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Objective: To determine possible effects of prolonged marijuana use on the cerebrovascular system during a month of monitored abstinence and to assess how the intensity of current use might have influenced cerebrovascular perfusion in these marijuana users. Blood flow velocity was recorded within 3 days of admission and 28 to 30 days of monitored abstinence on an inpatient research unit in order to evaluate subacute effects of the drug and any abstinence-generated changes. Results: Pulsatility index, a measure of cerebrovascular resistance, and systolic velocity were significantly increased in the marijuana users vs control subjects. These increases persisted in the heavy marijuana users after a month of monitored abstinence. Conclusions: Chronic marijuana use is associated with increased cerebrovascular resistance through changes mediated, in part, in blood vessels or in the brain parenchyma. These findings might provide a partial explanation for the cognitive deficits observed in a similar group of marijuana users. Abstract Objective: To determine possible effects of prolonged marijuana use on the cerebrovascular system during a month of monitored abstinence and to assess how the intensity of current use might have influenced cerebrovascular perfusion in these marijuana users.

Marijuana Use Affects Blood Flow in Brain Even After Abstinence

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Official websites use. Share sensitive information only on official, secure websites. Address correspondence and reprint requests to Dr. Aron H. Marijuana Cannabis sativa is the most commonly used illicit drug worldwide as well as in the Unites States. The changes that occur with repeated cannabis use include alterations in behavioral, physiological, and biochemical responses. A variety of withdrawal responses occur in cannabis-dependent individuals: anger, aggression, irritability, anxiety and nervousness, decreased appetite or weight loss, restlessness, and sleep difficulties with strange dreams. But the long half-life and other pharmacokinetic properties of THC result in delayed expression of withdrawal symptoms, and because of the lack of contiguity between drug cessation and withdrawal responses the latter are not readily recognized as a clinically relevant syndrome. Over the past 30 years, a substantial body of clinical and laboratory animal research has emerged supporting the assertion that chronic exposure to cannabinoids produces physical dependence and may contribute to drug maintenance in cannabis-dependent individuals. However, no medications are approved to treat cannabis dependence and withdrawal. In this review, we describe preclinical and clinical research that supports the existence of a cannabinoid withdrawal syndrome. In addition, we review research evaluating potential pharmacotherapies e. Although the perception persists that marijuana use is innocuous and lacks dependence liability, the first record of cannabis withdrawal was published in the s Wallace and Cunningham and the medical community is now beginning to accept the idea that cannabis-related disorders represent a clinically significant public health problem for review, Weinstein and Gorelick According to the Drug Abuse Warning Network, marijuana was involved in , hospital emergency department visits or In this review, we discuss data from human surveys, retrospective and clinical studies, and preclinical research characterizing cannabis dependence. The preponderance of evidence suggests that cannabis dependence should be considered an important medical condition that requires clinical intervention. Cannabis-dependent individuals who cease using the drug experience a variety of withdrawal symptoms that are sufficiently severe to contribute to drug maintenance, thus highlighting its addictive properties. We review both clinical and preclinical studies examining a variety of pharmacotherapies to alleviate withdrawal signs. Since then, more than 70 other phytocannabinoids have been discovered Elsohly and Slade and hundreds, if not thousands, of cannabinoids have been synthesized. Studies have shown that THC and many other cannabinoids bind to and activate two types of cannabinoid CB 1 receptors that have been cloned: CB 1 Matsuda et al. CB 1 receptors, which are heterogeneously expressed throughout the central nervous system CNS and periphery Felder and Glass ; Herkenham et al. CB 2 receptors are associated with immune cells Klein et al. A major breakthrough in cannabinoid pharmacology