liu.seSearch for publications in DiVA
Change search
Link to record
Permanent link

Direct link
BETA
Thorsell, Annika
Alternative names
Publications (10 of 49) Show all publications
Karlsson, C., Schank, J. R., Rehman, F., Stojakovic, A., Björk, K., Barbier, E., . . . Heilig, M. (2017). Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice. Addiction Biology, 22(5), 1279-1288
Open this publication in new window or tab >>Proinflammatory signaling regulates voluntary alcohol intake and stress-induced consumption after exposure to social defeat stress in mice
Show others...
2017 (English)In: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 22, no 5, p. 1279-1288Article in journal (Refereed) Published
Abstract [en]

Proinflammatory activity has been postulated to play a role in addictive processes and stress responses, but the underlying mechanisms remain largely unknown. Here, we examined the role of interleukin 1 (IL-1) and tumor necrosis factor-a (TNF-a) in regulation of voluntary alcohol consumption, alcohol reward and stress-induced drinking. Mice with a deletion of the IL-1 receptor I gene (IL-1RI KO) exhibited modestly decreased alcohol consumption. However, IL-1RI deletion affected neither the rewarding properties of alcohol, measured by conditioned place preference (CPP), nor stress-induced drinking induced by social defeat stress. TNF-a signaling can compensate for phenotypic consequences of IL1-RI deletion. We therefore hypothesized that double deletion of both IL-1RI and TNF-1 receptors (TNF-1R) may reveal the role of these pathways in regulation of alcohol intake. Double KOs consumed significantly less alcohol than control mice over a range of alcohol concentrations. The combined deletion of TNF-1R and IL-1RI did not influence alcohol reward, but did prevent increased alcohol consumption resulting from exposure to repeated bouts of social defeat stress. Taken together, these data indicate that IL-1RI and TNF-1R contribute to regulation of stress-induced, negatively reinforced drinking perhaps through overlapping signaling events downstream of these receptors, while leaving rewarding properties of alcohol largely unaffected.

Place, publisher, year, edition, pages
John Wiley & Sons, 2017
Keywords
CPP; IL-1RI; TNF-1R; alcohol; cytokines; social defeat stress
National Category
Substance Abuse
Identifiers
urn:nbn:se:liu:diva-146330 (URN)10.1111/adb.12416 (DOI)000408409700012 ()27273552 (PubMedID)
Available from: 2018-04-07 Created: 2018-04-07 Last updated: 2018-04-07
Karlsson, C., Rehman, F., Damdazic, R., Atkins, A. L., Schank, J. R., Gehlert, D. R., . . . Heilig, M. (2016). The melanin-concentrating hormone-1 receptor modulates alcohol-induced reward and DARPP-32 phosphorylation. Psychopharmacology, 233(12), 2355-2363
Open this publication in new window or tab >>The melanin-concentrating hormone-1 receptor modulates alcohol-induced reward and DARPP-32 phosphorylation
Show others...
2016 (English)In: Psychopharmacology, ISSN 0033-3158, E-ISSN 1432-2072, Vol. 233, no 12, p. 2355-2363Article in journal (Refereed) Published
Abstract [en]

Melanin-concentrating hormone (MCH) is involved in the regulation of food intake and has recently been associated with alcohol-related behaviors. Blockade of MCH-1 receptors (MCH1-Rs) attenuates operant alcohol self-administration and decreases cue-induced reinstatement, but the mechanism through which the MCH1-R influences these behaviors remains unknown. MCH1-Rs are highly expressed in the nucleus accumbens shell (NAcSh) where they are co-expressed with dopamine (DA) receptors. MCH has been shown to potentiate responses to dopamine and to increase phosphorylation of DARPP-32, an intracellular marker of DA receptor activation, in the NAcSh. In the present study, we investigated the role of the MCH1-R in alcohol reward using the conditioned place preference (CPP) paradigm. We then used immunohistochemistry (IHC) to assess activation of downstream signaling after administration of a rewarding dose of alcohol. We found that alcohol-induced CPP was markedly decreased in mice with a genetic deletion of the MCH1-R as well as after pharmacological treatment with an MCH1-R antagonist, GW803430. In contrast, an isocaloric dose of dextrose did not produce CPP. The increase in DARPP-32 phosphorylation seen in wildtype (WT) mice after acute alcohol administration in the NAcSh was markedly reduced in MCH1-R knock-out (KO) mice. Our results suggest that MCH1-Rs regulate the rewarding properties of alcohol through interactions with signaling cascades downstream of DA receptors in the NAcSh.

