About

Glen R. Hanson, DDS, PhD, is a faculty member at the Spencer Fox Eccles School of Medicine. His educational background includes an undergraduate degree from Brigham Young University, a DDS from the University of California at Los Angeles, a PhD from the University of Utah, and postdoctoral training at the National Institutes of Health (National Heart, Lung and Blood Institute). His research focuses on neuropharmacology, particularly the regulation of dopamine and vesicular monoamine transporters, with implications for disease and pharmacological targets. Hanson has contributed to understanding the neurochemical effects of substances such as methamphetamine and nicotine, including their impact on dopaminergic systems and neurotoxicity. His work involves the study of neuropeptides, metal complexes, and receptor ligands, advancing knowledge in neurochemical mechanisms related to substance abuse and neurotoxicity.

Research topics

• Internal medicine
• Chemistry
• Medicine
• Biochemistry
• Pharmacology
• Biology
• Endocrinology

Selected publications

• Differential Effects of Neurotensin NTS1 and NTS2 Receptors on Locomotion

  Brain and Behavior · 2025-11-01

  articleOpen accessSenior author

  INTRODUCTION: Neurotensin (NT) is an endogenous neuropeptide with diverse central and peripheral effects, particularly as related to modulation of central nervous system dopaminergic activity. For example, interactions between dopamine and NT have been associated with the motivation to use, and the motor consequences of drugs abuse, including nicotine. However, the relative contribution of the two subtypes of cell surface G-protein coupled NT receptors (NTS1 and NTS2) to dopamine-related drug-induced effects is unclear. METHODS: We investigated the locomotor behavior and exploratory drive of C57BL/6J mice deficient in either NTS1 (NTS1 -/-) or NTS2 (NTS2 -/-) compared to wild-type C57BL/6J (WT +/+) mice in an open-field. In addition, the effect of nicotine on locomotion and intra-session habituation to a novel open field was compared in each of these genetic strains. RESULTS: When compared to WT (+/+) mice, the results demonstrated less intra-session habituation across time (i.e., less accommodation (as assessed by distanced travelled, horizontal activity, and vertical activity) in mice deficient in the NTS1 receptor. In contrast, mice deficient in the NTS2 receptor accommodated more rapidly. Nicotine injection reduced all three parameters of locomotor activity in WT (+/+) and NTS1 (-/-) mice. In contrast to effects in both WT (+/+) and NTS1 (-/-) mice, NIC exposure had a negligible effect on TD in the NTS2 (-/-) mice. CONCLUSION: These results suggest opposing effects of the NTS1 and NTS2 receptor subtypes in modulating natural and nicotine-induced dopaminergic transmission and consequent locomotor behavior.

  PublisherOA PDFDOI

• Methcathinone decreases dopamine transporter function: Role of protein kinase C

  Journal of Neurochemistry · 2021 · 2 citations

  • Chemistry
  • Internal medicine
  • Endocrinology

  Abstract Methcathinone (MCAT) is a psychostimulant of abuse that can cause both persistent striatal dopaminergic and serotonergic, as well as hippocampal serotonergic, deficits. Evidence suggests that the rapid effects of stimulants that are structurally and mechanistically similar to MCAT on monoamine transporter function may contribute to the abuse liability and/or persistent monoaminergic deficits caused by these agents. Thus, effects of MCAT on 1) striatal dopamine (DA) transporter (DAT); and 2) striatal and hippocampal serotonin transporter (SERT) function, as determined in tissues from adult male rats, were assessed. As reported previously, a single administration of MCAT rapidly (within 1 hr) decreases striatal [ 3 H]DA uptake. Similarly, incubation of rat synaptosomes with MCAT at 37℃ (but not 4˚C) decreased striatal [ 3 H]DA uptake. Incubation with MCAT likewise decreased [ 3 H]5HT but not vesicular [ 3 H]DA uptake. MCAT incubation in vitro was without effect on [ 3 H]DA uptake in striatal synaptosomes prepared from MCAT‐treated rats. The decrease in [ 3 H]DA uptake caused by MCAT incubation: (a) reflected a decrease in V max , with minimal change in K m , and (b) was attenuated by co‐incubation with the cell‐permeable calcium chelator, N , N '‐[1,2‐ethanediylbis(oxy‐2,1‐phenylene)]bis[ N ‐[2‐[(acetyloxy)methoxy]‐2‐oxoethyl]‐1,1'‐bis[(acetyloxy)methyl] ester‐glycine (BAPTA‐AM), as well as the non‐selective protein kinase‐C (PKC) inhibitors bisindolylmaleimide‐1 (BIM‐1) and 2‐[1‐3(Aminopropyl)indol‐3‐yl]‐3(1‐methyl‐1H‐indol‐3‐yl)maleimide (or Bisindolylmaleimide VIII; Ro‐31‐7549). Taken together, these results suggest that in vitro MCAT incubation may model important aspects of MCAT administration in vivo, and that calcium and PKC contribute to the in vitro effects of MCAT on DAT. image

