Abstract:
:To test the hypothesis that prepubertal exposure of LHRH neurons to a source of catecholamines and neuropeptides accelerates the onset of puberty, we examined the effects of autologous adrenal transplantation into the base of the third ventricle of the brain in juvenile female rhesus monkeys at 11-13 months of age. The adrenal medulla, which contains catecholamines and neuropeptide Y (NPY), was cut into small pieces and mixed with gelfoam in artificial CSF and injected into the third ventricle, adjacent to LHRH neurons and their neuroterminals. Sham control monkeys received artificial CSF with gelfoam alone. Animals were monitored for signs of pubertal development. While menarche was not altered by adrenal transplantation, the timing of first and second ovulations occurred significantly (P < 0.05) earlier in adrenal-transplanted monkeys. Histological examination indicated that the grafts survived in all transplanted monkeys. The presence of catecholamines and NPY in graft tissue was confirmed by tyrosine-hydroxylase-positive, dopamine beta-hydroxylase-positive, and NPY-positive cells. Endogenous LHRH fibers were observed innervating the graft tissue. We conclude that: (1) adrenal medulla transplantation into the third ventricle accelerates the age of first ovulation; (2) this is likely due to neuroactive substances (e.g., catecholamines and NPY) from the graft tissue; and (3) grafted adrenal medulla tissue can survive for at least 30-40 months. However, the age of menarche was not accelerated by this grafting, suggesting that an additional mechanism (e.g., removal of tonic inhibition) may be necessary for the onset of puberty.
journal_name
Exp Neuroljournal_title
Experimental neurologyauthors
Gore AC,Saitoh Y,Terasawa Edoi
10.1006/exnr.1996.0127subject
Has Abstractpub_date
1996-08-01 00:00:00pages
172-83issue
2eissn
0014-4886issn
1090-2430pii
S0014-4886(96)90127-2journal_volume
140pub_type
杂志文章abstract::c-Fos protein-like immunoreactivity (IR) was investigated in the rat brain following an application of weak anodal direct current to the surface of the unilateral sensorimotor cortex in an attempt to elucidate the cellular and molecular bases of central plasticity. Anodal polarization resulted in a massive increase in...
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章,评审
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.1999.7163
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2004.04.003
更新日期:2004-07-01 00:00:00
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2005.12.033
更新日期:2006-06-01 00:00:00
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journal_title:Experimental neurology
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journal_title:Experimental neurology
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doi:10.1006/exnr.2001.7849
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journal_title:Experimental neurology
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journal_title:Experimental neurology
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journal_title:Experimental neurology
pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2020-01-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1006/exnr.2000.7555
更新日期:2001-02-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
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更新日期:1990-11-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
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journal_title:Experimental neurology
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更新日期:1983-09-01 00:00:00
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journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2012.02.010
更新日期:2012-05-01 00:00:00
abstract::Ischemic stroke (IS) is one of the most common cerebrovascular diseases worldwide. The aberrant expression of BCL6 has been previously implicated in the pathogenesis of IS. Meanwhile, miR-31 is known as a target of BCL6, and has also been suggested to diminish cell damage by suppressing the PKD1 expression. Expanding ...
journal_title:Experimental neurology
pub_type: 杂志文章
doi:10.1016/j.expneurol.2020.113528
更新日期:2021-01-01 00:00:00