Microarray proﬁle analysis of toxic cocaine‐induced alterations in the expression of mouse brain gene sequences: a possible ‘protective’ effect of buprenorphine

Hayase, Tamaki; Yamamoto, Yoshiko; Yamamoto, Keiichi; Muso, Eri; Shiota, Kohei

doi:10.1002/jat.939

Cited by 9 publications

(6 citation statements)

References 29 publications

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“…In this respect, a surprisingly large number of differentially expressed genes were detected in the whole mouse cerebrum following repeated administration of a high dose of cocaine (40 mg/kg, i.p., for 4 days) (Hayase et al, 2004). Whole cerebrum RNA samples were collected 24 hours after the last cocaine administration, and were pooled for analysis with a mouse 'discovery array' containing 2688 probes and dual-dye labelling (Cy5/Cy3).…”

Section: Single-cell Rna Amplification and Microarray Analysismentioning

confidence: 99%

Microarray Studies of Psychostimulant-Induced Changes in Gene Expression

et al. 2005

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Alterations in the expression of multiple genes in many brain regions are likely to contribute to psychostimulant-induced behaviours. Microarray technology provides a powerful tool for the simultaneous interrogation of gene expression levels of a large number of genes. Several recent experimental studies, reviewed here, demonstrate the power, limitations and progress of microarray technology in the field of psychostimulant addiction. These studies vary in the paradigms of cocaine or amphetamine administration, drug doses, route and also mode of administration, duration of treatment, animal species, brain regions studied and time of tissue collection after final drug administration. The studies also utilize different microarray platforms and statistical techniques for analysis of differentially expressed genes. These variables influence substantially the results of these studies. It is clear that current microarray techniques cannot detect small changes reliably in gene expression of genes with low expression levels, including functionally significant changes in components of major neurotransmission systems such as glutamate, dopamine, opioid and GABA receptors, especially those that may occur after chronic drug administration or drug withdrawal. However, the microarray studies reviewed here showed cocaine- or amphetamine-induced alterations in the expression of numerous genes involved in the modulation of neuronal growth, cytoskeletal structures, synaptogenesis, signal transduction, apoptosis and cell metabolism. Application of laser capture microdissection and single-cell cDNA amplification may greatly enhance microarray studies of gene expression profiling. The combination of rapidly evolving microarray technology with established methods of neuroscience, molecular biology and genetics, as well as appropriate behavioural models of drug reinforcement, may provide a productive approach for delineating the neurobiological underpinnings of drug responses that lead to addiction.

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Section: Single-cell Rna Amplification and Microarray Analysismentioning

confidence: 99%

Microarray Studies of Psychostimulant-Induced Changes in Gene Expression

et al. 2005

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“…Not surprisingly, a large majority focused on the mesocorticolimbic dopaminergic pathway: the NAc (21 articles [8,22,26,28–30,32,40–53]), frontal cortex (13 articles [8,25,27,29,51,54–61]), whole/unspecified striatal complex (11 articles [24,33,62–70]), dorsal striatum (7 articles [8,30,48–50,71,72]) and ventral tegmental area (VTA, 5 articles [28,51,73–75]). Other regions included the spinal cord (7 articles [62,76– 81]); hippocampus (5 articles [8,63,82–84]); amygdala (3 articles [8,85,86]); locus coeruleus [74, 87], ventral midbrain [42, 88], hypothalamus [89, 90], whole brain with [91] or without [92] cerebellum (1 each); periaqueductal gray matter [93], pituitary gland [90], arcuate nucleus [94], nucleus of the tractus solitarius [31], brainstem [23], cerebellum [84] or dorsal root ganglia [95] (DRG, 1 each). Below, we briefly describe the rationale for studying such diverse structures.…”

Section: Resultsmentioning

confidence: 99%

Functional genomic mechanisms of opioid action and opioid use disorder: a systematic review of animal models and human studies