  PublisherDOI

• 3,4-Methylenedioxypyrovalerone: Neuropharmacological Impact of a Designer Stimulant of Abuse on Monoamine Transporters

  Journal of Pharmacology and Experimental Therapeutics · 2020 · 6 citations

  • Pharmacology
  • Chemistry
  • Medicine
  PublisherOA PDFDOI

• Methcathinone Rapidly Decreases Dopamine Transporter Function: Role of Calcium and Protein Kinase C

  The FASEB Journal · 2020

  • Chemistry
  • Pharmacology
  • Internal medicine

  Methcathinone (MCAT) is a synthetic cathinone that causes both persistent striatal dopaminergic as well as striatal and hippocampal serotonergic deficits. It has been demonstrated that the rapid effects of similar stimulants on dopamine (DA) transporter (DAT) function contribute to persistent monoaminergic deficits. Thus, the effect of MCAT on DAT was assessed. Results revealed that MCAT self‐administration (SA) decreased striatal [ 3 H]DA uptake, as assessed ex vivo in synaptosomes prepared from male rats 1 h after the final MCAT SA session. In vitro co‐incubation of synaptosomes with MCAT (1, 10, 100 μM) at 37°C likewise decreased striatal [ 3 H]DA uptake. There was no effect of in vitro co‐incubation with MCAT at 4°C, suggesting that decreases in [ 3 H]DA uptake are not due to residual drug. These effects were not limited to DAT as MCAT SA decreased hippocampal [ 3 H]serotonin uptake. Further, in vitro co‐incubation of synaptosomes with MCAT decreased both striatal and hippocampal [ 3 H]serotonin uptake. The in vitro effect on DAT function was attenuated by co‐incubation with the cell‐permeable calcium chelator, 1,2‐bis (2‐aminophenoxy) ethane‐N, N, N, N‐tetraacetic acid acetoxymethyl ester (BAPTA‐AM), as well as with the structurally related non‐specific protein kinase C (PKC) inhibitors bisindolylmaleimide I and Ro‐31‐7549. In contrast, this in vitro decrease in DAT function was not attenuated by co‐incubation with other non‐specific PKC inhibitors (NPC‐15437 and Go6976), nor with the PKC‐β inhibitor ruboxistaurin. Neither co‐incubation with the Ca 2+ /calmodulin‐dependent protein kinase II inhibitor, KN‐93, nor the glycogen synthase kinase 3β inhibitor, SB‐216763, attenuated the MCAT‐induced decrease in [ 3 H]DA uptake. Taken together, these results suggest that MCAT self‐administration and in vitro MCAT exposure have comparable effects to investigator administered MCAT on DAT and SERT function in the striatum and hippocampus; further, in vitro data suggest that the MCAT‐induced effect on DAT is dependent upon calcium and some, but not all, PKC isoforms. Support or Funding Information R01‐DA039145

  PublisherDOI

• Comprehensive oral care improves treatment outcomes in male and female patients with high-severity and chronic substance use disorders

