About

Arturo Andrade, Ph.D., is an Associate Professor of Brain Science (Research) and Neuroscience (Research) at Brown University. His research focuses on elucidating cell-specific mechanisms of neuronal activity and drug action, including opioids and cannabinoids. His main research areas include the function and expression of presynaptic calcium channels in anxiety and pain, the development of calcium-dependent bioluminescence sensors for neuronal activity control and imaging, and the development of biochemical sensors for neurotransmitters such as glutamate, GABA, and serotonin. His studies have implications for conditions like epilepsy, Parkinson's disease, neuropathic pain, Alzheimer's disease, schizophrenia, and bipolar disorder. Andrade's lab employs various systems and techniques, including mammalian expression systems, mouse genetic models, electrophysiology, biochemistry, molecular biology, bioluminescence, and calcium imaging. In addition to his research, he directs the Rodent Behavioral Phenotyping Core under the Carney Institute for Brain Science at Brown, coordinating behavioral studies in rodents among a group of researchers.

Research topics

• Biology
• Neuroscience
• Biochemistry
• Chemistry
• Materials science
• Medicine
• Internal medicine
• Chromatography
• Cell biology

Selected publications

• Continuous monitoring of glutamate using electroactive templated polymers as synthetic molecular receptors

  The Analyst · 2026-01-01

  articleOpen access

  Selective and spatiotemporally resolved monitoring of glutamate in the brain is essential for understanding its role in many brain functions as well as in the progression of various mental disorders. However, achieving accurate time resolved glutamate detection has been challenging due in part to the lack of glutamate-binding receptors that can offer both target selectivity and continuous measurement capability. To address this challenge, we have developed a novel polymer-based electrochemical biosensor designed to enhance selectivity for glutamate. Our proposed biosensor incorporates an innovative templated polymer-based target receptor, which selectively binds to the glutamate molecule. Furthermore, the reversible binding kinetics enable continuous glutamate detection with a time resolution of approximately 1 minute and a detection limit of 88.5 nM in artificial cerebrospinal fluid (ACSF) buffer. Additionally, due to the synthetic target-imprinted receptors, the sensor exhibited high selectivity for glutamate in the presence of other interfering neurochemicals GABA, glycine, and aspartate. These results indicate that the proposed sensor technology holds potential for monitoring glutamate in real physiological samples with possible use in clinical settings.

  PublisherOA PDFDOI

• Spatial memory in Alzheimer’s disease 5XFAD mice is enhanced by XPO1 inhibitor KPT-330

  GeroScience · 2026-02-06 · 1 citations

  articleOpen access

  The proteostatic decline in Alzheimer's disease is well established, and improvement in proteostasis could potentially delay cognitive impairment. One emerging entry point to modulate proteostasis is the regulation of nucleo-cytoplasmic partitioning of proteins across the nuclear pore via karyopherins. The nuclear exportin XPO1 is a key regulator of proteostasis by driving the assembly of ribosomes and by modulating the process of autophagy. We recently found that the XPO1 inhibitor KPT-330 (Selinexor), an FDA-approved drug against multiple myelomas, enhances proteostasis, leading to benefits in models of neurodegenerative diseases in C. elegans and Drosophila. Here, we find that KPT-330 increases autophagy in murine neuronal cells. In a murine model of Alzheimer's disease (5XFAD), KPT-330 improved spatial memory performance. Unexpectedly, general amyloid deposition in several brain regions was significantly increased by KPT-330, but specific regions, especially the thalamus, displayed significantly lower deposition, suggesting that XPO1 inhibition has regional-specific effects on proteostasis and amyloid plaque formation. Altogether, we conclude that, despite overall increases in amyloid plaque burden, XPO1 inhibition can improve cognition via spatially-specific reductions in amyloid deposition.

