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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Cocaine is a highly addictive psychostimulant drug of abuse that constitutes an ongoing public health threat. Emerging research is revealing that numerous peripheral effects of this drug may serve as conditioned stimuli for its central reinforcing properties. The gut microbiota is emerging as one of these peripheral sources of input to cocaine reward. The primary objective of the present study was to determine how cocaine HCl and methylenedioxypyrovalerone, both of which powerfully activate central reward pathways, alter the gut microbiota. Cocaine methiodide, a quaternary derivative of cocaine that does not enter the brain, was included to assess peripheral influences on the gut microbiota. Both cocaine congeners caused significant and similar alterations of the gut microbiota after a day course of treatment. Functional predictions of metabolic alterations caused by the treatment drugs reaffirmed that the cocaine congeners were similar whereas MDPV was most dissimilar from the other two drugs and controls. It appears that the monoamine transporters in the gut mediate the effects of the treatment drugs. The effects of the cocaine congeners and MDPV on the gut microbiome may form the basis of interoceptive cues that can influence their abuse properties. Cocaine is a powerful addictive drug of abuse that remains a significant threat to public health. In addition to its abuse properties, habitual cocaine use is associated with numerous comorbid medical conditions that range in severity from irritation of the nasal septum to increased risk for stroke and seizures 1 , a wide variety of cardiovascular abnormalities 2 , 3 and ischemic injury to the gastrointestinal GI tract 4. Chronic cocaine use leads to a vast array of changes in the CNS to include persistent alterations in synaptic properties in neurons of the dopamine DA reward pathway 5 , and plasticity changes in excitatory transmission in the nucleus accumbens 6 and along corticostriatal pathways 7. These processes likely act in concert through all phases of cocaine abuse disorder to modulate acquisition of self-administration, extinction, craving and relapse. Although numerous targets for therapeutic intervention have emerged, it is generally accepted by experts in the field that an effective treatment for cocaine addiction is lacking 8. While emphasis on achieving a better understanding of substance use disorders has naturally focused on intrinsic CNS mechanisms, it is possible that signals from outside of the CNS could play a role in cocaine abuse. While gut microbiota is a target of peripheral action for abused drugs, the mechanisms underlying this interaction remain elusive. The bulk of the microbiota resides in the GI tract and is composed of bacteria, fungi, viruses and archaea. Normal functioning of the gut microbiota is essential to the maintenance of human health. An imbalance in the microbiota composition i. It is also emerging that gut microbiota dysbiosis can play a role in numerous neurological e. With regard to drugs of abuse, a small but growing literature is implicating the gut microbiota in alcohol abuse and withdrawal 17 , 18 , 19 , nicotine and smoking 20 , 21 and in methamphetamine-induced conditioned place preference CPP Despite the paucity of published papers in the area of drug abuse and gut microbiota interactions, the premise for undertaking such studies with regard to cocaine is actually quite compelling. Emerging results have shown that cocaine causes dysbiosis in the gut microbiota of humans 24 and rodents 25 , 26 and that dysbiosis affects responses to cocaine Depletion of gut bacteria by treatment with a prolonged course of antibiotics increased sensitivity to cocaine CPP and enhanced its locomotor stimulating properties The report by Buch and colleagues 26 also documented cocaine-induced upregulation of proinflammatory mediators in the gut along with a compromise of mucosal barrier integrity. The current status of gut microbiota roles in substance use disorders has been reviewed recently 31 , In the present study, we report the effects of cocaine hydrochloride HCl , cocaine methiodide MI and methylenedioxypyrovalerone MDPV on the gut microbiota. Cocaine HCl was chosen for this study to broaden the understanding of its actions on the gut microbiota and for comparison to its MI analog. The rewarding and reinforcing effects of cocaine have all been primarily associated with its blockade of the DA transporter DAT and the resulting elevation in extracellular DA levels Cocaine MI is a quaternary derivative of cocaine that cannot cross the blood—brain barrier 34 and may