Transcription Factor Modulation and Expression in the Rat Auditory Brainstem Following Electrical Intracochlear Stimulation

Illing, Robert‐Benjamin; Michler, Steffen A.; Kraus, Kari Suzanne; Laszig, Roland

doi:10.1006/exnr.2002.7895

Cited by 40 publications

(22 citation statements)

References 92 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Stimulation of the cochlear and vestibular systems activates brain structures involved in autonomic regulation similar to those activated by altered gravity, including PB (8,9). Consistent with these data, it has been shown that the vestibular system alone or in conjunction with gravity receptors in the body exert certain effects on autonomic regulation.…”

mentioning

confidence: 56%

Evidence for vestibular regulation of autonomic functions in a mouse genetic model

Murakami

Erkman

Hermanson

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

mentioning

confidence: 56%

Evidence for vestibular regulation of autonomic functions in a mouse genetic model

Murakami

Erkman

Hermanson

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…All signaling pathways that activate CREB lead to phosphorylation of the protein at serine 133 (Ser133) (Shaywitz and Greenberg 1999;Lonze and Ginty, 2002). It has been shown previously that the phosphorylational state of CREB in the auditory brainstem can be modulated through changes in cochlear input (Illing et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Loss of Kv3.1 Tonotopicity and Alterations in cAMP Response Element-Binding Protein Signaling in Central Auditory Neurons of Hearing Impaired Mice

Hehn

Bhattacharjee²,

Kaczmarek³

2004

J. Neurosci.

101

View full text Add to dashboard Cite

The promoter for the kv3.1 potassium channel gene is regulated by a Ca 2ϩ -cAMP responsive element, which binds the transcription factor cAMP response element-binding protein (CREB). Kv3.1 is expressed in a tonotopic gradient within the medial nucleus of the trapezoid body (MNTB) of the auditory brainstem, where Kv3.1 levels are highest at the medial end, which corresponds to high auditory frequencies. We have compared the levels of Kv3.1, CREB, and the phosphorylated form of CREB (pCREB) in a mouse strain that maintains good hearing throughout life, CBA/J (CBA), with one that suffers early cochlear hair cell loss, C57BL/6 (BL/6). A gradient of Kv3.1 immunoreactivity in the MNTB was detected in both young (6 week) and older (8 month) CBA mice. Although no gradient of CREB was detected, pCREB-immunopositive cells were grouped together in distinct clusters along the tonotopic axis. The same pattern of Kv3.1, CREB, and pCREB localization was also found in young BL/6 mice at a time (6 weeks) when hearing is normal. In contrast, at 8 months, when hearing is impaired, the gradient of Kv3.1 was abolished. Moreover, in the older BL/6 mice there was a decrease in CREB expression along the tonotopic axis, and the pattern of pCREB labeling appeared random, with no discrete clusters of pCREB-positive cells along the tonotopic axis. Our findings are consistent with the hypothesis that ongoing activity in auditory brainstem neurons is necessary for the maintenance of Kv3.1 tonotopicity through the CREB pathway.

show abstract

“…In both cases, activation takes place through the Egr-1 sites previously mentioned. Therefore, it is reasonable to expect that other physiological stimuli that increase Egr-1 expression (see [22] for a review), such as the ones driving to neuronal stimulation [23,24], could also activate the nAChR a7 subunit gene. Fig.…”

Section: Resultsmentioning

confidence: 99%

Glucocorticoid activation of the neuronal nicotinic acetylcholine receptor $alpha;7 subunit gene: involvement of transcription factor Egr-1

CARRASCOSERRANO¹

2004

FEBS Letters

View full text Add to dashboard Cite

The a7 subunit is a component of nicotinic acetylcholine receptors expressed in bovine chromaffin cells. The peculiar localization of these receptors at adrenomedullary areas adjacent to the adrenal cortex suggests that factors, probably glucocorticoids, arising from the cortex might diffuse and regulate a7 receptor expression. In reporter gene transfection experiments, dexamethasone increased a7 promoter activity by up to fivefold in a concentration-and time-dependent manner despite the absence of consensus glucocorticoid receptor elements at the a7 promoter. Transcriptional activation induced by glucocorticoids was abolished through simultaneous mutation of at least two of the three sites for the immediate early transcription factor Egr-1, present in the proximal promoter region of the a7 subunit gene. Therefore, glucocorticoids activate the a7 subunit gene through Egr-1 in an indirect way.

show abstract

Transcription Factor Modulation and Expression in the Rat Auditory Brainstem Following Electrical Intracochlear Stimulation

Cited by 40 publications

References 92 publications

Evidence for vestibular regulation of autonomic functions in a mouse genetic model

Evidence for vestibular regulation of autonomic functions in a mouse genetic model

Loss of Kv3.1 Tonotopicity and Alterations in cAMP Response Element-Binding Protein Signaling in Central Auditory Neurons of Hearing Impaired Mice

Glucocorticoid activation of the neuronal nicotinic acetylcholine receptor $alpha;7 subunit gene: involvement of transcription factor Egr-1

Contact Info

Product

Resources

About