  The Journal of the American Dental Association · 2019-05-20 · 16 citations

  articleOpen access1st authorCorresponding
  PublisherOA PDFDOI

• Methylenedioxypryovalerone (MDPV) Rapidly Increases Dopamine Transporter and Vesicular Monoamine Transporter‐2 Function

  The FASEB Journal · 2018-04-01

  article

  Methylenedioxypyrovalerone (MDPV) is a synthetic cathinone designer drug primarily abused for its psychostimulant properties. Rapid dysregulation of central monoamine neurotransmitter transport into presynaptic terminals and synaptic vesicles are principal mechanisms of psychostimulant action, and contribute to the development of persistent monoaminergic deficits. Still, the impact of in vivo MDPV administration on the function of central monoamine transporters is not fully elucidated. Consequently, this study examined the response of the striatal dopamine transporter (DAT) and vesicular monoamine transporter‐2 (VMAT2) to a single MDPV exposure in adult male rats. A single in vivo MDPV administration rapidly (within 1 h) and reversibly (effect diminishes after 6 h) increased both DAT and VMAT2 function when assessed ex vivo in striatal synaptosomes and non‐membrane‐associated (presumably cytoplasmic) synaptic vesicles, respectively. MDPV treatment did not increase VMAT2 immunoreactivity within the cytoplasmic synaptic vesicle fraction, suggesting increased VMAT2 activity is unlikely due to intracellular trafficking increasing the number of available cytoplasmic VMAT2‐associated synaptic vesicles. In contrast to other psychostimulants, most notably methamphetamine and methylphenidate, MDPV acutely increases both DAT and VMAT2 function, and increased VMAT2 function is likely independent of vesicular trafficking‐mediated mechanisms. Together, these data suggest that MDPV has a unique and undescribed mechanism of action on striatal dopaminergic neurons. Support or Funding Information This work was supported by National Institutes of Health grants DA039145 and DA031883. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

  PublisherDOI

• Increased risk of diseases of the basal ganglia and cerebellum in patients with a history of attention-deficit/hyperactivity disorder

  Neuropsychopharmacology · 2018-09-11 · 64 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Lack of Evidence for Methylenedioxypyrovalerone (MDPV)‐Induced Persistent Dopaminergic or Serotonergic Deficits: Comparison with Methamphetamine and Mephedrone

  The FASEB Journal · 2018-04-01

  article

  β‐Ketoamphetamines such as methylenedioxypyrovalerone (MDPV) and mephedrone (MEPH) are synthetic cathinones with a structural similarity to methamphetamine (METH) that may account for some similarities in behavioral effects. However, the persistent effects of repeated high‐dose MDPV exposures on striatal dopaminergic and hippocampal serotonergic systems remain to be fully elucidated. Accordingly, the persistent effects of repeated high‐dose MPDV administrations were investigated. Results revealed that MDPV treatment did not alter striatal dopaminergic or hippocampal serotonergic systems as assessed 7 days later in synaptosomes prepared from treated rats. Further, MDPV did not alter hippocampal serotonin or 5‐hydroxyindoleacetic acid content at this time point. These data stand in contrast to our previous report that repeated high‐dose MEPH administrations cause persistent hippocampal serotonergic deficits. These data also stand in contrast to effects of repeated high‐dose METH administrations that include persistent striatal dopaminergic and hippocampal serotonergic deficits. Noteworthy, in these studies MDPV did not induce hyperthermia to the degree reported in previous studies of MEPH and METH. Further, the impact of MDPV on the dopamine transporter and vesicular monoamine transporter‐2 appears distinct from that of MEPH and METH. Taken together, these latter findings may contribute to the differential impact of MDPV, MEPH, and METH on dopaminergic and serotonergic systems. Support or Funding Information DA039145 and DA031883 This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