differentiate the peripheral and central effects that contribute to the rewarding effects of cocaine HCl MDPV was included because it shares many of the rewarding properties of cocaine HCl based on its ability to support self-administration 36 , 37 , 38 , form a CPP 39 , 40 , 41 and facilitate intracranial self-stimulation 42 , 43 , Therefore, this study sheds light on the mechanisms by which cocaine can affect the gut microbiome by pointing the role of monoamine transporters differentially activated by cocaine and analog drugs in the gut, and it also contributes to understand the crosstalk between gut microbiome and brain axis in responses to cocaine. This was possible through the use of cocaine methiodide, which does not cross the blood-brain barrier, limiting its effects to peripheral targets. Females were used in order to maintain consistency with our previous study that examined effects of synthetic psychoactive cathinone drugs and amphetamine stimulants on the gut microbiota In addition, studies in humans and rodents indicate that females are more vulnerable to the reinforcing effects of cocaine Given that sex hormones can drive differences in gut microbiome, a stand-alone sex comparison is more suitable as an independent and subsequent study Mice had free access to food and water. Diet consisted of standard laboratory rodent chow LabDiet containing All mice used in these studies were from the same cohort. Doses of the study drugs were chosen from published accounts showing self-administration for cocaine HCl and MDPV and are based on average daily drug intake achieved for each drug 36 , This treatment regimen is similar to the one used for cocaine HCl treatment of mice by Chivero and colleagues in their recent paper Additionally, we are modeling repeated cocaine use in a similar time frame used in the context of well-established paradigms modeling cocaine addiction-like behaviors such as CPP and behavioral sensitization 28 , Mice were sacrificed 2 days after the final treatment with each study drug. Stressors such as noise and handling by multiple persons were avoided. Mice were monitored daily for signs of distress or injury by visualization of general parameters such as separation from the group, decreased grooming, piloerection, abnormal posture e. The ASVs were classified taxonomically using the Silva reference database v and the bacterial community data was thereafter visualized and statistically analyzed using PAST software v3. High-dimensional class comparisons were carried out with linear discriminant analysis effect size LEfSe in an online interface 54 using default parameters with the exception that LDA score was set to 3. Heat maps were generated using MetaboAnalyst 4. MetaCyc ontology predictions 57 were used for metabolic pathways classification. Taxonomic distributions at the phylum level were analyzed with a mixed-effects model fixed effects of treatment X phylum controlled for multiple comparisons using Benjamini—Hochberg correction. Chao-1 is a richness estimator, whereas Simpson and Shannon are two different measures of richness and evenness of the microbial composition Simpson's complementary diversity 1-D index relies on Simpson's dominance D , which indicates the species dominance Thus, greater values of Simpson 1-D indicate increases in diversity. The Shannon index places a greater weight on species richness and its value increases as both the number of species and their evenness increase Post hoc analysis revealed that all pairwise comparisons between drugs were significantly different with the exception of cocaine HCl versus cocaine MI. All pairwise comparisons between study drugs were statistically significant in the Bray—Curtis analysis. Bray—Curtis index, b of gut microbiome profiles among mice treated with the different study drugs. All pairwise statistical comparisons are included in Supplementary Table S1. The treatment drugs caused changes in percent relative abundance across the represented phylogenetic tree i. Both cocaine groups showed higher relative abundances of those taxa with greater overall percent relative abundance and lower relative abundances of taxa with overall lower percent relative abundance. The ASV profiles of MDPV, on the other hand, were different from controls and both cocaine groups showing decreased abundance of taxa with overall intermediate and lower relative abundance and increased abundance of taxa with overall higher relative abundance. All subjects in each treatment group are arrayed in columns and bacterial taxonomies are arrayed in rows. Taxonomic clustering was done using the Ward algorithm. LEfSe determines the features e. The discriminant taxa for all drugs spanned several phyla