  PublisherOA PDFDOI

• <i>Cacna1b</i> alternative splicing is linked to associative learning

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-18

  articleOpen accessSenior authorCorresponding

  ABSTRACT Voltage-gated Ca V 2.2 channels are essential for neurotransmitter release throughout the nervous system including areas related to learning and memory like the hippocampus. Previous results have shown that Ca V 2.2 channels are involved in cognitive processes. However, a link between alternative splicing of the Cacna1b (gene that encodes for Ca V 2.2) pre-mRNA and cognitive processes has not been described. The Cacna1b pre-mRNA undergoes extensive cell-specific alternative splicing. In this body of work, we focus on the cassette exon 18a. Alternative splicing of exon 18a generates two splice variants, +18a- Cacna1b and Δ18a- Cacna1b . Exon 18a encodes a 21-amino acid sequence within the SYNaptic PRotein INTeraction ( synprint ) site. Splice variants containing exon 18a (+18a-Ca V 2.2) show reduced cumulative inactivation and increased Ca²⁺ current density compared to splice variants lacking exon 18a (Δ18a-Ca V 2.2), suggesting functional specialization. We previously showed that +18a- Cacna1b splice variants are enriched in cholecystokinin-expressing interneurons (CCK + INs). This neuronal type is strongly implicated in associative learning. Therefore, we tested whether alternative splicing of exon 18a contributes to associative learning. To test this hypothesis, we used genetically engineered mice that constitutively express either +18a- Cacna1b (+18a) or Δ18a- Cacna1b (Δ18a). We first validated that restricted splicing of exon 18a did not alter downstream alternative or constitutive spliced exons in the Cacna1b pre-mRNA, nor total Ca V 2.2 protein levels. We then performed a comprehensive behavioral analysis that included assessment of associate learning. We found that in the trace fear conditioning task, +18a mice exhibited less freezing during the trace interval in both the acquisition and memory phases compared to WT mice. Whereas Δ18a mice showed enhanced freezing during the same intervals relative to WT mice. These bidirectional phenotypes reveal that exon 18a shapes aversive associative learning. Furthermore, exon 18a splicing did not influence spatial working memory, spatial navigation under stress, nociceptive responses in basal and inflammatory conditions, overall locomotion or exploratory behavior. These results suggest that the behavioral impact of exon 18a splicing is highly selective. Together, our findings identify alternative splicing of exon 18a as a molecular contributor to associative learning.

  PublisherOA PDFDOI

• CaBLAM: a high-contrast bioluminescent Ca2+ indicator derived from an engineered Oplophorus gracilirostris luciferase

  Nature Methods · 2025-12-02 · 9 citations

  articleOpen access

  Monitoring intracellular calcium is central to understanding cell signaling across nearly all cell types and organisms. Fluorescent genetically encoded calcium indicators (GECIs) remain the standard tools for in vivo calcium imaging, but require intense excitation light, leading to photobleaching, background autofluorescence and phototoxicity. Bioluminescent GECIs, which generate light enzymatically, eliminate these artifacts but have been constrained by low dynamic range and suboptimal calcium affinities. Here we show that CaBLAM ('calcium bioluminescence activity monitor'), an engineered bioluminescent calcium indicator, achieves an order-of-magnitude improvement in signal contrast and a tunable affinity matched to physiological cytosolic calcium. CaBLAM enables single-cell and subcellular activity imaging at video frame rates in cultured neurons and sustained imaging over hours in awake, behaving animals. These capabilities establish CaBLAM as a robust and general alternative to fluorescent GECIs, extending calcium imaging to regimes where excitation light is undesirable or infeasible.