came with the discovery of the endogenous cannabinoids endocannabinoids N -arachidonylethanolamine anandamide Devane et al. The endocannabinoid system comprises the CB receptors, the endocannabinoids, and the enzymes that regulate endocannabinoid biosynthesis and degradation Ahn et al. These catabolic enzymes are targets for the development of selective inhibitors to treat cannabis-related disorders as well as pain, inflammation, and anxiety. We review evidence from laboratory animal and human studies showing that repeated administration of cannabinoids can result in physical dependence. Emerging data indicate that cannabinoid-dependent laboratory animals and humans display physical withdrawal responses upon drug cessation. In addition, we provide an overview of preclinical and clinical research examining pharmacotherapies to treat cannabis dependence. In animal studies, THC administration and inhibition of endocannabinoid catabolic enzymes represent promising approaches to reduce cannabinoid withdrawal responses. We discuss several clinical studies showing that oral THC reduces cannabis withdrawal responses in cannabis-dependent patients. The DSM-IV reflects the attitude of many in medicine and the general public that cannabis is not a physically addictive substance in which a withdrawal syndrome can produce clinically relevant symptoms of a severity and duration to affect substance-use behavior. This belief is probably due to a multitude of factors, such as the relatively slow onset and unique constellation of the withdrawal syndrome. Cannabis is the most commonly used illicit drug worldwide. This high prevalence allows for many people to have personal or anecdotal experience with marijuana without necessarily having personal interactions with dependent users. The severity of cannabis withdrawal is not generally associated with symptoms that require hospitalization or are viewed as potentially life threatening. Furthermore, only a subset of regular marijuana users experience a clustering of symptoms upon cessation of use; estimates range from 1 in 6 to half of all such users Budney et al. Common symptoms observed during cannabis withdrawal include anger, aggression, irritability, anxiety and nervousness, decreased appetite or weight loss, restlessness, and sleep difficulties with strange dreams Budney and Hughes Although the immediate physical impact of these symptoms is mild when compared with certain other drugs of abuse, as discussed below the comprehensive impact of the cannabis withdrawal syndrome is becoming better understood. Before the cloning of cannabinoid receptors, discovery of the endogenous cannabinoid system, and development of selective cannabinoid agonists and antagonists, early studies of marijuana smokers indicated potential signs of tolerance and withdrawal Williams et al. In the s, Jones and colleagues set out to define the physiological and psychoactive effects of cannabis in controlled laboratory settings Jones and Benowitz ; Jones et al. Human subjects were given varying oral doses of THC in a double-blind fashion, spaced evenly throughout the day to maintain consistent drug levels. THC produced profound tolerance after repeated administration, as assessed by the following: self-reported intoxication, time spent in REM sleep, psychomotor task performance, and numerous autonomic physiological effects. The investigators also identified a subset of behaviors that increased dramatically among subjects during the 4 days after cessation of the drug, including disturbances in sleeping and eating, sweats and chills, tremors and restlessness, and irritability. Most of these symptoms subsided after a resumption of THC intake or marijuana smoking Jones et al. Subsequent studies of marijuana smokers in the laboratory over periods of use and cessation replicated these findings but lacked the controls and precise measurements of the earlier laboratory studies Georgotas and Zeidenberg ; Nowlan and Cohen More recently, Haney and colleagues used data from both laboratory and survey findings to ascertain how heavy users of cannabis respond to use and abstinence in terms of cognitive function, subjective drug effects, and detailed cannabis-specific withdrawal symptoms. Parallel studies using identical methodologies evaluated the effects of oral THC and smoked marijuana. Both types of studies showed increases in ratings of anxiety and irritability and disturbances in food intake, but sleep patterns seemed more sensitive to abstinence from oral THC, and marijuana abstinence impaired performance on a task