but were primarily located within Bacteroidetes and Firmicutes. In general, the species linked to cocaine HCl e. Species determinant for controls e. Figure 5 shows the effect of treatments at the phylum level. The effect of treatment drug was not significant whereas the effect of phylum F 1. Multiple comparisons corrected with the Benjamini—Hochberg method revealed that significant drug-induced alterations occurred in the phylum Verrucomicrobia. For this phylum, every drug differed from controls and from each other, with the exception of the comparison between cocaine HCl and Cocaine MI. Stacked columns for the mean values for each phylum are included for each of the treatments and controls. The treatment drugs caused complex changes in the percent relative abundance at taxonomic levels of family in a manner that was largely drug specific. First, the phylum within which most drug-induced changes occurred was Firmicutes 4 of 10 panels of Fig. The greatest number of drug-induced changes from control were seen after cocaine HCl and cocaine MI treatments where both drugs caused significant decreases in families Deferribacteraceae Fig. The significant drug-induced effects were analyzed with STAMP and displayed in MetaCyc, a database that includes a collection of metabolic pathways and enzymes from a wide variety of microorganisms and plants. A summary analysis of these data revealed that 76 microbial pathways were modified significantly by one or more of the drug treatments used. All of the predicted drug-induced metabolic changes are presented in Supplementary Table S2. The number of metabolic pathways changed by each treatment is presented as a Venn diagram in Fig. A single pathway was shared among all three drugs. It is interesting that when cocaine HCl and cocaine MI altered the same metabolic pathway, the direction of alteration was always the same and these comparisons are included in Supplementary Table S3. On the other hand, when cocaine HCl and MDPV caused changes in the same metabolic pathway, the direction of the change was always in opposite directions. These findings further reinforce other observations that cocaine HCl and cocaine MI were most similar and MDPV was most dissimilar by comparison to the cocaine congeners. Finally, a random forest analysis was carried out to define those metabolic features that allowed discrimination among the drug treatment groups and the results are presented in Fig. Based on mean decrease in accuracy analysis, 11 pathways emerged that discriminate among the 3 drugs and controls, most of which 8 of 11 were in the major MetaCyc pathway of metabolism of cofactors and vitamins. The remaining classifiers fell within pathways of lipid metabolism and carbohydrate metabolism. The number of metabolic pathways that differed significantly from controls for each treatment drug are represented by the major circles. The intersections show the number of pathway alterations shared by two or three of the treatment drugs. Data for the pathway alterations by the treatment drugs is plotted versus mean decrease in accuracy. Higher values for mean decrease in accuracy indicates the importance of a pathway in predicting its association with a treatment drug. Predictions of how these drugs could alter the gut microbiome depend on whether these drugs are acting directly at the level of the gut or via the brain-to-gut axis. In the former possibility, it would be predicted that cocaine HCl would cause effects similar to those of cocaine MI, based on their sequence similarity, and MDPV would differ from both cocaine congeners. In the latter possibility, it would be predicted that cocaine HCl and MDPV would be most similar in their effects on the gut microbiome in light of the extensive overlap these drugs have on DA reward circuits in the CNS. These include the ability to support self-administration 36 , 37 , 38 , formation of a CPP 39 , 40 , 41 and enhancement of intracranial self-stimulation 42 , 43 , Taken together, the results suggest direct actions on the gut in light of the similarities between cocaine HCl and cocaine MI, and the dissimilarity of MDPV with the cocaine congeners. The phyla most altered by the study drugs were Verrucomicrobia and Firmicutes. MDPV significantly reduced the relative abundance of Verrucomicrobia by comparison to the cocaine congeners and significantly increased the relative abundance of Firmicutes versus both cocaine compounds. It is interesting that the differences between the cocaine congeners and MDPV remained evident in the alterations of the family taxa with cocaine HCl and cocaine MI changing in opposite directions from those caused by MDPV. For instance, MDPV was significantly lower in abundance