Postdoctoral Research Focus
*More details on recent projects will be added soon.
October 2019 - present. Postdoctoral scholar at Dr. Rebecca Calisi Rodríguez lab (B3 lab).
My work is focused on reproductive neurogenomics and science communication.
Research
My research will be focused on the characterization of the effects of single parenting on the amygdala, emotional center of the brain, in the parent and their offspring.
SciComm
Together with Dr. Calisi-Rodríguez I am leading the development of a Science Communications training program for faculty at UC Davis. This work is in collaboration with the University of California San Diego Research Communications Program and the UC Davis Office of Strategic Communications.
January 2017- September 2019. Postdoctoral scholar at Dr. Megan Dennis lab.
My research in the Dennis lab was focused on using zebrafish as a model to identify and characterize genetic mutations that lead to epilepsy and or autism spectrum disorder. There I successfully created zebrafish mutants for several genes including the large amino acid transporter LAT1 gene, slc7a5, and the SynGAP1 gene, synngap1b.
Together with the zebrafish team we characterized these two genes genetically, morphologically and behaviorally in stable lines. In addition, we identified/developed a higher-throughput approach to maximize the use of individual zebrafish larvae for these measurements. A manuscript (bioRxiv https://www.biorxiv.org/content/10.1101/2020.07.23.217273v1) for this work has been submitted for publication (July 2020).
Ph.D. Research Focus
My research as a graduate student was focused on understanding the mechanism of toxicity of an environmental neurotoxicant, methylmercury (MeHg), on spinal cord motor neurons.
Why?
Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in humans. It is characterized by the degeneration of upper and lower motor neurons, leading to death approximately five years after being diagnosed. There are two forms of ALS: familial (FALS) which accounts for 10% of all ALS cases and sporadic (SALS) which comprises 90% of all ALS cases. In both FALS and SALS the clinical and pathological manifestations are the same [1]. Genetic and environmental factors are considered possible contributors to the development of both forms [2,3]. One environmental toxicant that has been considered a possible contributor to the development of ALS is methylmercury (MeHg) [2-4].
MeHg is a persistent environmental neurotoxicant to which humans are exposed mainly through the consumption of seafood. Motor neurons are one of the targets of MeHg toxicity and exposure to mercury compounds has been reported to lead to ALS-like syndromes [2,4]. In a study using the ALS mouse model SOD1-G93A, exposure to MeHg led to early onset of ALS-like phenotype, presenting a possible gene environment interaction [5]. One of the factors contributing to MeHg-induced motor neuron degeneration is alterations in intracellular calcium [5]. These effects have not been well characterized and are the focus of my dissertation project. The findings of my work contribute to 1) the understanding of MeHg-induced toxicity in motor neurons, 2) provide a platform for ongoing studies in the Atchison lab focused on identifying the underlying mechanisms by which MeHg is contributing to the accelerated onset of ALS-like phenotype in the SOD1-G93A mouse.
References:
1. Cleveland, D. W. & Rothstein, J. D. From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS. Nat. Rev. Neurosci. 2, 806–19 (2001).
2. Johnson, F. O. & Atchison, W. D. The role of environmental mercury, lead and pesticide exposure in development of amyotrophic lateral sclerosis. Neurotoxicology 30, 761–5 (2009).
3. Trojsi, F., Monsurrò, M. R. & Tedeschi, G. Exposure to environmental toxicants and pathogenesis of amyotrophic lateral sclerosis: state of the art and research perspectives. Int. J. Mol. Sci. 14, 15286–311 (2013).
4. Praline, J. et al. ALS and mercury intoxication: a relationship? Clin. Neurol. Neurosurg. 109, 880–3 (2007).
5. Johnson, F. O. et al. Exposure to an environmental neurotoxicant hastens the onset of amyotrophic lateral sclerosis-like phenotype in human Cu2+/Zn2+ superoxide dismutase 1 G93A mice : J. Pharmacol. Exp. Ther. 338, 518–527 (2011).
Manuscripts related to this (PhD) research are below.
1. Effects of methylmercury on spinal cord afferents and efferents – A review. A. Colón-Rodríguez, H. E. Hannon, and W. D. Atchison. Neurotoxicology. In press, Dec 2016.
2. Evaluating a gene-environment interaction in amyotrophic lateral sclerosis: Methylmercury exposure and mutated SOD1. J. M. Bailey, A. Colón-Rodríguez, and W. D. Atchison. Current Environmental Health Reports. In press, April 2017.
3. Acute methylmercury exposure alters intracellular calcium concentrations in human induced pluripotent stem cell motor neurons through AMPA receptors. A. Colón-Rodríguez, N. M. Colón-Carrión, and W. D. Atchison. Neurotoxicology. Accepted, June 2020.
4. Low level methylmercury exposure alters steady state levels of ion channel mRNA in the cerebellum and brainstem of the developing rat. A. Colón-Rodríguez, Y. Yuan, and W. D. Atchison. In progress.
*More details on recent projects will be added soon.
October 2019 - present. Postdoctoral scholar at Dr. Rebecca Calisi Rodríguez lab (B3 lab).
My work is focused on reproductive neurogenomics and science communication.
Research
My research will be focused on the characterization of the effects of single parenting on the amygdala, emotional center of the brain, in the parent and their offspring.
SciComm
Together with Dr. Calisi-Rodríguez I am leading the development of a Science Communications training program for faculty at UC Davis. This work is in collaboration with the University of California San Diego Research Communications Program and the UC Davis Office of Strategic Communications.
January 2017- September 2019. Postdoctoral scholar at Dr. Megan Dennis lab.
My research in the Dennis lab was focused on using zebrafish as a model to identify and characterize genetic mutations that lead to epilepsy and or autism spectrum disorder. There I successfully created zebrafish mutants for several genes including the large amino acid transporter LAT1 gene, slc7a5, and the SynGAP1 gene, synngap1b.
Together with the zebrafish team we characterized these two genes genetically, morphologically and behaviorally in stable lines. In addition, we identified/developed a higher-throughput approach to maximize the use of individual zebrafish larvae for these measurements. A manuscript (bioRxiv https://www.biorxiv.org/content/10.1101/2020.07.23.217273v1) for this work has been submitted for publication (July 2020).
Ph.D. Research Focus
My research as a graduate student was focused on understanding the mechanism of toxicity of an environmental neurotoxicant, methylmercury (MeHg), on spinal cord motor neurons.
Why?
Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease in humans. It is characterized by the degeneration of upper and lower motor neurons, leading to death approximately five years after being diagnosed. There are two forms of ALS: familial (FALS) which accounts for 10% of all ALS cases and sporadic (SALS) which comprises 90% of all ALS cases. In both FALS and SALS the clinical and pathological manifestations are the same [1]. Genetic and environmental factors are considered possible contributors to the development of both forms [2,3]. One environmental toxicant that has been considered a possible contributor to the development of ALS is methylmercury (MeHg) [2-4].
MeHg is a persistent environmental neurotoxicant to which humans are exposed mainly through the consumption of seafood. Motor neurons are one of the targets of MeHg toxicity and exposure to mercury compounds has been reported to lead to ALS-like syndromes [2,4]. In a study using the ALS mouse model SOD1-G93A, exposure to MeHg led to early onset of ALS-like phenotype, presenting a possible gene environment interaction [5]. One of the factors contributing to MeHg-induced motor neuron degeneration is alterations in intracellular calcium [5]. These effects have not been well characterized and are the focus of my dissertation project. The findings of my work contribute to 1) the understanding of MeHg-induced toxicity in motor neurons, 2) provide a platform for ongoing studies in the Atchison lab focused on identifying the underlying mechanisms by which MeHg is contributing to the accelerated onset of ALS-like phenotype in the SOD1-G93A mouse.
References:
1. Cleveland, D. W. & Rothstein, J. D. From Charcot to Lou Gehrig: deciphering selective motor neuron death in ALS. Nat. Rev. Neurosci. 2, 806–19 (2001).
2. Johnson, F. O. & Atchison, W. D. The role of environmental mercury, lead and pesticide exposure in development of amyotrophic lateral sclerosis. Neurotoxicology 30, 761–5 (2009).
3. Trojsi, F., Monsurrò, M. R. & Tedeschi, G. Exposure to environmental toxicants and pathogenesis of amyotrophic lateral sclerosis: state of the art and research perspectives. Int. J. Mol. Sci. 14, 15286–311 (2013).
4. Praline, J. et al. ALS and mercury intoxication: a relationship? Clin. Neurol. Neurosurg. 109, 880–3 (2007).
5. Johnson, F. O. et al. Exposure to an environmental neurotoxicant hastens the onset of amyotrophic lateral sclerosis-like phenotype in human Cu2+/Zn2+ superoxide dismutase 1 G93A mice : J. Pharmacol. Exp. Ther. 338, 518–527 (2011).
Manuscripts related to this (PhD) research are below.
1. Effects of methylmercury on spinal cord afferents and efferents – A review. A. Colón-Rodríguez, H. E. Hannon, and W. D. Atchison. Neurotoxicology. In press, Dec 2016.
2. Evaluating a gene-environment interaction in amyotrophic lateral sclerosis: Methylmercury exposure and mutated SOD1. J. M. Bailey, A. Colón-Rodríguez, and W. D. Atchison. Current Environmental Health Reports. In press, April 2017.
3. Acute methylmercury exposure alters intracellular calcium concentrations in human induced pluripotent stem cell motor neurons through AMPA receptors. A. Colón-Rodríguez, N. M. Colón-Carrión, and W. D. Atchison. Neurotoxicology. Accepted, June 2020.
4. Low level methylmercury exposure alters steady state levels of ion channel mRNA in the cerebellum and brainstem of the developing rat. A. Colón-Rodríguez, Y. Yuan, and W. D. Atchison. In progress.