measuring attention. Other controlled studies reported that chronic marijuana users show deficits associated with complex decision making and cognitive planning Hermann et al. These studies marked a renewed effort to define the symptoms and impact of cannabis dependence. Although laboratory studies provide for a controlled environment, increased compliance, and around-the-clock data collection, they generally incorporate relatively small sample sizes on the order of a few dozen and are conducted on a subset of relatively heavy cannabis users for a critique of these and other studies discussed in this review, see Smith In contrast, large datasets are used in retrospective studies in which subjects are asked to recall their own attempts to abstain from marijuana use, providing insight into real-world conditions. Examining for symptoms similar to those found in laboratory studies, the authors noted that only a small percentage of infrequent and even daily users reported each withdrawal symptom. Budney and colleagues conducted a retrospective study of a group seeking treatment for cannabis use and found that over half the subjects reported at least four moderate withdrawal symptoms during their last attempt to stop. A more recent multisite study established that retrospective reports of specific marijuana withdrawal symptoms were similar in a general population sample to symptoms in treatment-seeking individuals Mennes et al. Large-scale data collection, such as data mining of national surveys on drug use, has been a useful approach to investigate cannabis dependence. The incidence of symptoms correlated highly with the amount of cannabis used, levels of distress, and subsequent general substance use to relieve symptoms. This association supports the notion that cannabis withdrawal symptoms contribute to the maintenance of cannabis use in dependent individuals. The largest volume of published research describes self-report and monitored outpatient studies, which allow for immediate reporting of symptoms and timeline information without constant supervision and monitoring. Measurement of urinary drug metabolites is a common method to verify initial drug use and abstinence from cannabis or other drugs. Patients identified as heavy cannabis users typically show a moderate set of symptoms, both physical e. This time course corresponds to rather precipitous drops in THC metabolites in the urine during the first few days of abstinence. Other common symptoms, such as irritability and aggression, can persist for weeks Budney et al. Although many of these studies contain sample sizes not much larger than those of laboratory studies, they allow a more thorough examination of how cannabis withdrawal symptoms affect the daily life of users and can be readily performed by numerous treatment clinics to build a converging set of data from multiple sites. The exact timeline and symptoms of the cannabis withdrawal syndrome vary across studies, but the growing consensus is that withdrawal symptoms contribute to continued drug use. Cannabis withdrawal is comparable in severity and scope to tobacco withdrawal and contributes to relapse to only a slightly lesser extent Budney et al. Bonn-Miller and Moos evaluated marijuana use in male inpatients treated for substance use disorders in Department of Veterans Affairs residential substance abuse programs and reported that anxiety symptoms at treatment discharge were associated with a month relapse to marijuana use. Although this finding is consistent with the idea that increases in anxiety after marijuana discontinuation may be predictive of relapse, the study did not report whether these patients were marijuana dependent. Other studies also show that the occurrence of withdrawal symptoms may predict marijuana users who will relapse soon after a prolonged outpatient abstinence period Chung et al. Withdrawal symptoms do not, however, appear to predict relapse after 2 or more years of abstinence Arendt et al. Studies are beginning to examine the interactions of cannabis use with other drug use and have shown that concurrent cessation of tobacco and cannabis use is associated with temporary increases in withdrawal severity compared with cessation of either alone Vandrey et al. Cannabis users often differentially use alcohol, tobacco, or cannabis to reduce the severity of specific symptoms Copersino et al. Taken together, the evidence shows that withdrawal from cannabis use produces a distinct syndrome that increases drug craving and use, thus necessitating research into therapeutic