Place, publisher, year, edition, pages
SPRINGER, 2016
Keywords
Alcohol; Conditioned place preference (CPP); Knock-out mice; MCH1-R; p-DARPP-32; Reward
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:liu:diva-129488 (URN)10.1007/s00213-016-4285-y (DOI)000376410800013 ()27044354 (PubMedID)
Available from: 2016-06-21 Created: 2016-06-20 Last updated: 2018-01-10
Bilbao, A., Robinson, J. E., Heilig, M., Malanga, C. J., Spanagel, R., Sommer, W. H. & Thorsell, A. (2015). A Pharmacogenetic Determinant of Mu-Opioid Receptor Antagonist Effects on Alcohol Reward and Consumption: Evidence from Humanized Mice.. Biological Psychiatry, 77(10), 850-858
Open this publication in new window or tab >>A Pharmacogenetic Determinant of Mu-Opioid Receptor Antagonist Effects on Alcohol Reward and Consumption: Evidence from Humanized Mice.
Show others...
2015 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 77, no 10, p. 850-858Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: It has been proposed that therapeutic responses to naltrexone in alcoholism are moderated by variation at the mu-opioid receptor gene locus (OPRM1). This remains controversial because human results vary and no prospectively genotyped studies have been reported. We generated humanized mice carrying the respective human OPRM1 A118G alleles. Here, we used this model system to examine the role of OPRM1 A118G variation for opioid antagonist effects on alcohol responses.

METHODS: Effects of naltrexone on alcohol reward were examined using intracranial self-stimulation. Effects of naltrexone or nalmefene on alcohol intake were examined in continuous access home cage two-bottle free-choice drinking and operant alcohol self-administration paradigms.

RESULTS: Alcohol lowered brain stimulation reward thresholds in 118GG mice in a manner characteristic of rewarding drugs, and this effect was blocked by naltrexone. Brain stimulation reward thresholds were unchanged by alcohol or naltrexone in 118AA mice. In the home cage, increased alcohol intake emerged in 118GG mice with increasing alcohol concentrations and was 33% higher at 17% alcohol. At this concentration, naltrexone selectively suppressed alcohol intake in 118GG animals to a level virtually identical to that of 118AA mice. No effect of naltrexone was found in the latter group. Similarly, both naltrexone and nalmefene were more effective in suppressing operant alcohol self-administration in 118GG mice.

CONCLUSIONS: In a model that allows close experimental control, OPRM1 A118G variation robustly moderates effects of opioid antagonism on alcohol reward and consumption. These findings strongly support a personalized medicine approach to alcoholism treatment that takes into account OPRM1 genotype.

Place, publisher, year, edition, pages
Elsevier, 2015
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:liu:diva-116656 (URN)10.1016/j.biopsych.2014.08.021 (DOI)000353559600004 ()25442002 (PubMedID)
Available from: 2015-03-30 Created: 2015-03-30 Last updated: 2018-01-11
Nätt, D., Johansson, I., Faresjö, T., Ludvigsson, J. & Thorsell, A. (2015). High cortisol in 5-year-old children causes loss of DNA methylation in SINE retrotransposons: a possible role for ZNF263 in stress-related diseases. Clinical Epigenetics, 7(1), Article ID 91.
Open this publication in new window or tab >>High cortisol in 5-year-old children causes loss of DNA methylation in SINE retrotransposons: a possible role for ZNF263 in stress-related diseases
Show others...
2015 (English)In: Clinical Epigenetics, E-ISSN 1868-7083, ISSN 1868-7083, Vol. 7, no 1, article id 91Article in journal (Refereed) Published
Abstract [en]

