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Novel Targets for Treating Methamphetamine Use Disorder
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Novel Targets for Treating Methamphetamine Use Disorder

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 6013

Special Issue Editor

Prof. Dr. Karen Szumlinski

E-Mail Website
Guest Editor
Department of Psychological and Brain Sciences, University of California Santa Barbara, Santa Barbara, CA, USA
Interests: behavioral neuroscience; addiction; alcoholism; stimulants; opioids; animal models; anxiety; psychosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Methamphetamine use disorder is a serious neuropsychiatric condition, characterized by intense drug-craving, compulsive drug-seeking and taking, and pronounced cognitive impairment.  In the wake of the opioid crisis and COVD-19 pandemic, methamphetamine-related deaths have risen to epidemic levels. This rise in methamphetamine-related deaths is concerning as currently, there exists no approved pharmacotherapy for treating methamphetamine use disorder and the available cognitive/behavioral therapies have proven relatively ineffective at reducing drug use and preventing relapse to the addicted state. Methamphetamine is well-characterized to impact monoaminergic neurotransmission in the brain and to do so via effects on plasmalemmal and vesicular transporters, as well as interactions with the TAAR1 receptor. In addition to affecting monoamine neurotransmission, methamphetamine is also reported to exert both short- and long-lasting effects upon several other neurotransmitters systems, as well as to perturb neuroimmune function.  This Special Topic will examine the neuropsychopharmacology of methamphetamine use disorder and focus on the latest developments from basic science, preclinical and clinical research regarding its pharmacotherapy. The discovery of a broad range of druggable targets to ameliorate the different symptoms of methamphetamine use disorder will inform biomedical strategies for predicting disease susceptibility, early and late intervention in the disease process, and promoting recovery.

Prof. Dr. Karen Szumlinski
Guest Editor

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Keywords

  • methamphetamine use disorder
  • pharmacotherapy
  • addiction
  • relapse
  • vulnerability
  • drug self-administration
  • craving

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Published Papers (2 papers)

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Research

28 pages, 9204 KiB  
Article
Alterations of Mitochondrial Structure in Methamphetamine Toxicity
by Paola Lenzi, Francesca Biagioni, Carla L. Busceti, Gloria Lazzeri, Maico Polzella, Alessandro Frati, Michela Ferrucci and Francesco Fornai
Int. J. Mol. Sci. 2022, 23(16), 8926; https://doi.org/10.3390/ijms23168926 - 10 Aug 2022
Cited by 13 | Viewed by 2896
Abstract
Recent evidence shows that methamphetamine (METH) produces mitochondrial alterations that contribute to neurotoxicity. Nonetheless, most of these studies focus on mitochondrial activity, whereas mitochondrial morphology remains poorly investigated. In fact, morphological evidence about the fine structure of mitochondria during METH toxicity is not [...] Read more.
Recent evidence shows that methamphetamine (METH) produces mitochondrial alterations that contribute to neurotoxicity. Nonetheless, most of these studies focus on mitochondrial activity, whereas mitochondrial morphology remains poorly investigated. In fact, morphological evidence about the fine structure of mitochondria during METH toxicity is not available. Thus, in the present study we analyzed dose-dependent mitochondrial structural alterations during METH exposure. Light and transmission electron microscopy were used, along with ultrastructural stoichiometry of catecholamine cells following various doses of METH. In the first part of the study cell death and cell degeneration were assessed and they were correlated with mitochondrial alterations observed using light microscopy. In the second part of the study, ultrastructural evidence of specific mitochondrial alterations of crests, inner and outer membranes and matrix were quantified, along with in situ alterations of mitochondrial proteins. Neurodegeneration induced by METH correlates significantly with specific mitochondrial damage, which allows definition of a scoring system for mitochondrial integrity. In turn, mitochondrial alterations are concomitant with a decrease in fission/mitophagy protein Fis1 and DRP1 and an increase in Pink1 and Parkin in situ, at the mitochondrial level. These findings provide structural evidence that mitochondria represent both direct and indirect targets of METH-induced toxicity. Full article
(This article belongs to the Special Issue Novel Targets for Treating Methamphetamine Use Disorder)
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20 pages, 4164 KiB  
Article
Selective Inhibition of PDE4B Reduces Methamphetamine Reinforcement in Two C57BL/6 Substrains
by Kevin M. Honeywell, Eliyana Van Doren and Karen K. Szumlinski
Int. J. Mol. Sci. 2022, 23(9), 4872; https://doi.org/10.3390/ijms23094872 - 28 Apr 2022
Cited by 7 | Viewed by 2483
Abstract
Methamphetamine (MA) is a highly addictive psychostimulant drug, and the number of MA-related overdose deaths has reached epidemic proportions. Repeated MA exposure induces a robust and persistent neuroinflammatory response, and the evidence supports the potential utility of targeting neuroimmune function using non-selective phosphodiesterase [...] Read more.
Methamphetamine (MA) is a highly addictive psychostimulant drug, and the number of MA-related overdose deaths has reached epidemic proportions. Repeated MA exposure induces a robust and persistent neuroinflammatory response, and the evidence supports the potential utility of targeting neuroimmune function using non-selective phosphodiesterase 4 (PDE4) inhibitors as a therapeutic strategy for attenuating addiction-related behavior. Off-target, emetic effects associated with non-selective PDE4 blockade led to the development of isozyme-selective inhibitors, of which the PDE4B-selective inhibitor A33 was demonstrated recently to reduce binge drinking in two genetically related C57BL/6 (B6) substrains (C57BL/6NJ (B6NJ) and C57BL/6J (B6J)) that differ in their innate neuroimmune response. Herein, we determined the efficacy of A33 for reducing MA self-administration and MA-seeking behavior in these two B6 substrains. Female and male mice of both substrains were first trained to nose poke for a 100 mg/L MA solution followed by a characterization of the dose–response function for oral MA reinforcement (20 mg/L–3.2 g/L), the demand-response function for 400 mg/L MA, and cue-elicited MA seeking following a period of forced abstinence. During this substrain comparison of MA self-administration, we also determined the dose–response function for A33 pretreatment (0–1 mg/kg) on the maintenance of MA self-administration and cue-elicited MA seeking. Relative to B6NJ mice, B6J mice earned fewer reinforcers, consumed less MA, and took longer to reach acquisition criterion with males of both substrains exhibiting some signs of lower MA reinforcement than their female counterparts during the acquisition phase of the study. A33 pretreatment reduced MA reinforcement at all doses tested. These findings provide the first evidence that pretreatment with a selective PDE4B inhibitor effectively reduces MA self-administration in both male and female mice of two genetically distinct substrains but does not impact cue-elicited MA seeking following abstinence. If relevant to humans, these results posit the potential clinical utility of A33 or other selective PDE4B inhibitors for curbing active drug-taking in MA use disorder. Full article
(This article belongs to the Special Issue Novel Targets for Treating Methamphetamine Use Disorder)
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