  PublisherDOI

• ML314: A Biased Neurotensin Receptor Ligand for Methamphetamine Abuse

  ACS Chemical Biology · 2016-04-27 · 44 citations

  article

  Pharmacological treatment for methamphetamine addiction will provide important societal benefits. Neurotensin receptor NTR1 and dopamine receptor distributions coincide in brain areas regulating methamphetamine-associated reward, and neurotensin peptides produce behaviors opposing psychostimulants. Therefore, undesirable methamphetamine-associated activities should be treatable with druggable NTR1 agonists, but no such FDA-approved therapeutics exist. We address this limitation with proof-of-concept data for ML314, a small-molecule, brain penetrant, β-arrestin biased, NTR1 agonist. ML314 attenuates amphetamine-like hyperlocomotion in dopamine transporter knockout mice, and in C57BL/6J mice it attenuates methamphetamine-induced hyperlocomotion, potentiates the psychostimulant inhibitory effects of a ghrelin antagonist, and reduces methamphetamine-associated conditioned place preference. In rats, ML314 blocks methamphetamine self-administration. ML314 acts as an allosteric enhancer of endogenous neurotensin, unmasking stoichiometric numbers of hidden NTR1 binding sites in transfected-cell membranes or mouse striatal membranes, while additionally supporting NTR1 endocytosis in cells in the absence of NT peptide. These results indicate ML314 is a viable, preclinical lead for methamphetamine abuse treatment and support an allosteric model of G protein-coupled receptor signaling.

  PublisherDOI

• Prior nicotine self-administration attenuates subsequent dopaminergic deficits of methamphetamine in rats: role of nicotinic acetylcholine receptors

  Behavioural Pharmacology · 2016-02-12 · 4 citations

  article

  Preclinical studies have demonstrated that oral nicotine exposure attenuates long-term dopaminergic damage induced by toxins, including repeated, high doses of methamphetamine. It is suggested that alterations in nicotinic acetylcholine receptor (nAChR) expression, including α4β2* and α6β2* subtypes, likely contribute to this protection. The current study extended these findings by investigating whether nicotine self-administration in male, Sprague-Dawley rats (a) attenuates short-term dopaminergic damage induced by methamphetamine and (b) causes alterations in levels of α4β2* and α6β2* nAChR subtypes. The findings indicate that nicotine self-administration (0.032 mg/kg/infusion for 14 days) per se did not alter α4β2* and α6β2* nAChR expression or dopamine transporter (DAT) expression and function. Interestingly, prior nicotine self-administration attenuated methamphetamine-induced decreases in DAT function when assessed 24 h, but not 1 h, after methamphetamine treatment (4×7.5 mg/kg/injection). The ability of nicotine to attenuate the effects of methamphetamine on DAT function corresponded with increases in α4β2*, but not α6β2*, nAChR binding density. Understanding the role of nAChRs in methamphetamine-induced damage has the potential to elucidate mechanisms underlying the etiology of disorders involving dopaminergic dysfunction, as well as to highlight potential new therapeutic strategies for prevention or reduction of dopaminergic neurodegeneration.

  PublisherDOI

Recent grants

• NIH Grant R01DA009407

  NIH · $3.1M · 2010

• NIH Grant K05DA000378

  NIH · $389k · 2013

• NIH Grant R01DA004222

  NIH · $3.9M · 2013

• NIH Grant R01DA000869

  NIH · $5.4M · 2013

• Role of Neurotensin Systems in Methamphetamine Self Administration

  NIH · $1.5M · 2012–2019

Frequent coauthors

• James W. Gibb

  131 shared

• Annette E. Fleckenstein

  University of Utah

  117 shared

• Lloyd G. Bush

  University of Utah

  40 shared

• Michel Johnson

  University of Utah

  36 shared

• Diana G. Wilkins

  University of Utah

  29 shared

• Mario E. Alburges

  University of Utah

  26 shared

• Lisa M. McFadden

  University of South Dakota

  22 shared

• Evan L. Riddle

  Biogen (United States)

  21 shared

Education

• B.S.

  Brigham Young University

• Other

  University of California at Los Angeles

• Ph.D.

  University of Utah

• Other

  National Institutes of Health (National Heart, Lung and Blood Institute)