Background: Childhood stress leads to increased risk of many adult diseases, such as major depression and cardiovascular disease. Studies show that adults with experienced childhood stress have specific epigenetic changes, but to understand the pathways that lead to disease, we also need to study the epigenetic link prospectively in children. Results: Here, we studied a homogenous group of 48 5-year-old children. By combining hair cortisol measurements (a well-documented biomarker for chronic stress), with whole-genome DNA-methylation sequencing, we show that high cortisol associates with a genome-wide decrease in DNA methylation and targets short interspersed nuclear elements (SINEs; a type of retrotransposon) and genes important for calcium transport: phenomena commonly affected in stress-related diseases and in biological aging. More importantly, we identify a zinc-finger transcription factor, ZNF263, whose binding sites where highly overrepresented in regions experiencing methylation loss. This type of zinc-finger protein has previously shown to be involved in the defense against retrotransposons. Conclusions: Our results show that stress in preschool children leads to changes in DNA methylation similar to those seen in biological aging. We suggest that this may affect future disease susceptibility by alterations in the epigenetic mechanisms that keep retrotransposons dormant. Future treatments for stress-and age-related diseases may therefore seek to target zinc-finger proteins that epigenetically control retrotransposon reactivation, such as ZNF263.

Place, publisher, year, edition, pages
BioMed Central, 2015
Keywords
Stress; DNA methylation; ZNF263; Children; Retrotransposon; Cortisol; Transcription factor; EGR1; Blood; Hair
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:liu:diva-122055 (URN)10.1186/s13148-015-0123-z (DOI)000360619500001 ()26339299 (PubMedID)
Note

Funding Agencies|Centre for Systems Neurobiology at Linkoping University; Swedish Research Council [K2005-72X-11242-11A, K2008-69X-20826-01-4]; Swedish Child Diabetes Foundation; JDRF Wallenberg Foundation [K 98-99D-12813-01A]; Medical Research Council of Southeast Sweden (FORSS); Swedish Council for Working Life and Social Research [FAS2004-1775]

Available from: 2015-12-18 Created: 2015-10-19 Last updated: 2017-12-01
Elliott Robinson, J., Vardy, E., DiBerto, J. F., Chefer, V. I., White, K. L., Fish, E. W., . . . Malanga, C. J. (2015). Receptor Reserve Moderates Mesolimbic Responses to Opioids in a Humanized Mouse Model of the OPRM1 A118G Polymorphism. Neuropsychopharmacology, 40(11), 2614-2622
Open this publication in new window or tab >>Receptor Reserve Moderates Mesolimbic Responses to Opioids in a Humanized Mouse Model of the OPRM1 A118G Polymorphism
Show others...
2015 (English)In: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 40, no 11, p. 2614-2622Article in journal (Refereed) Published
Abstract [en]

The OPRM1 A118G polymorphism is the most widely studied mu-opioid receptor (MOR) variant. Although its involvement in acute alcohol effects is well characterized, less is known about the extent to which it alters responses to opioids. Prior work has shown that both electrophysiological and analgesic responses to morphine but not to fentanyl are moderated by OPRM1 A118G variation, but the mechanism behind this dissociation is not known. Here we found that humanized mice carrying the 118GG allele (h/mOPRM1-118GG) were less sensitive than h/mOPRM1-118AA littermates to the rewarding effects of morphine and hydrocodone but not those of other opioids measured with intracranial self-stimulation. Reduced morphine reward in 118GG mice was associated with decreased dopamine release in the nucleus accumbens and reduced effects on GABA release in the ventral tegmental area that were not due to changes in drug potency or efficacy in vitro or receptor-binding affinity. Fewer MOR-binding sites were observed in h/mOPRM1-118GG mice, and pharmacological reduction of MOR availability unmasked genotypic differences in fentanyl sensitivity. These findings suggest that the OPRM1 A118G polymorphism decreases sensitivity to low-potency agonists by decreasing receptor reserve without significantly altering receptor function.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-121737 (URN)10.1038/npp.2015.109 (DOI)000361138300014 ()25881115 (PubMedID)
Note

Funding Agencies|National Institute on Alcohol Abuse and Alcoholism [F30 AA021312, R01 AA018335]; National Institute on Drug Abuse [R01 DA017204]; Swedish Research Council [2010-3219]; intramural programs of the National Institute on Drug Abuse; NIH; Dai Nippon Sumitomo; Merck; Asubio Pharmaceuticals