Falconnier

Caparros-Roissard

Decraene

et al. 2022

Preprint

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In the past two decades, over-prescription of opioids for pain management has driven a steep increase in opioid use disorder (OUD) and death by overdose, exerting a dramatic toll on western countries. OUD is a chronic relapsing disease associated with a lifetime struggle to control drug consumption, suggesting that opioids trigger long-lasting brain adaptations, notably through functional genomic and epigenomic mechanisms. Current understanding of these processes, however, remain scarce, and have not been previously reviewed systematically. To do so, the goal of the present work was to synthesize current knowledge on genome-wide transcriptomic and epigenetic mechanisms of opioid action, in primate and rodent species. Using a prospectively registered methodology, comprehensive literature searches were completed in PubMed, Embase, and Web of Science. Of the 2705 articles identified, 69 met our inclusion criteria and were considered for qualitative analysis. Focusing on the 5 most studied nervous system structures (nucleus accumbens, frontal cortex, whole striatum, dorsal striatum, spinal cord; 44 articles), we also conducted a quantitative analysis of differentially expressed genes, in an effort to identify a putative core transcriptional signature of opioids. Only one gene, Cdkn1a, was replicated in six studies and, globally, our results unveil surprisingly low consistency across published work, even when considering most recent single-cell approaches. Analysis of putative sources for this poor reproducibility suggest contributions from species, brain structures, duration of opioid exposure, as well as batch effects. To go beyond those limitations, we leveraged threshold-free methods to illustrate how genome-wide comparisons may generate new findings and hypotheses. Finally, we discuss current methodological development in the field, and their implication for future research and, ultimately, better care.

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“…For example, the antioxidant compound selenium has been shown to protect against cocaine‐induced myocardial oxidative stress 46 . Animal experiments also suggest cocaine‐induced hepatotoxic neurobehavioral and biochemical changes can be ameliorated by the mixed opioid agonist‐antagonist buprenorphine 47,48 . Protection against cocaine and combined cocaine‐ethanol toxicities by a partial inverse agonist of benzodiazepine receptors Ro 15‐4513 has also been shown in mice 49,80 .…”

Section: Direct Toxic Actions Of Abused Drugsmentioning

confidence: 99%

“…46 Animal experiments also suggest cocaine-induced hepatotoxic neurobehavioral and biochemical changes can be ameliorated by the mixed opioid agonistantagonist buprenorphine. 47,48 Protection against cocaine and combined cocaine-ethanol toxicities by a partial inverse agonist of benzodiazepine receptors Ro 15-4513 has also been shown in mice. 49,80 Other strategies such as liver detoxification and prevention of renal failure have also been proposed.…”

Section: Cocaine Abuse and Encephalopathymentioning

confidence: 99%

Neuroprotective strategies in drug abuse‐evoked encephalopathy

Virmani

Ali²,

Binienda

2010

Annals of the New York Academy of Sciences

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Encephalopathy is evidenced as an altered mental state with various neurological symptoms, such as memory and cognitive problems. The type of a substance-evoked encephalopathy will depend on the drug, substance, or combination being abused. The categories into which we could place the various abused substances could be tentatively divided into stimulants, amphetamines, hallucinogens, narcotics, inhalants, anesthetics, anabolic steroids, and antipsychotics/antidepressants. Other factors that may underlie encephalopathy, such as infectious agents, environmental, and other factors have also to be taken into account. Drugs of abuse can be highly toxic to the CNS following acute, but more so in chronic exposure, and can produce significant damage to other organs, such as the heart, lungs, liver, and kidneys. The damage to these organs may be at least partially reversible when drug abuse is stopped but CNS damage from repeated or prolonged abuse is often irreversible. The major pathways for the organ and CNS toxicity could be related to ischemic events as well as increased cell damage due to metabolic or mitochondrial dysfunction resulting in increased excitotoxicity, reduced energy production, and lowered antioxidant potential. These susceptibilities could be strengthened by the use of antioxidants to combat free radicals (e.g., vitamin E, lipoic acid); trying to improve energy generation by using mitochondriotropic/metabolic compounds (e.g., thiamine, coenzyme Q10, carnitine, riboflavin); by reducing excitotoxicity (e.g., glutamate antagonists) and other possible strategies, such as robust gene response, need to be investigated further. The drug-abuse-evoked encephalopathy still needs to be studied further to enable better preventative and protective strategies.

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Microarray proﬁle analysis of toxic cocaine‐induced alterations in the expression of mouse brain gene sequences: a possible ‘protective’ effect of buprenorphine

Cited by 9 publications

References 29 publications

Microarray Studies of Psychostimulant-Induced Changes in Gene Expression

Microarray Studies of Psychostimulant-Induced Changes in Gene Expression

Functional genomic mechanisms of opioid action and opioid use disorder: a systematic review of animal models and human studies

Neuroprotective strategies in drug abuse‐evoked encephalopathy

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