Psychostimulant use disorder emphasizing methamphetamine and the opioid -dopamine connection: Digging out of a hypodopaminergic ditch.

BACKGROUND: Approved food and drug administration (FDA) medications to treat Psychostimulant Use Disorder (PUD) are needed. Both acute and chronic neurological deficits related to the neurophysiological effects of these powerfully addictive drugs can cause stroke and alterations in mood and cognition.
OBJECTIVE: This article presents a brief review of the psychiatric and neurobiological sequelae of methamphetamine use disorder, some known neurogenetic associations impacted by psychostimulants, and explores treatment modalities and outcomes. HYPOTHESIS: The authors propose that gentle D2 receptor stimulation accomplished via some treatment modalities can induce dopamine release, causing alteration of D2-directed mRNA and thus enhanced function of D2 receptors in the human. This proliferation of D2 receptors, in turn, will induce the attenuation of craving behavior, especially in genetically compromised high-risk populations. DISCUSSION: A better understanding of the involvement of molecular neurogenetic opioid, mesolimbic dopamine, and psychostimulant connections in "wanting" supports this hypothesis. While both scientific and, clinical professionals search for an FDA approved treatment for PUD the induction of dopamine homeostasis, via activation of the brain reward circuitry, offers treatment for underlying neurotransmitter functional deficits, potential prophylaxis, and support for recovery efforts.
CONCLUSION: Dopamine regulation may help people dig out of their hypodopaminergia ditch.