Available from: 2015-10-06 Created: 2015-10-05 Last updated: 2017-12-01
Kwako, L. E., Spagnolo, P. A., Schwandt, M. L., Thorsell, A., George, D. T., Momenan, R., . . . Heilig, M. (2015). The Corticotropin Releasing Hormone-1 (CRH1) Receptor Antagonist Pexacerfont in Alcohol Dependence: A Randomized Controlled Experimental Medicine Study. Neuropsychopharmacology, 40(5), 1053-1063
Open this publication in new window or tab >>The Corticotropin Releasing Hormone-1 (CRH1) Receptor Antagonist Pexacerfont in Alcohol Dependence: A Randomized Controlled Experimental Medicine Study
Show others...
2015 (English)In: Neuropsychopharmacology, ISSN 0893-133X, E-ISSN 1740-634X, Vol. 40, no 5, p. 1053-1063Article in journal (Refereed) Published
Abstract [en]

Extensive preclinical data implicate corticotropin-releasing hormone (CRH), acting through its CRH1 receptor, in stress- and dependence-induced alcohol seeking. We evaluated pexacerfont, an orally available, brain penetrant CRH1 antagonist for its ability to suppress stress-induced alcohol craving and brain responses in treatment seeking alcohol-dependent patients in early abstinence. Fifty-four anxious alcohol-dependent participants were admitted to an inpatient unit at the NIH Clinical Center, completed withdrawal treatment, and were enrolled in a double-blind, randomized, placebo-controlled study with pexacerfont (300 mg/day for 7 days, followed by I 00 mg/day for 23 days). After reaching steady state, participants were assessed for alcohol craving in response to stressful or alcohol-related cues, neuroendocrine responses to these stimuli, and functional magnetic resonance imaging (fMRI) responses to alcohol-related stimuli or stimuli with positive or negative emotional valence. A separate group of 10 patients received open-label pexacerfont following the same dosing regimen and had cerebrospinal fluid sampled to estimate central nervous system exposure. Pexacerfont treatment had no effect on alcohol craving, emotional responses, or anxiety. There was no effect of pexacerfont on neural responses to alcohol-related or affective stimuli. These results were obtained despite drug levels in cerebrospinal fluid (CSF) that predict close to 90% central CRH1 receptor occupancy. CRH1 antagonists have been grouped based on their receptor dissociation kinetics, with pexacerfont falling in a category characterized by fast dissociation. Our results may indicate that antagonists with slow offset are required for therapeutic efficacy. Alternatively, the extensive preclinical data on CRH1 antagonism as a mechanism to suppress alcohol seeking may not translate to humans.

Place, publisher, year, edition, pages
Nature Publishing Group: Open Access Hybrid Model Option A, 2015
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-117224 (URN)10.1038/npp.2014.306 (DOI)000351022900001 ()25409596 (PubMedID)
Note

Funding Agencies|NIAAA DICBR; Cooperative Research and Development Agreement (CRADA) between the NIAAA; BristolMeyersSquibb

Available from: 2015-04-23 Created: 2015-04-21 Last updated: 2017-12-04
Holm, L., Liang, W., Thorsell, A. & Hilke, S. (2014). Acute effects on brain cholecystokinin-like concentration and anxiety-like behaviour in the female rat upon a single injection of 17β-estradiol. Pharmacology, Biochemistry and Behavior, 122, 222-227
Open this publication in new window or tab >>Acute effects on brain cholecystokinin-like concentration and anxiety-like behaviour in the female rat upon a single injection of 17β-estradiol
2014 (English)In: Pharmacology, Biochemistry and Behavior, ISSN 0091-3057, E-ISSN 1873-5177, Vol. 122, p. 222-227Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: The neuropeptide cholecystokinin (CCK) has been implicated in the neurobiology of anxiety and panic disorders, as well as in dopamine-related behaviours. Anxiety and panic-disorders are twice as common in females compared to males, but studies of females are rare, although increasing in number. Limited studies have found that CCK fluctuates in limbic regions during the estrous cycle, and that CCK and its receptors are sensitive to estrogen.