  PublisherDOI

• <i>Trpv1</i>-dependent <i>Cacna1b</i> gene inactivation reveals cell-specific functions of Ca_V2.2 channels <i>in vivo</i>

  Figshare · 2025-01-01

  datasetOpen access

  Voltage-gated Ca_V2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for Ca_V2.2 channels has been well established in the transmission of sensory signals including noxious information using pharmacological and global gene knockout mouse models. However, investigation of the cell-specific actions of Ca_V2.2 channels has been difficult due to the lack of gene-dependent knockout mouse models and particularly in dissecting behavioral responses that depend on Ca_V2.2 channel activity. Here, we show the importance of Ca_V2.2 channels in <i>Trpv1</i>-lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the <i>Cacna1b</i> gene. Our work shows the cell-type specificity of Ca_V2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of <i>Cacna1b</i> to discern cell-specific Ca_V2.2 channel functions.

  PublisherDOI

• <i>Trpv1</i> -dependent <i>Cacna1b</i> gene inactivation reveals cell-specific functions of Ca _V 2.2 channels <i>in vivo</i>

  Channels · 2025-12-22 · 1 citations

  articleOpen access

  2.2 channel functions.

  PublisherDOI

• <i>Trpv1</i>-dependent <i>Cacna1b</i> gene inactivation reveals cell-specific functions of Ca_V2.2 channels <i>in vivo</i>

  Figshare · 2025-01-01

  datasetOpen access

  Voltage-gated Ca_V2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for Ca_V2.2 channels has been well established in the transmission of sensory signals including noxious information using pharmacological and global gene knockout mouse models. However, investigation of the cell-specific actions of Ca_V2.2 channels has been difficult due to the lack of gene-dependent knockout mouse models and particularly in dissecting behavioral responses that depend on Ca_V2.2 channel activity. Here, we show the importance of Ca_V2.2 channels in <i>Trpv1</i>-lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the <i>Cacna1b</i> gene. Our work shows the cell-type specificity of Ca_V2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of <i>Cacna1b</i> to discern cell-specific Ca_V2.2 channel functions.

  PublisherDOI

• <i>Trpv1</i> -dependent <i>Cacna1b</i> gene inactivation reveals cell-specific functions of Ca _V 2.2 channels <i>in vivo</i>

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-05-10 · 1 citations

  preprintOpen access

  ABSTRACT Voltage-gated Ca V 2.2 channels underlie the N-type current, and they regulate calcium entry at many presynaptic nerve endings to control transmitter release. A role for Ca V 2.2 channels has been well-established in the transmission of pain information using pharmacological and global gene inactivated mouse models. However, investigation of the cell-specific actions of Ca V 2.2 channels would benefit from the availability of cell-restricted knockout mouse models and particularly in dissecting behavioral responses that depend on Ca V 2.2 channel activity. Here, we show the importance of Ca V 2.2 channels in Trpv1 -lineage neurons in behavioral responses to sensory stimuli using Cre-dependent inactivation of the Cacna1b gene. Our work shows the cell- type specificity of Ca V 2.2 channels in mediating rapidly developing heat hypersensitivity and the utility of Cre-dependent inactivation of Cacna1b to discern cell-specific Ca V 2.2 channel functions.

  PublisherOA PDFDOI

• Electrochemical Detection of Glutamate and Histamine Using Redox-Labeled Stimuli-Responsive Polymer as a Synthetic Target Receptor

