable of antagonizing some behavioral effects of pharmacological stimulation of the GABA(B) receptor. METHODS: Experiments on sedation/hypnosis induced by the GABA(B) receptor agonists baclofen, SKF 97541, CGP 44532 and gamma-hydroxybutyric acid (GHB) in DBA mice and selectively bred GHB-sensitive (GHB-S) rats, and a GHB drug discrimination study in Long Evans rats were conducted. Specificity of the DTT action on the GABA(B) receptor was investigated by assessing its effect on the sedative/hypnotic effect induced by diazepam, ketamine and ethanol. RESULTS: DTT prevented the sedative/hypnotic effect of all GABA(B) receptor agonists tested and also reversed baclofen-induced sedation/hypnosis. In contrast, DTT had no effect on, or even potentiated, sedation/hypnosis produced by diazepam, ketamine or ethanol. DTT completely blocked the discriminative stimulus effects of GHB. CONCLUSIONS: These results are discussed in terms of DTT altering the stability of the binding domain of the GABA(B) receptor, hindering the drug-receptor interaction.

Stimulation of voluntary ethanol intake by cannabinoid receptor agonists in ethanol-preferring sP rats.

RATIONALE: Recent studies have shown that the cannabinoid CB1 receptor antagonist, SR 141716, is capable of reducing voluntary ethanol intake in rodents, suggesting the involvement of the CB1 receptor in the neural circuitry mediating the positive reinforcing properties of ethanol. OBJECTIVES: The present study extended to the agonists the investigation on the pharmacological manipulation of ethanol intake by cannabinoid agents. METHODS: Selectively bred, Sardinian alcohol-preferring (sP) rats were offered ethanol and water under the two-bottle free choice procedure with unlimited access for 24 h/day. RESULTS: The acute administration of WIN 55,212-2 (0.5-2 mg/kg; IP) and CP 55,940 (3-30 microg/kg; IP) induced a significant, dose-dependent increase in ethanol intake. Conversely, water consumption and intake of regular food and a highly palatable sucrose solution were not affected by treatment with WIN 55,212-2 and CP 55,940. The stimulatory effect of WIN 55,212-2 and CP 55,940 on ethanol intake was completely prevented by administration of SR 141716 (0.3 mg/kg; IP) and the opioid receptor antagonist, naloxone (0.1 mg/kg; IP). CONCLUSIONS: Administration of WIN 55,212-2 and CP 55,940 promoted voluntary ethanol intake in sP rats. This effect was mediated by stimulation of the cannabinoid CB1 receptor and required the activation of the endogenous opioid system. The results of the present study add further support to the hypothesis that the cannabinoid CB1 receptor is part of the neural substrate regulating ethanol intake. These results are also discussed in terms of WIN 55,212-2 and CP 55,940 administration possibly fixing to a higher level the hedonic set-point mechanism regulating ethanol drinking behavior in sP rats.

Suppressing effect of the cannabinoid CB1 receptor antagonist, SR 141716, on alcohol's motivational properties in alcohol-preferring rats.

Administration of the cannabinoid CB(1) receptor antagonist, SR 141716 [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide], has been reported to reduce alcohol intake and alcohol self-administration in different models of excessive alcohol consumption, including the selectively bred Sardinian alcohol-preferring (sP) rats. The present study investigated whether SR 141716 was also capable of decreasing, in this rat line, alcohol's motivational properties. Extinction responding for alcohol, defined as the maximal number of lever responses reached in the absence of alcohol in rats trained to lever-press for alcohol, was used as index of alcohol's motivational properties. Rats were initially trained to lever-press for oral alcohol (15%, v/v) under a fixed ratio (FR) schedule of FR4. Once self-administration behavior was established, extinction sessions were conducted. SR 141716 (0, 0.3, 1 and 3 mg/kg; i.p.) was acutely administered before extinction sessions. In order to assess the specificity of SR 141716 action on extinction responding for alcohol, a separate group of sP rats was trained to lever-press for a 3% (w/v) sucrose solution under an FR4 schedule. SR 141716 administration produced a dose-dependent, virtually complete suppression of extinction responding for alcohol. In contrast, extinction responding for sucrose was not significantly altered by treatment with SR 141716. Further to the consummatory aspects, these results also extend the suppressing effect of SR 141716 to the appetitive aspects of alcohol drinking behavior in sP rats. The results also implicate the cannabinoid CB1 receptor in the neural substrate mediating alcohol's motivational properties in this rat line.

Suppression by baclofen of the stimulation of alcohol intake induced by morphine and WIN 55,212-2 in alcohol-preferring rats.

Administration of morphine and cannabinoids stimulates alcohol intake in rats. The present study investigated whether the promoting effect of morphine and of the cannabinoid receptor agonist, WIN 55,212-2 [(R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone], on alcohol intake was prevented by the gamma-aminobutyric (GABA)(B) receptor agonist, baclofen. Sardinian alcohol-preferring (sP) rats were given alcohol (10%, v/v) and water under the standard homecage two-bottle-free choice regimen with unlimited access for 24 h/day. Baclofen (0, 0.5 and 1 mg/kg; i.p.) was administered acutely 30 min before lights off. Morphine (0 and 1 mg/kg, s.c.) or WIN 55,212-2 (0 and 2 mg/kg, i.p.) was administered acutely 10 min after baclofen. Alcohol intake was recorded 60 min after lights off. As predicted, both morphine and WIN 55,212-2 produced a specific and marked increase in alcohol intake. Pretreatment with baclofen, which failed to alter alcohol intake when given alone, dose-dependently suppressed morphine- and WIN 55,212-2-induced promotion of alcohol drinking. These results suggest the involvement of the GABA(B) receptor in the neural circuitry mediating the stimulating effect of morphine and cannabinoids on alcohol consumption in sP rats.