AIM/PURPOSE: The aim of the present work was to study the acute effects of 17β-estradiol on anxiety-like behaviour and on CCK-like immunoreactivity (LI) in the female rat brain (amygdala, hippocampus, nucleus accumbens, and cingulate cortex).

METHODS: Four groups of female Sprague-Dawley rats were used: ovariectomized, ovariectomized+17β-estradiol-replacement, sham, and sham+17β-estradiol-replacement. The effect of 17β-estradiol-replacement on anxiety-related behaviour was measured in all animals on the elevated plus maze 2-24h after injection. CCK-LI concentration was measured in punch biopsies by means of radioimmunoassay.

RESULTS: 17β-estradiol decreased anxiety-like behaviour 2h after administration in ovariectomized and sham-operated animals, as demonstrated by increased exploration of the open arms compared to respective sesame oil-treated controls. This effect was not present when testing occurred 24h post-treatment. The rapid behavioural effect of 17β-estradiol was accompanied by changes in CCK-LI concentrations in regions of the limbic system including cingulate cortex, hippocampus, amygdala and nucleus accumbens.

CONCLUSION: Although the interpretation of these data requires caution since the data were collected from two different experiments, our results suggest that estrogen-induced anxiolytic effects may be associated with changes of the CCK-system in brain regions controlling anxiety-like behaviour.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Anxiety, Cholecystokinin, Estrogen
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-106089 (URN)10.1016/j.pbb.2014.04.004 (DOI)000338597000025 ()24732637 (PubMedID)
Available from: 2014-04-24 Created: 2014-04-24 Last updated: 2017-12-05Bibliographically approved
Cippitelli, A., Damadzic, R., Hamelink, C., Brunnquell, M., Thorsell, A., Heilig, M. & Eskay, R. L. (2014). Binge-like ethanol consumption increases corticosterone levels and neurodegneration whereas occupancy of type II glucocorticoid receptors with mifepristone is neuroprotective. Addiction Biology, 19(1), 27-36
Open this publication in new window or tab >>Binge-like ethanol consumption increases corticosterone levels and neurodegneration whereas occupancy of type II glucocorticoid receptors with mifepristone is neuroprotective
Show others...
2014 (English)In: Addiction Biology, ISSN 1355-6215, E-ISSN 1369-1600, Vol. 19, no 1, p. 27-36Article in journal (Refereed) Published
Abstract [en]

Excessive ethanol (EtOH) use leads to impaired memory and cognition. Using a rat model of binge-like intoxication, we tested whether elevated corticosterone (Cort) levels contribute to the neurotoxic consequences of EtOH exposure. Rats were adrenalectomized (Adx) and implanted with cholesterol pellets, or cholesterol pellets containing Cort in order to achieve basal, medium, or high blood concentrations of Cort. Intragastric EtOH or an isocaloric control solution was given three times daily for 4 days to achieve blood alcohol levels ranging between 200 and 350 mg/dl. Mean 24-hour plasma levels of Cort were ∼110 and ∼40 ng/ml in intact EtOH-treated and intact control animals, respectively. Basal Cort replacement concentrations in EtOH-treated Adx animals did not exacerbate alcohol-induced neurodegeneration in the hippocampal dentate gyrus (DG) or the entorhinal cortex (EC) as observed by amino-cupric silver staining. In contrast, Cort replacement pellets resulting in plasma Cort levels twofold higher (medium) than normal, or greater than twofold higher (high) in Adx-Cort-EtOH animals increased neurodegeneration. In separate experiments, pharmacological blockade of the Type II glucocorticoid (GC) receptor was initiated with mifepristone (RU38486; 0, 5, 15 mg/kg/day, i.p.). At the higher dose, mifepristone decreased the number of degenerating hippocampal DG cells in binge-EtOH-treated intact animals, whereas, only a trend for reduction was observed in 15 mg/kg/day mifepristone-treated animals in the EC, as determined by fluoro-jade B staining. These results suggest that elevated circulating Cort in part mediates EtOH-induced neurotoxicity in the brain through activation of Type II GC receptors.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2014
Keywords
corticosterone, ethanol, FJ-B, hippocampus, mifepristone, neurodegeneration
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-101831 (URN)10.1111/j.1369-1600.2012.00451.x (DOI)000328610300004 ()22500955 (PubMedID)
Available from: 2013-11-24 Created: 2013-11-24 Last updated: 2018-01-11
Thorsell, A., Tapocik, J. D., Liu, K., Zook, M., Bell, L., Flanigan, M., . . . Heilig, M. (2013). A Novel Brain Penetrant NPS Receptor Antagonist, NCGC00185684, Blocks Alcohol-Induced ERK-Phosphorylation in the Central Amygdala and Decreases Operant Alcohol Self-Administration in Rats. Journal of Neuroscience, 33(24), 10132-10142
Open this publication in new window or tab >>A Novel Brain Penetrant NPS Receptor Antagonist, NCGC00185684, Blocks Alcohol-Induced ERK-Phosphorylation in the Central Amygdala and Decreases Operant Alcohol Self-Administration in Rats
Show others...
2013 (English)In: Journal of Neuroscience, ISSN 0270-6474, E-ISSN 1529-2401, Vol. 33, no 24, p. 10132-10142Article in journal (Refereed) Published
Abstract [en]