of Akkermansiaceae by comparison to the cocaine drugs whereas MDPV was significantly higher in abundance in the Rikenellaceae family by comparison to the cocaine drugs. The only family in which all three drugs had the same effect was in Desulfovibrionaceae where abundance was significantly reduced by comparison to controls. Cocaine HCl also caused changes in relative abundance increases and decreases throughout the bacterial taxonomy 24 , 25 , While we did not assess alterations in gut function presently, Chivero et al. With their results in mind, we attempted to link drug-induced changes in the gut microbiota to taxa known to alter gut function and inflammation. In general, A. Lower levels of Porphyromonadaceae have been associated with suppression of inflammation in mice lacking the fat mass and obesity-associated gene These latter effects indicate that cocaine HCl is exerting inflammatory effects in the gut and the increase in A. A similar situation exists for cocaine MI with regard to its signature on the gut microbiota. These findings suggest the association of Lachnospiraceae with inflammatory conditions or with attempts to mount an anti-inflammatory response, depending on the provoking GI condition. The outcomes of the PICRUSt metabolic and functional analyses were parallel to the drug-induced alterations in the gut microbiome, showing that cocaine HCl significantly increased whereas MDPV resulted in significant reductions in the same metabolic pathways. Overall, cocaine HCl and cocaine MI to a lesser extent increased activity in the major metabolic pathways for nucleotide metabolism, cofactors and vitamins whereas MDPV had the opposite effect on these pathways. Taken together, the results from gut microbiota analyses and the metabolic and functional predictions confirm that cocaine HCl and cocaine MI were very similar whereas MDPV was very different from the cocaine congeners in its effects. This suggests that the treatments drugs are exerting their effects on the gut microbiome directly at the level of the gut and not through an indirect brain-to-gut axis. If it is assumed that the treatment drugs are acting locally in the gut to alter the microbiome, monoamine transporters emerge as likely mediators that can explain cocaine HCl — cocaine MI similarities and MDPV differences from the cocaine congeners. Cocaine MI blocks all three transporters but with much lower potency All three transporters are expressed in the gut 73 , 74 , 75 , 76 and can influence intestinal motility and function 74 , 77 , 78 , 79 , It therefore appears that 5-HT is the factor that differentiates the actions of the cocaine congeners from MDPV with regard to alterations in the gut microbiota. Sitte and colleagues showed that cocaine HCl dissociates rapidly from the DAT and has short-lived behavioral effects whereas MDPV has significantly slower off-kinetics and exerts long-lasting effects Therefore, the differences between cocaine HCl and MDPV in terms of the specificity of transporter blockade could be amplified in the gut because of the widely differing duration of their inhibition of monoamine uptake. It is known that cocaine HCl and MDPV share the ability to cause vasoconstriction and increases in blood pressure 83 , 84 , 85 and that the gut microbiome can regulate blood pressure However, it does not appear that the cardiovascular effects of these drugs can account for their differing effects on the gut microbiome or metabolome. The ability of cocaine HCl and MDPV to block monoamine transporters in the gut suggests the unrecognized possibility that they could influence pathogen colonization and virulence which are now known to be mediated by 5-HT 87 and NE Cocaine is known to be markedly immunomodulatory which can increase susceptibility to infection We also hypothesized that cocaine HCl would overlap with cocaine MI in its effects on the gut microbiome and metabolome if their actions on the gut microbiota were peripheral. The cocaine congeners do share extensive overlap in their ability to alter CNS excitation and hyperthermia via blockade of peripheral voltage-gated sodium channels 92 , 93 , In addition, the conditioned taste aversion properties of cocaine HCl are shared by cocaine MI, an effect that has been attributed in part to peripheral sodium channel inhibition 95 by these drugs. In animals with prior exposure to cocaine HCl, cocaine MI causes DA 96 and glutamate 34 , 97 release in the nucleus accumbens, reinstates an extinguished cocaine HCl CPP, and rapidly alters the activity of ventral tegmental neurons Wise and Kiyatkin 35 have shown convincingly that peripheral interoceptive cues associated with cocaine HCl become conditioned to its central actions, explaining