treatment. Preclinical studies in a variety of laboratory animals show that repeated administration of THC or other cannabinoid agonists results in dependence. Animal models for assessing dependence also measure reinforcing and rewarding properties—such as self-administration, conditioned place preference, and intracranial self-stimulation for a complete review, Panagis et al. The two general approaches used to induce a state of drug withdrawal in preclinical drug dependence studies are spontaneous withdrawal and precipitated withdrawal. Spontaneous withdrawal occurs after abrupt cessation of the drug, which is metabolized and cleared from the body. In precipitated withdrawal, an appropriate selective receptor antagonist is used to displace the agonist from the receptor, resulting in the rapid onset of withdrawal symptoms. The specific withdrawal symptoms, intensity, and duration depend on the pharmacological characteristics of the compound; drugs from the same class generally share similar withdrawal syndromes. The precipitated withdrawal model is used more often than the spontaneous model because of the long half-life of THC and because subtle withdrawal effects in the latter model are difficult to observe and quantify. The results of preclinical studies using precipitated and spontaneous withdrawal procedures are shown in Table 1. Preclinical studies investigating cannabinoid withdrawal using precipitated and spontaneous withdrawal procedures. AEA, anandamide; b. Abrupt cessation of THC after prolonged administration results in delayed onset and long-duration withdrawal symptoms, so the quantification of abrupt withdrawal signs in laboratory animals is challenging Huestis and often yields yields mixed results. The study of somatic withdrawal signs from repeated administration of THC and other cannabinoids has been examined in different animal species. Although one study in rats reported a variety of abnormal behavior signs, such as tremors, wet-dog shakes, and hyperirritability Kaymakcalan et al. In contrast, rhesus monkeys chronically infused with intravenously administered THC 0. In another study, food-reinforced operant responding was decreased in monkeys after abrupt cessation of drug infusions Beardsley et al. Spontaneous withdrawal responses also occurred after discontinuation of chronic administration of the full cannabinoid receptor agonists WIN in rats Aceto et al. The data from these studies suggest that the ability to observe and quantify spontaneous withdrawal effects in experimental animals depends on many factors including species, cannabinoid selection, duration of drug administration, time point at which withdrawal is assessed, and specific endpoints. Yet, although the spontaneous withdrawal approach presents with considerable challenges and may be prone to false negatives because of the slow elimination of THC and its metabolites Huestis , it is considered to be more valid than precipitated withdrawal for modeling human cannabis withdrawal. The development of CB 1 receptor antagonists e. Rimonabant binds with high affinity to the CB 1 receptor and antagonizes the pharmacological effects of many cannabinoid receptor agonist activities in both laboratory animals and humans Compton et al. Soon after the discovery of rimonabant, two independent groups used this antagonist in rats to demonstrate somatic precipitated withdrawal signs—wet-dog shakes, forepaw fluttering, chewing, increased horizontal and vertical activity, retropulsion, and ptosis Aceto et al. Rimonabant also precipitated a profound withdrawal syndrome in mice that were chronically exposed to either THC or marijuana smoke Wilson et al. Withdrawal signs such as paw tremors and wet-dog shakes are observed consistently across all strains Cook et al. Other signs such as mastication, sniffing, and piloerection are of low frequency but are scored in a cannabinoid composite withdrawal index Hutcheson et al. In THC-dependent dogs, rimonabant precipitated a withdrawal syndrome that included distinct gastrointestinal signs e. These studies show that it is critical to include appropriate vehicle-treated control groups in studies using a CB 1 antagonist to precipitate cannabinoid withdrawal to control for intrinsic effects of the drug at testing. Nonetheless, the observation that rimonabant elicits a far greater magnitude of withdrawal-like behavior e. There are few reports examining aversive or emotional responses in rodents undergoing cannabinoid withdrawal. Rimonabant challenge to THC-dependent mice led to less time in the open-arm component