  ACS Applied Polymer Materials · 2024-05-10 · 8 citations

  articleOpen access

  Glutamate (Glu) and histamine (His) are two major neurotransmitters that play many critical roles in brain physiological functions and neurological disorders. Therefore, specific and sensitive monitoring of Glu and His is essential in the diagnosis and treatment of various mental health and neurodegenerative disorders. Both being nonelectroactive species, direct electrochemical detection of Glu and His has been challenging. Herein, we report a stimuli-responsive polymer-based biosensor for the electrochemical detection of Glu and His. The polymer-based target receptors consist of a linear chain stimuli-responsive templated polymer hybrid that is labeled with an osmium-based redox-active reporter molecule to elicit conformation-dependent electrochemical responses. The polymers are then attached to a gold electrode to implement an electrochemical sensor. The cyclic voltammetry (CV) and square-wave voltammetry (SWV) results confirmed the polymers’ conformational changes due to the specific target (i.e., Glu and His) recognition and the corresponding electrochemical detection capabilities. The voltammetry results indicate that this biosensor can be used as a “signal-on” and “signal-off” sensors for the detection of Glu and His concentrations, respectively. The developed biosensor also showed excellent regeneration capability by fully recovering the initial current signal after being rinsed with deionized water. To further validate the polymer’s utility as a target bioreceptor, the surface plasmon resonance (SPR) technique was used to characterize the binding affinity between the designed polymers and the target chemical. The SPR results exhibited the equilibrium dissociation constants (KD) of 2.40 μM and 1.54 μM for the polymer–Glu and polymer–His interactions, respectively. The results obtained in this work strongly suggest that the proposed sensing technology could potentially be used as a platform for monitoring nonelectroactive neurochemicals from animal models.

  PublisherOA PDFDOI

• Electrochemical detection of glutamate and histamine using redox-labeled stimuli-responsive polymer as a synthetic target receptor

  ChemRxiv · 2024-01-12 · 1 citations

  preprintOpen access

  Glutamate (Glu) and histamine (His) are two major neurotransmitters that play many critical roles in brain physiological functions and neurological disorders. Therefore, specific and sensitive monitoring of Glu and His is essential in the diagnosis and treatment of various mental health and neurodegenerative disorders. Both being non-electroactive species, direct electrochemical detection of Glu and His has been challenging. Herein, we report a stimuli-responsive polymer-based biosensor for the electrochemical detection of Glu and His. The polymer-based target receptors consist of a linear chain stimuli-responsive templated polymer hybrid that is labeled with an osmium-based redox-active reporter molecules to elicit conformation-dependent electrochemical responses. The polymers are then attached to a gold electrode to implement an electrochemical sensor. The cyclic voltammetry (CV) and square-wave voltammetry (SWV) results confirmed the polymers’ conformational changes due to the specific target (i.e., Glu and His) recognition and the corresponding electrochemical detection capabilities. The voltammetry results indicate that this biosensor can be used as a ‘signal-on’ and ‘signal-off’ sensors for the detection of Glu and His concentrations, respectively. The developed biosensor also showed excellent regeneration capability by fully recovering the initial current signal after rinsing with deionized water. To further validate the polymer’s utility as a target bioreceptor, the surface plasmon resonance (SPR) technique was used to characterize the binding affinity between the designed polymers and the target chemical. The SPR results exhibited the equilibrium dissociation constants (KD) of 2.40 µM and 1.54 µM for the polymer-Glu and polymer-His interactions, respectively. The results obtained this work strongly suggest that the proposed sensing technology could potentially be used as a platform for monitoring non-electroactive neurochemicals from animal models.

  PublisherOA PDFDOI

Recent grants

• NIH Grant K99MH099405

  NIH · $180k · 2015

• NIH Grant R00MH099405

  NIH · $738k · 2019

Frequent coauthors

• Diane Lipscombe

  Providence College

  40 shared

• Ricardo Felix

  Center for Research and Advanced Studies of the National Polytechnic Institute

  35 shared

• Sylvia A. Denome

  Brown Institute for Media Innovation

  28 shared

• Alejandro Sandoval

  Universidad Nacional Autónoma de México

  18 shared

• A. J. Castiglioni

  16 shared

• Thomas D. Helton

  National Institute of Environmental Health Sciences

  16 shared

• Spiro Marangoudakis

  Brown University

  14 shared

• Alexandra Bunda

  Bristol-Myers Squibb (United States)

  11 shared

Labs

• Neuroscience Department at Brown UniversityPI

Awards & honors

• Outstanding Advisor Award (2021)
• K99/R00 Pathway to Independence Award (2012-2018)
• National Network of Investigators, Category I (2008-present)
• Miguel Hidalgo Award to Academic Merit (1996-2001)
• Telmex Foundation Award (2000-2007)