how cocaine MI can exert central effects. Mice treated with cocaine MI in the present experiments were not pre-exposed to cocaine HCl, making it unlikely that cocaine MI was causing effects on the gut microbiota via the CNS. The current study has several principal strengths. First, it expands existing research on cocaine HCl-gut microbiota interactions and extends it to other drugs with similar pharmacological and structural properties. Second, it establishes that drugs with very similar CNS properties can have distinct effects on the gut microbiota, as observed recently for methamphetamine and synthetic psychoactive cathinone drugs Third, the results suggest that earlier demonstrations of cocaine effects can now be subjected to reinterpretation in light of the extensive impact of these treatments on the gut microbiota. These include the attenuation of the addictive properties of cocaine HCl with a high fat diet, sodium butyrate used as a histone deacetylase inhibitor and with ceftriaxone to upregulate expression of the neuronal glutamate transporter. Our study also has several primary limitations. First, it did not include measures of drug-induced gut or CNS alterations. Second, the method of drug administration used presently and in other studies of cocaine HCl-gut microbiota interactions 25 , 26 simulated self-administration schedules and dosages versus contingent intravenous intake as used in self-administration studies. This limitation would be difficult to overcome because cocaine MI is not self-administered It also appears that the pharmacological effects of abused drugs override the method of administration or the behavioral assay used, at least in the case of methamphetamine Third, we cannot yet determine the mechanism by which the study drugs are altering the structure and composition of the gut microbiota. This will be addressed in future studies. Raw data or further methodological information from the current study are available upon reasonable request from the corresponding author. Fonseca, A. Drug abuse and stroke. Maraj, S. Cocaine and the heart. Havakuk, O. The cardiovascular effects of cocaine. Riezzo, I. Side effects of cocaine abuse: Multiorgan toxicity and pathological consequences. Francis, T. Synaptic and intrinsic plasticity in the ventral tegmental area after chronic cocaine. Wolf, M. Synaptic mechanisms underlying persistent cocaine craving. Bobadilla, A. Corticostriatal plasticity, neuronal ensembles, and regulation of drug-seeking behavior. Brain Res. Kampman, K. The treatment of cocaine use disorder. Sender, R. Revised estimates for the number of human and bacteria cells in the body. PLoS Biol. Savage, D. Microbial ecology of the gastrointestinal tract. Hamady, M. Microbial community profiling for human microbiome projects: Tools, techniques, and challenges. Genome Res. Shreiner, A. The gut microbiome in health and in disease. Pflughoeft, K. Human microbiome in health and disease. Tremlett, H. The gut microbiome in human neurological disease: A review. Article PubMed Google Scholar. Dinan, T. The microbiome-gut-brain axis in health and disease. Article Google Scholar. Foster, J. Gut-brain axis: How the microbiome influences anxiety and depression. Trends Neurosci. Barr, T. Concurrent gut transcriptome and microbiota profiling following chronic ethanol consumption in nonhuman primates. Gut Microbes 9 , — Peterson, V. Drunk bugs: Chronic vapour alcohol exposure induces marked changes in the gut microbiome in mice. Xiao, H. Gut microbiota modulates alcohol withdrawal-induced anxiety in mice. Chi, L. Nicotine alters the gut microbiome and metabolites of gut-brain interactions in a sex-specific manner. Allais, L. Chronic cigarette smoke exposure induces microbial and inflammatory shifts and mucin changes in the murine gut. Ning, T. Gut microbiota analysis in rats with methamphetamine-induced conditioned place preference. Cluny, N. Prevention of diet-induced obesity effects on body weight and gut microbiota in mice treated chronically with delta9-tetrahydrocannabinol. Volpe, G. Associations of cocaine use and HIV infection with the intestinal microbiota, microbial translocation, and inflammation. Drugs 75 , — Scorza, C. Alterations in the gut microbiota of rats chronically exposed to volatilized cocaine and its active adulterants caffeine and phenacetin. Neurotox Res. Chivero, E. Cocaine induces inflammatory gut milieu by compromising the mucosal barrier integrity and altering the gut microbiota colonization. Cuesta, S. Gut colonization by Proteobacteria alters host metabolism and modulates cocaine neurobehavioral responses. Cell Host Microbe 30 , — Kiraly, D. Alterations of the host microbiome affect behavioral responses to cocaine. Bertacco, A. Modulation of intestinal microbiome prevents intestinal ischemic injury. Yoshiya, K. Liver Physiol. Meckel, K. A potential role for the gut microbiome in substance use disorders. Psychopharmacology , — Angoa Perez, M. Evidence for modulation of substance use disorders by the gut microbiome: Hidden in plain sight. Yamamoto, D. Rats classified as low or high cocaine locomotor responders: A unique model involving striatal dopamine transporters that predicts cocaine addiction-like behaviors. Wise, R. Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release. Differentiating the rapid actions of cocaine. Gannon, B. The abuse-related effects of pyrrolidine-containing cathinones are related to their potency and selectivity to inhibit the dopamine transporter. Neuropsychopharmacology 43 , — Aarde, S. In vivo potency and efficacy of the novel cathinone alpha-pyrrolidinopentiophenone and 3,4-methylenedioxypyrovalerone: Self-administration and locomotor stimulation in male rats. Geste, J. Self-administration of the synthetic cathinone MDPV enhances reward function via a nicotinic receptor dependent mechanism. Neuropharmacology , — Karlsson, L. Mephedrone, methylone and 3,4-methylenedioxypyrovalerone MDPV induce conditioned place preference in mice. Basic Clin. King, H. Drug Alcohol. Atehortua-Martinez, L. Acute and chronic neurobehavioral effects of the designer drug and bath salt constituent 3,4-methylenedioxypyrovalerone in the rat. Kolanos, R. Stereoselective actions of methylenedioxypyrovalerone MDPV to inhibit dopamine and norepinephrine transporters and facilitate intracranial self-stimulation in rats. ACS Chem. Bonano, J. Watterson, L. Potent rewarding and reinforcing effects of the synthetic cathinone 3,4-methylenedioxypyrovalerone MDPV. Baumann, M. Neuropsychopharmacology 38 , — Angoa-Perez, M. Differential effects of synthetic psychoactive cathinones and amphetamine stimulants on the gut microbiome in mice. Martini, M. Sex chromosome complement influences vulnerability to cocaine in mice. He, S. The gut microbiome and sex hormone-related diseases. Inhibition of cocaine and 3,4-methylenedioxypyrovalerone MDPV self-administration by lorcaserin is mediated by 5-HT2C receptors in rats. Chen, H. Minocycline affects cocaine sensitization in mice. Kozich, J. Development of a dual-index sequencing strategy and curation pipeline for analyzing amplicon sequence data on the MiSeq Illumina sequencing platform. Effects of gut microbiota remodeling on the dysbiosis induced by high fat diet in a mouse model of Gulf war illness. Life Sci. Hammer, O. PAST: Paleontological statistics software package for education and data analysis. Palaeontologia Electonica 4 , 1—9 Google Scholar. Segata, N. Metagenomic biomarker discovery and explanation. Genome Biol. Chong, J. MetaboAnalyst 4. Nucleic Acids Res. Langille, M. Predictive functional profiling of microbial communities using 16S rRNA marker gene sequences. Caspi, R. The MetaCyc database of metabolic pathways and enzymes: A update. Kim, B. Deciphering diversity indices for a better understanding of microbial communities. Schneeberger, M. Akkermansia muciniphila inversely correlates with the onset of inflammation, altered adipose tissue metabolism and metabolic disorders during obesity in mice. Addolorato, G. Gut microbiota compositional and functional fingerprint in patients with alcohol use disorder and alcohol-associated liver disease. Liver Int. Derrien, M. Akkermansia muciniphila and its role in regulating host functions. Zhai, R. Strain-specific anti-inflammatory properties of two Akkermansia muciniphila strains on chronic colitis in mice. Front Cell Infect Microbiol 9 , Sun, L. Fto deficiency reduces anxiety- and depression-like behaviors in mice via alterations in gut microbiota. Theranostics 9 , — Crouch, L. Prominent members of the human gut microbiota express endo-acting O-glycanases to initiate mucin breakdown. Ren, T. Rodriguez, J. Discovery of the gut microbial signature driving the efficacy of prebiotic intervention in obese patients. Zeng, H. Lai, F. Haikal, C. Eshleman, A. Substituted methcathinones differ in transporter and receptor interactions. Simmler, L. Pharmacological characterization of designer cathinones in vitro. Hill, E. Potencies of cocaine methiodide on major cocaine targets in mice. Li, Z. Dependence of serotonergic and other nonadrenergic enteric neurons on norepinephrine transporter expression. Physiological modulation of intestinal motility by enteric dopaminergic neurons and the D2 receptor: Analysis of dopamine receptor expression, location, development, and function in wild-type and knock-out mice. Gill, R. Function, expression, and characterization of the