of the elevated plus-maze test Huang et al. Other studies have focused on subjective signs of cannabinoid withdrawal. The data suggest that the interoceptive cues of THC cessation—induced abstinence are mediated by the CB 1 receptor. Rimonabant has precipitated withdrawal signs after chronic administration of other cannabinoid agonists such as anandamide, methanandamide, WIN , CP , and HU Aceto et al. The withdrawal syndrome precipitated after chronic anandamide administration is not as robust as that precipitated with other cannabinoids Costa et al. In contrast, rimonabant elicited a mild intensity of somatic withdrawal signs in mice treated chronically with the irreversible MAGL inhibitor JZL that produced a tenfold increase in levels of 2-AG Schlosburg et al. Thus, increases of the two primary endocannabinoids in the brain result in different consequences of physical dependence. This difference may be related to brain 2-AG levels that are already two orders of magnitude greater than the brain levels of anandamide and to the fact that 2-AG is a full CB 1 agonist and anandamide a partial CB 1 agonist Howlett and Mukhopadhyay Preclinical studies are now beginning to identify the molecular changes that result from repeated exposure to and cessation of cannabinoid use. Such studies provide indicators of the adaptations that drive withdrawal symptomatology and thus improve strategic targeting of therapeutics. Chronic administration of cannabinoid agonists results in downregulation of the CB 1 receptor in several brain regions as measured by radioligand binding Breivogel et al. Similarly, chronic treatment with THC produces a time- and region-dependent desensitization of CB 1 activity in the G protein Breivogel et al. Other evidence of dysregulation in the endocannabinoid system includes region-specific alterations in endocannabinoid content after precipitated withdrawal in rats and mice Gonzalez et al. Alterations in numerous other neurotransmitter systems are also associated with withdrawal from THC in rodents. After chronic administration of THC, brain levels of serotonin decrease concurrent with increases in its primary metabolite Taylor and Fennessy , The finding that various serotonin uptake inhibitors elicited writhing, backward kicks, jumps, and wet-dog shakes in THC-dependent rats suggests serotonergic involvement in cannabinoid withdrawal-like behavior Verberne et al. In addition, histamine levels in the brain decrease during initial exposure to THC and during somatic withdrawal induced by the serotonin reuptake inhibitor clomipramine Verberne et al. Several studies have shown evidence of upregulation and release of the stress-related peptide corticotropin-releasing factor upon precipitated withdrawal, a common phenomenon during withdrawal from many drugs of abuse Gonzalez et al. At the intracellular level, the cyclic adenosine mono-phosphate cAMP second messenger signaling system appears to be involved in modulating cannabinoid withdrawal. Rimonabant administered to THC-dependent mice resulted in significant increases in basal and forskolin-stimulated adenylyl cyclase activity in the cerebellum but not in other regions Hutcheson et al. Similar results were obtained with calcium-calmodulin-stimulated cyclase activity from the cerebella of THC-dependent rats undergoing precipitated withdrawal Rubino et al. These findings provide strong evidence for the functional role of the cAMP cascade, particularly in the cerebellum, in modulating withdrawal from cannabinoids. The development of preclinical cannabinoid withdrawal models has made it possible to evaluate potential therapeutic agents for the treatment of cannabis dependence. Compounds investigated for reducing cannabinoid withdrawal responses include cannabinoid substitutes, such as THC and inhibitors of endocannabinoid catabolic enzymes, and non-cannabinoid drugs, such as lithium and clonidine Table 2. Preclinical and clinical studies evaluating pharmacological agents in reducing cannabinoid withdrawal responses. Abbreviations: b. Early studies reported that reintroduction of THC 1 alleviated decreases in operant responding in nonhuman primates undergoing spontaneous withdrawal Beardsley et al. In contrast, THC dose-dependently attenuated the intensity of rimonabant-precipitated paw tremors in mice rendered dependent on marijuana smoke, but marijuana itself failed to reverse the precipitated withdrawal effect Wilson et al. The lack of effect of marijuana itself was attributed to the lower THC brain levels after exposure to marijuana smoke ng of THC per