The mu-opioid receptors (MOR, OPRM1) mediate the effects of beta-endorphin and modulate many biological functions including reward processing and addiction.
This study provides preliminary evidence that DRD2 dopamine receptor gene SNPs are associated with indoor tanning addiction and young women with variant genotypes and elevated depressive symptoms may be at higher risk.
These findings suggest that combining strong NET and weak DAT inhibition could lead to the development of a highly effective cognitive enhancer that lacks the potential for addiction.
Mu opioid receptor (MOR) is involved in various brain functions, such as pain modulation, reward processing, and addictive behaviors, and mediates the main pharmacologic effects of morphine and other opioid compounds.
Moreover, using multinomial regression analysis, the homozygous 7/7 and 2/2 VNTR genotypes of DRD4 gene were nominally significantly associated with a lower risk of addiction (OR = 0.285 with P = 0.003 and OR = 0.447 with P = 0.031, respectively) after adjusting for other covariates.
Continuation of EGFR TKI beyond progressive disease is confined to patients in asymptomatic stage when the EGFRaddiction is still preserved in some subclones.
The dynorphin (DYN)/kappa opioid receptor (KOR) system plays an important role in the development of addiction, and dysregulation of this system could lead to abnormal activity in the reward pathway.
Sequentially, we looked into the detail of (1) the addiction to cocaine and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug-drug interaction of cocaine and fentanyl via p-glycoprotein (P-gp) efflux, (3) the metabolism of cocaine and fentanyl in CYP3A4, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug-drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
The conceptual framework of this review is to focus on hormonal, chromosomal, and epigenetic organizational and contingent, sex-dependent mechanisms of four neural systems that are known-primarily in males-to be key players in addiction: dopamine, mu-opioid receptors (MOR), kappa opioid receptors (KOR), and brain-derived neurotrophic factor (BDNF).
Sequentially, we looked into the detail of (1) the addiction to cocaine and fentanyl by binding to the dopamine transporter and the μ opioid receptor (DAT and μOR, respectively), (2) the potential drug-drug interaction of cocaine and fentanyl via p-glycoprotein (P-gp) efflux, (3) the metabolism of cocaine and fentanyl in CYP3A4, and (4) the physiologically based pharmacokinetic (PBPK) model for two drugs and their drug-drug interaction at the absorption, distribution, metabolism, and excretion (ADME) level.
The findings regarding an association with alcohol craving and tobacco consumption point towards a crucial role of DRD2-gene methylation in the neurobiology of addictive behavior.
Kappa opioid receptor (KOR) agonists show promise in ameliorating disorders, such as addiction and chronic pain, but are limited by dysphoric and aversive side effects.
As evidence indicates that brain-derived neurotrophic factor (BDNF) is associated with METH addiction, the present study aimed to investigate whether BDNF and the proteins regulating the BDNF signaling pathway might be implicated in the cognitive impairment of the METH abusers during early withdrawal.
Opioid activation of the mu opioid receptor (MOR) promotes signaling cascades that evoke both analgesic responses to pain and side effects like addiction and dependence.
A single, albeit aversive treatment that is able to reduce relapse long-term warrants further consideration of the therapeutic potential of KOR agonists in the treatment of addiction.
The class B corticotropin-releasing hormone type 1 receptor (CRHR1) is a key player in the stress response whose dysregulation is critically involved in stress-related disorders: psychiatric conditions (i.e. depression, anxiety, and addictions), neuroendocrinological alterations, and neurodegenerative diseases.