About

Jay Baraban MD, PhD is a Professor of Neuroscience at The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine. He is involved in both undergraduate and graduate education in neuroscience at Hopkins. For undergraduate neuroscience majors, he co-directs the Diseases and Disorders of the Nervous System elective with Dr. Dani Smith, where leading experts present overviews of major neurological or psychiatric diseases along with the latest developments in their fields. He also teaches a seminar course titled Great Discoveries in Neuroscience, covering key breakthroughs from classical insights such as the neuron doctrine and chemical neurotransmission to modern topics like endocannabinoids, leptin, and prions. Additionally, he supervises the Neuroscience BS/MS program, enabling highly qualified neuroscience majors to conduct intensive research for a full year. For graduate students, he delivers several lectures in the NeuroCog sequence, and for first-year medical students, he runs neuroanatomy lab sections and provides introductory lectures on neurotransmitters and synaptic plasticity.

Research topics

• Neuroscience
• Genetics
• Psychology
• Biology

Selected publications

• Translin deletion impairs cocaine-induced locomotor sensitization and RGS8 expression in the nucleus accumbens

  Acta Pharmacologica Sinica · 2025-05-12 · 2 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Genetic inactivation of the Translin/Trax RNase activity alters small RNAs including miRNAs, disrupts gene expression and impairs distinct forms of hippocampal synaptic plasticity and memory

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-11 · 2 citations

  preprintOpen access

  Neurons utilize RNA interference in the reversible translational repression of synaptically localized mRNAs, enabling rapid translation in response to synaptic activity. Two evolutionarily conserved proteins, Translin and Trax, form an RNase complex which processes miRNAs, tRNAs and siRNAs. To determine the specific role of the RNase activity of this complex in brain function, we employed a mouse line harboring a point mutation in Trax (E126A) that renders the Translin/Trax RNase inactive. At the molecular level, we found alterations in the levels of multiple small RNAs including miRNAs, tsRNAs and substantial downregulation of gene expression at the mRNA level in the hippocampus of TraxE126A mice. At the synaptic level, TraxE126A mice exhibit deficits in specific forms of long-term hippocampal synaptic plasticity. At the behavioral level, TraxE126A mice display impaired long-term spatial memory and altered openfield and acoustic-startle behavior. These studies reveal the functional role of Translin/Trax RNase in the mammalian brain.

  PublisherOA PDFDOI

• Ventral tegmental area astrocytes modulate cocaine reward by tonically releasing GABA

  Neuron · 2023 · 63 citations

  • Neuroscience
  • Psychology
  PublisherOA PDFDOI

• Adenosine A _2A Receptor Regulates microRNA‐181b Expression in Aorta: Therapeutic Implications for Large‐Artery Stiffness

  Journal of the American Heart Association · 2023-07-08 · 2 citations

  articleOpen access

  Background The identification of large‐artery stiffness as a major, independent risk factor for cardiovascular disease–associated morbidity and death has focused attention on identifying therapeutic strategies to combat this disorder. Genetic manipulations that delete or inactivate the translin/trax microRNA‐degrading enzyme confer protection against aortic stiffness induced by chronic ingestion of high‐salt water (4%NaCl in drinking water for 3 weeks) or associated with aging. Therefore, there is heightened interest in identifying interventions capable of inhibiting translin/trax RNase activity, as these may have therapeutic efficacy in large‐artery stiffness. Methods and Results Activation of neuronal adenosine A 2A receptors (A 2A Rs) triggers dissociation of trax from its C‐terminus. As A 2A Rs are expressed by vascular smooth muscle cells (VSMCs), we investigated whether stimulation of A 2A R on vascular smooth muscle cells promotes the association of translin with trax and, thereby increases translin/trax complex activity. We found that treatment of A7r5 cells with the A 2A R agonist CGS21680 leads to increased association of trax with translin. Furthermore, this treatment decreases levels of pre‐microRNA‐181b, a target of translin/trax, and those of its downstream product, mature microRNA‐181b. To check whether A 2A R activation might contribute to high‐salt water–induced aortic stiffening, we assessed the impact of daily treatment with the selective A 2A R antagonist SCH58261 in this paradigm. We found that this treatment blocked aortic stiffening induced by high‐salt water. Further, we confirmed that the age‐associated decline in aortic pre‐microRNA‐181b/microRNA‐181b levels observed in mice also occurs in humans. Conclusions These findings suggest that further studies are warranted to evaluate whether blockade of A 2A Rs may have therapeutic potential in treating large‐artery stiffness.