g of brain tissue compared with intravenous injection of THC ng of THC per g of brain tissue. Morphine also reduced the intensity of rimonabant-precipitated withdrawal signs in THC-dependent mice Lichtman et al. With the discovery of endocannabinoids, there has been interest in targeting the degradative enzymes of these naturally occurring ligands Clapper et al. If targeting endocannabinoid catabolic enzymes is indeed a viable approach to treat cannabis withdrawal, it is important to know whether these inhibitors would themselves have abuse or dependence liability. FAAH inhibitors have been extensively investigated in a variety of such paradigms. Importantly, it has been demonstrated that URB does not produce rewarding effects in the rat conditioned place preference paradigm, does not substitute for THC in the drug discrimination paradigm, and is not self-administered by nonhuman primates Gobbi et al. In addition, rimonabant does not precipitate any apparent withdrawal symptoms in mice treated subchronically with URB Schlosburg et al. There is also supporting biochemical evidence that chronic treatment with FAAH inhibitors does not lead to long-term neural adaptations. Likewise, repeated dosing of PF did not lead to desensitization or downregulation of CB 1 receptors and did not alter CB 1 receptor—mediated synaptic plasticity of hippocampal neurons. In contrast, repeated treatment with a high dose of the MAGL inhibitor JZL led to mild cannabinoid withdrawal signs after rimonabant administration, as well as regionally dependent changes in CB 1 receptor downregulation and desensitization in the brain and impaired endocannabinoid-mediated synaptic plasticity Schlosburg et al. It remains to be established whether repeated administration of lower doses of JZL leads to cannabinoid dependence or changes in CB 1 receptor function. Nonetheless, these studies provide proof of principle that bolstering endogenous anandamide or 2-AG through the inhibition of their respective catabolic enzymes may be viable approaches to reduce cannabis withdrawal symptoms. In recent years efforts to identify treatments for cannabis dependence disorders have increased considerably. Most of the current research is limited to small-scale laboratory models and small open-label trials. Medications investigated in the clinical laboratory setting include cannabinoid substitutes e. Many of these compounds were selected because of their effectiveness in treating specific symptom clusters or their overall clinical evidence in treating opiate or tobacco-use disorders. For a recent review of pharmacological treatment of cannabis dependence, see Weinstein and Gorelick Dronabinol, or oral synthetic THC, has been reliably reported to reduce withdrawal symptoms in cannabis-dependent individuals. In a subsequent study, dronabinol administered at 20 mg, three times a day for 8 days, decreased symptoms of cannabis withdrawal such as restlessness, anorexia, and chills Haney et al. However, clonidine has not been evaluated for efficacy in reducing withdrawal in cannabis-dependent patients, and lofexidine has yet to be examined in preclinical models of cannabinoid withdrawal. In addition, the use of pharmacotherapy for cannabis withdrawal needs to be weighed against side effects, as clonidine and, to a lesser extent, lofexidine produce orthostatic hypotension. In all of the studies described above, dronabinol itself did not produce any adverse effects, was well tolerated, and lower doses were not significantly distinguishable from placebo treatment. Various other medications have been evaluated in inpatient studies for the treatment of cannabis withdrawal, largely with mixed results. However, hepatotoxicity with this drug resulted in its removal from the market. The failure of bupropion to treat marijuana withdrawal underscores the need to treat cannabinoid withdrawal as a unique syndrome and not simply as another form of smoking cessation. However, the potential benefit of this medication was negated by adverse gastrointestinal effects nausea, vomiting, dyspepsia, and loose stools in the majority of patients. An open-label study reported that the anxiolytic agent buspirone did not significantly decrease cannabis withdrawal symptoms McRae-Clark et al. There was, however, increased incidence of divalproex-related adverse reactions and poor patient compliance during the trial Levin et al. Lithium has been tested for effectiveness in the treatment of cannabis withdrawal. Following results from preclinical studies Cui et al. A case study with varying doses of