Boosting effect of morphine on alcohol drinking is suppressed not only by naloxone but also by the cannabinoid CB1 receptor antagonist, SR 141716.

The present study investigated the effect of the cannabinoid CB(1) receptor antagonist, SR 141716 (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide), on the ability of low and high doses of morphine to, respectively, augment and suppress voluntary alcohol intake in selectively bred Sardinian alcohol-preferring rats. Acute administration of a low dose of morphine (1 mg/kg, s.c.) produced a specific and marked increase in alcohol intake, which correlated with an increase in blood alcohol levels and was prevented by either SR 141716 (0.3 mg/kg, i.p.) or naloxone (0.1 mg/kg, i.p.). A higher dose (10 mg/kg, s.c.) of morphine reduced both alcohol and food intakes and produced sedation and hypomotility. The suppressant effect of morphine on alcohol intake was blocked by naloxone (0.1 mg/kg, i.p.) but not by SR 141716 (0.3 mg/kg, i.p.). These results are in agreement with those showing the ability of SR 141716 to antagonize the appetitive and positive reinforcing properties of morphine and add further support to the hypothesis of the existence of a functional link between the action of opioids and of cannabinoids.

Central effects of 1,4-butanediol are mediated by GABA(B) receptors via its conversion into gamma-hydroxybutyric acid.

The aliphatic alcohol 1,4-butanediol in converted into gamma-hydroxybutyric acid (GHB) via two enzymatic steps: first, it is oxidised by alcohol dehydrogenase in gamma-hydroxybutyraldehyde; second, the latter is transformed, likely by aldehyde dehydrogenase, into GHB. Initially, the present study compared the sedative/hypnotic effect of GHB and 1,4-butanediol, measured as loss of righting reflex. 1,4-Butanediol was more potent than GHB, presumably because of a more rapid penetration of the blood brain barrier. Further alcohol dehydrogenase inhibitors, 4-methylpyrazole and ethanol, totally prevented the sedative/hypnotic effect of 1,4-butanediol; the aldehyde dehydrogenase inhibitor disulfiram partially blocked the sedative/hypnotic effect of 1,4-butanediol. Finally, the sedative/hypnotic effect of 1,4-butanediol was antagonised by the GABA(B) receptor antagonists, SCH 50911 [(2S)(+)-5,5-dimethyl-2-morpholineacetic acid] and CGP 46381 [(3-aminopropyl)(cyclohexylmethyl)phosphinic acid], but not by the putative GHB receptor antagonist NCS-382 (6,7,8,9-tetrahydro-5-hydroxy-5H-benzocyclohept-6-ylideneacetic acid), indicating that it is mediated by GABA(B) but not GHB receptors. Taken together, these results suggest that the sedative/hypnotic effect of 1,4-butanediol is mediated by its conversion in vivo into GHB which, in turn, binds to GABA(B) receptors. Accordingly 1,4-butanediol, unlike GHB, failed to displace [(3)H]GHB and [(3)H]baclofen in brain membranes.

Proconvulsive effect of the GABA(B) receptor antagonist, SCH 50911, in rats undergoing ethanol withdrawal syndrome.

The present study investigated the effect of the GABA(B) receptor antagonist, SCH 50911 [(2S)(+)-5,5-dimethyl-2-morpholineacetic acid], on the occurrence of seizures in ethanol-dependent rats undergoing ethanol withdrawal syndrome. The acute administration of nonconvulsive doses of SCH 50911 (0, 100, 170 and 300 mg/kg, i.p.) resulted in a dramatic facilitation of spontaneous seizure occurrence. This finding, together with the reported ability of the GABA(B) receptor agonist, baclofen, to suppress seizures associated to ethanol withdrawal syndrome, suggests that the GABA(B) receptor may be part of the neural substrate underlying the hyperexcitability of ethanol withdrawal syndrome.

Blockade by the cannabinoid CB(1) receptor antagonist, SR 141716, of alcohol deprivation effect in alcohol-preferring rats.

The present study investigated the effect of the cannabinoid CB(1) receptor antagonist, SR 141716 (N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide), on alcohol deprivation effect (i.e. the temporary increase in alcohol intake after a period of alcohol withdrawal) in Sardinian alcohol-preferring (sP) rats. As expected, alcohol-deprived rats virtually doubled voluntary alcohol intake during the first hour of re-access. Acute administration of SR 141716 (0, 0.3, 1 and 3 mg/kg, i.p.) completely abolished the alcohol deprivation effect. These results suggest that the cannabinoid CB(1) receptor is part of the neural substrate mediating the alcohol deprivation effect and that SR 141716 may possess anti-relapse properties.