  PublisherOA PDFDOI

• Deficient mitochondrial respiration in astrocytes impairs trace fear conditioning and increases naloxone‐precipitated aversion in morphine‐dependent mice

  Glia · 2022-03-11 · 7 citations

  articleOpen access

  Mitochondria are abundant in the fine processes of astrocytes, however, potential roles for astrocyte mitochondria remain poorly understood. In the present study, we performed a systematic examination of the effects of abnormal oxidative phosphorylation in astrocytes on several mouse behaviors. Impaired astrocyte oxidative phosphorylation was produced by astrocyte-specific deletion of the nuclear mitochondrial gene, Cox10, that encodes an accessory protein of complex IV, the protoheme:heme-O-farnesyl transferase. As expected, conditional deletion of the Cox10 gene in mice (cKO mice) significantly reduced expression of COX10 and Cytochrome c oxidase subunit I (MTCO1) of Complex IV, resulting in decreased oxidative phosphorylation without significantly affecting glycolysis. No effects of the deletion were observed on locomotor activity, anxiety-like behavior, nociception, or spontaneous alternation. Cox10 cKO female mice exhibited mildly impaired novel object recognition, while Cox10 cKO male mice were moderately deficient in trace fear conditioning. No group-related changes were observed in conditional place preference (CPP) that assessed effects of morphine on reward. In contrast to CPP, Cox10 cKO mice demonstrated significantly increased aversive behaviors produced by naloxone-precipitated withdrawal following chronic exposure to morphine, that is, jumping and avoidance behavior as assessed by conditional place aversion (CPA). Our study suggests that astrocyte oxidative phosphorylation may contribute to behaviors associated with greater cognitive load and/or aversive and stressful conditions.

  PublisherOA PDFDOI

• Deciphering the Role of microRNAs in Large-Artery Stiffness Associated With Aging: Focus on miR-181b

  Frontiers in Physiology · 2021-09-27 · 2 citations

  reviewOpen access1st author

  Large artery stiffness (LAS) is a major, independent risk factor underlying cardiovascular disease that increases with aging. The emergence of microRNA signaling as a key regulator of vascular structure and function has stimulated interest in assessing its role in the pathophysiology of LAS. Identification of several microRNAs that display age-associated changes in expression in aorta has focused attention on defining their molecular targets and deciphering their role in age-associated arterial stiffening. Inactivation of the microRNA-degrading enzyme, translin/trax, which reverses the age-dependent decline in miR-181b, confers protection from aging-associated arterial stiffening, suggesting that inhibitors targeting this enzyme may have translational potential. As LAS poses a major public health challenge, we anticipate that future studies based on these advances will yield innovative strategies to combat aging-associated arterial stiffening.

  PublisherOA PDFDOI

• Elevated body fat increases amphetamine accumulation in brain: evidence from genetic and diet-induced forms of adiposity

  Translational Psychiatry · 2021-08-14 · 4 citations

  articleOpen accessSenior author

  Despite the high prevalence of obesity, little is known about its potential impact on the pharmacokinetics of psychotropic drugs. In the course of investigating the role of the microRNA system on neuronal signaling, we found that mice lacking the translin/trax microRNA-degrading enzyme display an exaggerated locomotor response to amphetamine. As these mice display robust adiposity in the context of normal body weight, we checked whether this phenotype might reflect elevated brain levels of amphetamine. To assess this hypothesis, we compared plasma and brain amphetamine levels of wild type and Tsn KO mice. Furthermore, we checked the effect of diet-induced increases in adiposity on plasma and brain amphetamine levels in wild type mice. Brain amphetamine levels were higher in Tsn KO mice than in wild type littermates and correlated with adiposity. Analysis of the effect of diet-induced increases in adiposity in wild type mice on brain amphetamine levels also demonstrated that brain amphetamine levels correlate with adiposity. Increased adiposity displayed by Tsn KO mice or by wild type mice fed a high-fat diet correlates with elevated brain amphetamine levels. As amphetamine and its analogues are widely used to treat attention deficit disorder, which is associated with obesity, further studies are warranted to assess the impact of adiposity on amphetamine levels in these patients.