the atypical antipsychotic quetiapine — mg for 6 months given to cannabis users with schizophrenia or bipolar disorder reported reduced cannabis use in these patients over the course of treatment Potvin et al. However, the results of the study were complicated by concurrent treatments with anti-depressants, gabapentin, or methadone in some patients. Research has firmly established the existence of a clinically significant and distinct cannabis withdrawal syndrome, characterized by anger, aggression, irritability, anxiety or nervousness, decreased appetite or weight loss, restlessness, and sleep difficulties with strange dreams. Dependent individuals may continue to use marijuana to avoid these and other withdrawal symptoms. Laboratory animal models of cannabinoid withdrawal have been useful not only for characterizing and investigating the neurobiology of cannabinoid dependence but also for assessing potential pharmacological agents for therapeutic use. However, not all positive results in preclinical testing translate to clinical success, probably because of the wide variety of symptoms, both physical and psychological, observed in humans. The clinical studies described in the preceding section indicate that cannabinoid substitutes, such as THC, show the greatest promise to treat cannabis withdrawal. Indeed, repeated THC administration has been well established to produce dependence. In contrast, inhibition of the endocannabinoid catabolic enzyme FAAH reduces the severity of cannabinoid withdrawal in animal models of THC dependence and, unlike THC, FAAH inhibitors do not appear to have reinforcing properties or dependence liability. Given the relatively mild nature of the withdrawal syndrome and the political and public perception of cannabis dependence as a public health concern, there would have to be negligible abuse potential and side effects associated with any pharmacotherapeutic option. Further clinical studies are necessary to ascertain whether endocannabinoid catabolic enzyme inhibitors are effective for reducing withdrawal in cannabis-dependent individuals with minimal adverse impacts. Joel E. As a library, NLM provides access to scientific literature. ILAR J. Find articles by Divya Ramesh. Find articles by Joel E Schlosburg. Find articles by Jason M Wiebelhaus. Find articles by Aron H Lichtman. PMC Copyright notice. Somatic signs Cook et al. Somatic signs, adenylyl cyclase overshoot in cerebellum Hutcheson et al. Somatic signs Valverde et al. Somatic signs Lichtman et al. Somatic signs, body weight Anggadiredja et al. Increased locomotor activity, endocrine gene transcription levels Oliva et al. Somatic signs Wilson et al. Somatic signs Tourino et al. Somatic signs, activity Huang et al. Somatic signs Schlosburg et al. Somatic signs Falenski et al. Anxiogenic effects plus maze Huang et al. Somatic signs Aceto et al. Activity Tsou et al. Somatic signs with precipitated only Aceto et al. Somatic signs Diana et al. Somatic signs, activity Rubino et al. Somatic signs, body weight Aceto et al. Somatic signs Breivogel et al. Somatic signs Cui et al. Somatic signs, activity Gonzalez et al. Operant rate suppression Beardsley et al. Somatic signs, operant rate suppression Stewart and McMahon Open in a new tab. Somatic signs Clonidine Attenuation Lichtman et al. Somatic signs, body weight Prostaglandin E 2 Attenuation Anggadiredja et al. Somatic signs Marijuana No effect Wilson et al. Somatic signs Lithium Attenuation Cui et al. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Cook et al. Somatic signs, adenylyl cyclase overshoot in cerebellum. Hutcheson et al. Valverde et al. Lichtman et al. Anggadiredja et al. Increased locomotor activity, endocrine gene transcription levels. Oliva et al. Wilson et al. Tourino et al. Huang et al. Schlosburg et al. Falenski et al. THC, 4 days: 0. Aceto et al. Tsou et al. THC, 4 days: Diana et al. Rubino et al. Beardsley and Martin Breivogel et al. Cui et al. Gonzalez et al. Beardsley et al. Stewart and McMahon Full attenuation Partial attenuation of drug discrimination No attenuation. Haney et al. Attenuation; decreased craving, but exacerbated other symptoms. Levin et al. Potvin et al. Bowen et al. McRae et al. Budney et al. Reversed anorexia weight loss, decreased some withdrawal symptoms, but increased sleep onset latency, did not decrease marijuana relapse; Worsened abstinence- related anorexia, did not attenuate withdrawal, but improved sleep decreased relapse. Tirado et al. McRae-Clark et al. Winstock et al.

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