The Neuropeptide S receptor, a Gs/Gq-coupled GPCR expressed in brain regions involved in mediating drug reward, has recently emerged as a candidate therapeutic target in addictive disorders. Here, we describe the in vitro and in vivo pharmacology of a novel, selective and brain penetrant NPSR antagonist with nanomolar affinity for the NPSR, NCGC00185684. In vitro, NCGC00185684 shows biased antagonist properties, and preferentially blocks ERK-phosphorylation over intracellular cAMP or calcium responses to NPS. In vivo, systemic NCGC00185684 blocks alcohol-induced ERK-phosphorylation in the rat central amygdala, a region involved in regulation of alcohol intake. NCGC00185684 also decreases operant alcohol self-administration, and lowers motivation for alcohol reward as measured using progressive ratio responding. These effects are behaviorally specific, in that they are observed at doses that do not influence locomotor activity or reinstatement responding following extinction. Together, these data provide an initial validation of the NPSR as a therapeutic target in alcoholism.

Place, publisher, year, edition, pages
Society for Neuroscience, 2013
Keywords
addiction, neuropeptide S, phosphorylation
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-94652 (URN)10.1523/JNEUROSCI.4742-12.2013 (DOI)000320235300028 ()23761908 (PubMedID)
Available from: 2013-06-28 Created: 2013-06-28 Last updated: 2018-01-11Bibliographically approved
Patnaik, S., Marugan, J. J., Liu, K., Zheng, W., Southall, N., Dehdashti, S. J., . . . Austin, C. P. (2013). Structure-Activity Relationship of Imidazopyridinium Analogues as Antagonists of Neuropeptide S Receptor. Journal of Medicinal Chemistry, 56(22), 9045-9056
Open this publication in new window or tab >>Structure-Activity Relationship of Imidazopyridinium Analogues as Antagonists of Neuropeptide S Receptor
Show others...
2013 (English)In: Journal of Medicinal Chemistry, ISSN 0022-2623, E-ISSN 1520-4804, Vol. 56, no 22, p. 9045-9056Article in journal (Refereed) Published
Abstract [en]

The discovery and characterization of a novel chemical series of phosphorothioyl-containing imidazopyridines as potent neuropeptide S receptor antagonists is presented. The synthesis of analogues and their structure-activity relationship with respect to the Gq, Gs, and ERK pathways is detailed. The pharmacokinetics and in vivo efficacy of a potent analogue in a food intake rodent model are also included, underscoring its potential therapeutic value for the treatment of sleep, anxiety, and addiction disorders.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2013
National Category
Neurosciences
Identifiers
urn:nbn:se:liu:diva-101828 (URN)10.1021/jm400904m (DOI)24171469 (PubMedID)
Available from: 2013-11-24 Created: 2013-11-24 Last updated: 2018-01-11Bibliographically approved
Organisations

Search in DiVA

Show all publications