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28 results on '"Burton, Frank H."'

4. Pituitary hyperplasia and gigantism in mice caused by a cholera toxin transgene

Author

Burton, Frank H., Hasel, Karl W., Bloom, Floyd E., and Sutcliffe, J. Gregor

Subjects
Cyclic adenylic acid -- Physiological aspects, Gigantism -- Causes of, Cholera toxin -- Physiological aspects, Hyperplasia -- Research, Somatotropin -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1991

22. TSOCDlike neuropotentiated mice are supersensitive to seizure induction

Author

Campbell, Keith M., Veldman, Matthew B., McGrath, Michael J., and Burton, Frank H.

Abstract

Seizures can be induced by systemic dopamine D1 receptor agonists or by cortical-limbic neurostimulation non-selectively. Seizures are also often associated with tics and compulsions, which likewise involve cortical-limbic hyperactivity. To determine if selective potentiation of cortical-limbic D1 receptor-expressing (D1) neurons increases seizure susceptibility, we administered pentylenetetrazole (PTZ) to mice that express a neuropotentiating transgene only in a glutamatergic, corticallimbic subset of D1 neurons (D1CT-7 line). These mice exhibited increased PTZ-dependent seizure incidence, onset rate and intensity. Because D1CT-7 mice also exhibit ticcompulsion-like behaviors, this implies that glutamatergic hyperactivity induced by cortical-limbic D1 neuropotentiation facilitates not only epilepsy but also tics and compulsions. This suggests a dopamine-regulated glutamatergic basis for all three states and may explain why they often co-exist in humans.

Published
2000

23. Characterization of a Transgenic Model of Volitional Tremor

Author

Burton, Frank H.

Subjects
Ataxia -- Physiological aspects, Biological models -- Analysis, Genetic disorders -- Models
Abstract

Ataxias encompass a variety of neurophysiological deficits in which neural networks involved in motor activity and coordination exhibit degeneration or abnormalities in neurotransmission. To develop potential treatments for them, we [...]

Published
1995

24. Human Chromosomal Localization, Tissue/Tumor Expression, and Regulatory Function of the etsFamily Gene EHF

Author

Kleinbaum, Laurie A., Duggan, Catherine, Ferreira, Elisabeth, Coffey, Greg P., Butticè, Giovanna, and Burton, Frank H.

Abstract

Etsfactors are members of an ancient multigene family of transcription factors including oncoproteins and possibly tumor suppressors. We previously characterized a novel divergent etsgene, Ehf(ets homologous factor) in mice. Here we report the cDNA sequence, chromosomal location, and tissue/tumor expression patterns of the human EHFgene and the regulatory activity of the EHF protein. EHFmaps to 11p12, which is deleted in many prostate, breast, and lung carcinomas and is a hot spot for inherited deletion- or amplification-associated developmental defects. EHFis differentially expressed in normal tissues and carcinomas and between tumor stages and is most highly expressed in the organs known to form carcinomas upon 11p12 deletion. EHF protein represses the ETS-2 induced activity of both stromelysin-1 and collagenase-1 promoters. These data suggest that EHFmay contribute to human development and carcinogenesis and is a candidate for the 11p12 tumor suppressor gene.

Published
1999
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28. Biochemical markers of striatal desensitization in cortical-limbic hyperglutamatergic TS- & OCD-like transgenic mice.

Author

O'Brien KB, Sharrief AZ, Nordstrom EJ, Travanty AJ, Huynh M, Romero MP, Bittner KC, Bowser MT, and Burton FH

Subjects
Animals, Brain metabolism, Disease Models, Animal, Glutamine metabolism, Male, Mice, Mice, Inbred BALB C, Mice, Transgenic, Obsessive-Compulsive Disorder metabolism, Tourette Syndrome metabolism, Biomarkers analysis, Brain physiopathology, Obsessive-Compulsive Disorder physiopathology, Tourette Syndrome physiopathology
Abstract

Tics and compulsions in comorbid Tourette's syndrome (TS) and obsessive-compulsive disorder (OCD) are associated with chronic hyperactivity of parallel cortico/amygdalo-striato-thalamo-cortical (CSTC) loop circuits. Comorbid TS- & OCD-like behaviors have likewise been observed in D1CT-7 mice, in which an artificial neuropotentiating transgene encoding the cAMP-elevating intracellular subunit of cholera toxin (CT) is chronically expressed selectively in somatosensory cortical & amygdalar dopamine (DA) D1 receptor-expressing neurons that activate cortico/amygdalo-striatal glutamate (GLU) output. We've now examined in D1CT-7 mice whether the chronic GLU output from their potentiated cortical/limbic CSTC subcircuit afferents associated with TS- & OCD-like behaviors elicits desensitizing neurochemical changes in the striatum (STR). Microdialysis-capillary electrophoresis and in situ hybridization reveal that the mice's chronic GLU-excited STR exhibits pharmacodynamic changes in three independently GLU-regulated measures of output neuron activation, co-excitation, and desensitization, signifying hyperactive striatal CSTC output and compensatory striatal glial and neuronal desensitization: 1) Striatal GABA, an output neurotransmitter induced by afferent GLU, is increased. 2) Striatal d-serine, a glial excitatory co-transmitter inhibited by afferent GLU, is decreased. 3) Striatal Period1 (Per1), which plays a non-circadian role in the STR as a GLU + DA D1- (cAMP-) dependent repressor thought to feedback-inhibit GLU + DA- triggered ultradian urges and motions, is transcriptionally abolished. These data imply that chronic cortical/limbic GLU excitation of the STR desensitizes its co-excitatory d-serine & DA inputs while freezing its GABA output in an active state to mediate chronic tics and compulsions - possibly in part by abolishing striatal Per1-dependent ultradian extinction of urges and motions., (Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.)

Published
2018
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