  PublisherOA PDFDOI

• Degradation of Premature-miR-181b by the Translin/Trax RNase Increases Vascular Smooth Muscle Cell Stiffness

  Hypertension · 2021-09-01 · 8 citations

  articleOpen access

  Large artery stiffness is a major risk factor underlying cardiovascular disease. However, the molecular mechanisms driving this pathological process are poorly understood. Previous studies indicate that the age-associated decline of miR-181b levels can accelerate aortic stiffening by activating TGF-β (transforming growth factor β) signaling. Here, we studied the physiological role of miR-181b in mediating arginine vasopressin (AVP)-induced stiffening of vascular smooth muscle cells (VSMCs) isolated from aorta. We found that AVP treatment increases VSMC stiffness and causes marked reductions in both pre-miR-181b and miR-181b expression. Transfecting VSMCs with a miR-181b mimic abolishes AVP-induced stiffening, indicating that this stiffening response is dependent on AVP’s ability to reduce miR-181b levels. In addition, deletion of translin or inactivation of the TN/TX (translin/trax) RNAse prevents the AVP-induced decrease in pre-miR-181b/miR-181b levels and VSMC stiffening, indicating that these effects are mediated by this microRNA-degrading enzyme. Interestingly, AVP exposure increases extracellular TGF-β levels in a TN/TX-dependent manner and pretreatment of VSMCs with TGF-β neutralizing antibodies inhibits AVP-induced stiffness. Lastly, we have ascertained that age-associated aortic stiffening in vivo is prevented in mice homozygous for the TX (E126A) point mutation, which abolishes TN/TX RNase activity. Taken together, these findings provide compelling evidence that TN/TX RNase activity plays a critical role in regulating VSMC stiffness via degradation of pre-miR-181b and TGF-β pathway activation. Our findings also indicate that therapeutic strategies capable of blocking TN/TX-mediated reductions in miR-181b levels may confer protection against large artery stiffness and associated cardiovascular diseases.

  PublisherDOI

• Correction to: Selective role of the translin/trax RNase complex in hippocampal synaptic plasticity

  Molecular Brain · 2021-03-05

  articleOpen access

  An amendment to this paper has been published and can be accessed via the original article.

  PublisherOA PDFDOI

• Genetic inactivation of the translin/trax microRNA-degrading enzyme phenocopies the robust adiposity induced by Translin (Tsn) deletion

  Molecular Metabolism · 2020-05-11 · 11 citations

  articleOpen accessSenior authorCorresponding

  Deletion of Translin (Tsn) from mice induces an unusual metabolic profile characterized by robust adiposity, normal body weight and glucose tolerance. Translin (TN) protein and its partner, trax (TX), form the TN/TX microRNA-degrading enzyme. Since the microRNA system plays a prominent role in regulating metabolism, we reasoned that the metabolic profile displayed by Tsn KO mice might reflect dysregulation of microRNA signaling. To test this hypothesis, we inserted a mutation, E126A, in Tsnax, the gene encoding TX, that abolishes the microRNA-degrading enzymatic activity of the TN/TX complex. In addition, to help define the cell types that drive the adiposity phenotype, we have also generated mice with floxed alleles of Tsn or Tsnax. Introduction of the E126A mutation in Tsnax does not impair expression of TN or TX proteins or their co-precipitation. Furthermore, these mice display selective increases in microRNAs that match those induced by Tsn deletion, confirming that this mutation in Tsnax inactivates the microRNA-degrading activity of the TN/TX complex. Mice homozygous for the Tsnax (E126A) mutation display a metabolic profile that closely mimics that of Tsn KO mice. Selective deletion of Tsn or Tsnax from either adipocytes or hepatocytes, two candidate cell types, does not phenocopy the elevated adiposity displayed by mice with constitutive Tsn deletion or the Tsnax (E126A) mutation. Furthermore, global, conditional deletion of Tsn in adulthood does not elicit increased adiposity. Taken together, these findings indicate that inactivation of the TN/TX microRNA-degrading enzyme during development is necessary to drive the robust adiposity displayed by Tsn KO mice.

  PublisherDOI

Recent grants

• NIH Grant K02DA000358

  NIH · $575k · 2003

• Research Project 1

  NIH · $91.2M · 2018

• NIH Grant R03MH062392

  NIH · $164k · 2002

• Role of Translin/Trax in Dopamine Signaling

  NIH · $18.0M · 2018–2024

• NIH Grant R01NS034473

  NIH · $791k · 2000

Frequent coauthors

• Paul F. Worley

  Johns Hopkins Medicine

  115 shared

• Aparna Shah

  Virginia Tech

  73 shared

• Kellie L. Tamashiro

  Johns Hopkins Medicine

  63 shared

• Timothy H. Murphy

  University of British Columbia

  58 shared

• Akira Sawa

  55 shared

• Jacqueline D. Keighron

  New York Institute of Technology

  52 shared

• Gianluigi Tanda

  National Institute on Drug Abuse

  52 shared

• Ta-Chung M. Mou

  University of Maryland, Baltimore

  51 shared

Labs

• Jay Baraban's LabPI

  The lab's research focus is not provided in the HTML snippet.

Education

• Ph.D., Neuroscience

  Johns Hopkins University

• M.D.

  Johns Hopkins University

• B.S.

  Johns Hopkins University