Antentor Hinton, Jr.
Antentor Hinton Jr. is a recent Ph.D. recipient from the Integrative Molecular Biomedical Science Program (IMBS) at Baylor College of Medicine. He worked in the laboratory of Dr. Yong Xu, an Associate Professor and Associate Director of the Children Nutrition Research Center (CNRC) Postdoctoral Training Program in the Department of Pediatrics. His graduate research elucidated the role of estrogen receptor alpha and steroid co-activator-1 in stress-induced hypertension in the brain. While in graduate school, Antentor served for a two year period as the President for the Association of Graduate Student of Diversity and has accumulated 26 research awards, travel awards, career development , and poster/oral awards. He has mentored 1 Minority Access Program (MAP) student and three graduate students and lectured in the Molecular and Cell Biology Post-bac course and Cell and Molecular Biology Review course. He also distributed his time between being a teacher’s assistant for two graduate courses - Organization of the Cell and Director’s Course - along with tutoring other graduate courses. He also has published one first author in Hypertension and co-authored 12 publications. He is in the process of submitting his second first author paper under the tutelage of Dr. Yong Xu. A.J. graduated from the NIH SMART Post baccalaureate Research Education Program at Baylor College of Medicine where he finished first in the class. Lastly, A.J. did his undergraduate studies in Biology and minored in Chemistry at the Winston-Salem State University. He graduated with the honor of magnum cum laude and was a leader on the Varsity Tennis Team his senior year.
Research Position: I am a post-doc at the University of Iowa– Carver Medical School in the Department of Internal Medicine. My PI is Dr. Dale Abel and he is the Chair and Department Executive Officer of the Department of Internal Medicine. Dr. Abel also holds the following positions: Chief in the Division of Endocrinology and Metabolism, Director of Fraternal Order of Eagles Diabetes Research Center (FOEDRC), Professor of Internal Medicine - Endocrinology and Metabolism and Professor of Biochemistry, Biomedical Engineering
Teaching Position: I have obtained a Visiting Instructorship at Winston–Salem State University to teach Cell Biology, Intro to Forensic Science, Ethics, and Honors 1300.
Supervisors: Dr. Dale Abel
Phone: 319-383-3095
Address: 169 Newton Road
Research Position: I am a post-doc at the University of Iowa– Carver Medical School in the Department of Internal Medicine. My PI is Dr. Dale Abel and he is the Chair and Department Executive Officer of the Department of Internal Medicine. Dr. Abel also holds the following positions: Chief in the Division of Endocrinology and Metabolism, Director of Fraternal Order of Eagles Diabetes Research Center (FOEDRC), Professor of Internal Medicine - Endocrinology and Metabolism and Professor of Biochemistry, Biomedical Engineering
Teaching Position: I have obtained a Visiting Instructorship at Winston–Salem State University to teach Cell Biology, Intro to Forensic Science, Ethics, and Honors 1300.
Supervisors: Dr. Dale Abel
Phone: 319-383-3095
Address: 169 Newton Road
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replacement substantially suppresses binge-like eating behavior in ovariectomized female mice. Estrogen-dependent
inhibition of binge-like eating was blocked in female mice specifically lacking estrogen receptor-α (ERα) in serotonin (5-HT)
neurons in the dorsal raphe nuclei (DRN). Administration of a recently developed glucagon-like peptide-1–estrogen
(GLP-1–estrogen) conjugate designed to deliver estrogen to GLP1 receptor–enhanced regions effectively targeted bioactive
estrogens to the DRN and substantially suppressed binge-like eating in ovariectomized female mice. Administration of GLP-1
alone reduced binge-like eating, but not to the same extent as the GLP-1–estrogen conjugate. Administration of ERα-selective
agonist propylpyrazole triol (PPT) to murine DRN 5-HT neurons activated these neurons in an ERα-dependent manner. PPT
also inhibited a small conductance Ca2+-activated K+
(SK) current; blockade of the SK current prevented PPT-induced activation
of DRN 5-HT neurons. Furthermore, local inhibition of the SK current in the DRN markedly suppressed binge-like eating in
female mice. Together, our data indicate that estrogens act upon ERα to inhibit the SK current in DRN 5-HT neurons, thereby
activating these neurons to suppress binge-like eating behavior and suggest ERα and/or SK current in DRN 5-HT neurons as
potential targets for anti-binge therapies
Co-administration of leptin and mCPP provided additive body weight-lowering effects in DIO mice. Further, mCPP pre-treatment in DIO mice enhanced leptin-induced pSTAT3 in the arcuate nucleus, the ventromedial hypothalamic nucleus, and the ventral premammillary nucleus. Finally, deletion of 5-HT2C Rs significantly blunted leptin-induced pSTAT3 in these same hypothalamic regions.
Our study provided evidence that drugs activating 5-HT2C Rs could function as leptin sensitizers and be used in combination with leptin to provide additive weight loss in DIO mice.
Results and conclusions. Here we generated a novel ERα-ZsGreen reporter mouse line in which expression of a green fluorescent reporter protein, ZsGreen, is driven by a 241 kb ERα gene promoter. We validated that ZsGreen is highly colocalized with endogenous ERα in the brain. Native ZsGreen signals were visualized in unfixed brain tissue, and were used to assist single cell collection and electrophysiological recordings. Finally, we demonstrated that this ERα-ZsGreen mouse allele can be used in combination with other genetic reporter alleles to allow experiments in highly selective neural populations.
Methods: We combined neuroanatomical, pharmacological, electrophysiological, Cre-lox, and chemogenetic approaches to investigate the functions of 5-HT 2C receptor (5-HT2CR) expressed by dopamine (DA) neurons in the regulation of binge-like eating behavior in mice.
Results: We showed that 5-HT stimulates DA neural activity through a 5-HT2CR-mediated mechansim,
and activation of this midbrain 5-HT-DA neural circuit effectively inhibits binge-like eating behavior in
mice. Notably, 5-HT medications, including fluoxetine, d-Fenfluramine, and lorcaserin (a selective 5-HT2CR agonist), act upon 5-HT2CRs expressed by DA neurons to inhibit binge-like eating in mice.
Conclusions: We identified the 5-HT2CR population in DA neurons as one potential target for anti-binge therapies, and provided pre-clinical evidence that 5-HT2CR agonists could be used to treat binge eating.
replacement substantially suppresses binge-like eating behavior in ovariectomized female mice. Estrogen-dependent
inhibition of binge-like eating was blocked in female mice specifically lacking estrogen receptor-α (ERα) in serotonin (5-HT)
neurons in the dorsal raphe nuclei (DRN). Administration of a recently developed glucagon-like peptide-1–estrogen
(GLP-1–estrogen) conjugate designed to deliver estrogen to GLP1 receptor–enhanced regions effectively targeted bioactive
estrogens to the DRN and substantially suppressed binge-like eating in ovariectomized female mice. Administration of GLP-1
alone reduced binge-like eating, but not to the same extent as the GLP-1–estrogen conjugate. Administration of ERα-selective
agonist propylpyrazole triol (PPT) to murine DRN 5-HT neurons activated these neurons in an ERα-dependent manner. PPT
also inhibited a small conductance Ca2+-activated K+
(SK) current; blockade of the SK current prevented PPT-induced activation
of DRN 5-HT neurons. Furthermore, local inhibition of the SK current in the DRN markedly suppressed binge-like eating in
female mice. Together, our data indicate that estrogens act upon ERα to inhibit the SK current in DRN 5-HT neurons, thereby
activating these neurons to suppress binge-like eating behavior and suggest ERα and/or SK current in DRN 5-HT neurons as
potential targets for anti-binge therapies
Co-administration of leptin and mCPP provided additive body weight-lowering effects in DIO mice. Further, mCPP pre-treatment in DIO mice enhanced leptin-induced pSTAT3 in the arcuate nucleus, the ventromedial hypothalamic nucleus, and the ventral premammillary nucleus. Finally, deletion of 5-HT2C Rs significantly blunted leptin-induced pSTAT3 in these same hypothalamic regions.
Our study provided evidence that drugs activating 5-HT2C Rs could function as leptin sensitizers and be used in combination with leptin to provide additive weight loss in DIO mice.
Results and conclusions. Here we generated a novel ERα-ZsGreen reporter mouse line in which expression of a green fluorescent reporter protein, ZsGreen, is driven by a 241 kb ERα gene promoter. We validated that ZsGreen is highly colocalized with endogenous ERα in the brain. Native ZsGreen signals were visualized in unfixed brain tissue, and were used to assist single cell collection and electrophysiological recordings. Finally, we demonstrated that this ERα-ZsGreen mouse allele can be used in combination with other genetic reporter alleles to allow experiments in highly selective neural populations.
Methods: We combined neuroanatomical, pharmacological, electrophysiological, Cre-lox, and chemogenetic approaches to investigate the functions of 5-HT 2C receptor (5-HT2CR) expressed by dopamine (DA) neurons in the regulation of binge-like eating behavior in mice.
Results: We showed that 5-HT stimulates DA neural activity through a 5-HT2CR-mediated mechansim,
and activation of this midbrain 5-HT-DA neural circuit effectively inhibits binge-like eating behavior in
mice. Notably, 5-HT medications, including fluoxetine, d-Fenfluramine, and lorcaserin (a selective 5-HT2CR agonist), act upon 5-HT2CRs expressed by DA neurons to inhibit binge-like eating in mice.
Conclusions: We identified the 5-HT2CR population in DA neurons as one potential target for anti-binge therapies, and provided pre-clinical evidence that 5-HT2CR agonists could be used to treat binge eating.