serotonin transporter in the native human intestine. Wade, P. Localization and function of a 5-HT transporter in crypt epithelia of the gastrointestinal tract. Neuhuber, W. Monoamines in the enteric nervous system. Cell Biol. Cao, H. Dysbiosis contributes to chronic constipation development via regulation of serotonin transporter in the intestine. Singhal, M. Serotonin transporter deficiency is associated with dysbiosis and changes in metabolic function of the mouse intestinal microbiome. El Aidy, S. Serotonin transporter genotype modulates the gut microbiota composition in young rats, an effect augmented by early life stress. Niello, M. Persistent binding at dopamine transporters determines sustained psychostimulant effects. USA , e Cussotto, S. Differential effects of psychotropic drugs on microbiome composition and gastrointestinal function. McClenahan, S. Luo, F. Characterization of effects of mean arterial blood pressure induced by cocaine and cocaine methiodide on BOLD signals in rat brain. Wakabayashi, K. Methylenedioxypyrovalerone MDPV mimics cocaine in its physiological and behavioral effects but induces distinct changes in NAc glucose. Marques, F. Beyond gut feelings: How the gut microbiota regulates blood pressure. Kumar, A. The serotonin neurotransmitter modulates virulence of enteric pathogens. Cell Host Microbe 28 , 41— Friedman, H. Addictive drugs and their relationship with infectious diseases. FEMS Immunol. Ait Chait, Y. Unravelling the antimicrobial action of antidepressants on gut commensal microbes. Jin, M. Antidepressant fluoxetine induces multiple antibiotics resistance in Escherichia coli via ROS-mediated mutagenesis. Wang, Y. Antidepressants can induce mutation and enhance persistence toward multiple antibiotics. Kiyatkin, E. The role of peripheral and central sodium channels in mediating brain temperature fluctuations induced by intravenous cocaine. Rapid EEG desynchronization and EMG activation induced by intravenous cocaine in freely moving rats: A peripheral, nondopamine neural triggering. Brown, P. Freeman, K. Wang, B. Conditioned contribution of peripheral cocaine actions to cocaine reward and cocaine-seeking. Critical role of peripheral drug actions in experience-dependent changes in nucleus accumbens glutamate release induced by intravenous cocaine. Mejias-Aponte, C. Neuroscience , — Differential perturbations of gut microbial profiles and co-occurrence networks among phases of methamphetamine-induced conditioned place preference. Download references. Research and Development Service, John D. You can also search for this author in PubMed Google Scholar. All authors read, edited, and approved the manuscript. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. Reprints and permissions. Cocaine hydrochloride, cocaine methiodide and methylenedioxypyrovalerone MDPV cause distinct alterations in the structure and composition of the gut microbiota. Sci Rep 13 , Download citation. Received : 27 February Accepted : 17 August Published : 23 August Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily. Skip to main content Thank you for visiting nature. Download PDF. Subjects Computational biology and bioinformatics Neuroscience. Abstract Cocaine is a highly addictive psychostimulant drug of abuse that constitutes an ongoing public health threat. Microbial short-chain fatty acids regulate drug seeking and transcriptional control in a model of cocaine seeking Article 02 August Dual action of ketamine confines addiction liability Article 27 July Heroin and its metabolites: relevance to heroin use disorder Article Open access 08 April Full size image. Figure 2. Figure 3. Figure 4. Full size table. Figure 5. Figure 6. Figure 7. Figure 8. Data availability Raw data or further methodological information from the current study are available upon reasonable request from the corresponding author. References Fonseca, A. Article Google Scholar Foster, J. Article Google Scholar Cluny, N. Google Scholar Segata, N. Article Google Scholar Chong, J. View author publications. Ethics declarations Competing interests The authors declare no competing interests. Additional information Publisher's note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Supplementary Information. About this article. Copy to clipboard. This article is cited by Bridging the gap: associations between gut microbiota and psychiatric disorders Gellan K. Haridy Middle East Current Psychiatry Publish with us For authors Language editing services Submit manuscript. Search Search articles by subject, keyword or author. Show results from All journals This journal. Advanced search. Close banner Close. Email address Sign up. Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing.