Abstract:
:Rats were injected (i.p.) once daily with either 1 mg/kg CGP 56999A, a gamma-aminobutyric acid(B) (GABA(B)) receptor antagonist, or an equivalent volume of saline beginning 7 days prior to, and continuing for 7 days following, a unilateral 6-hydroxydopamine lesion of the nigrostriatal dopamine (DA) pathway. At the end of the CGP 56999A treatment period the concentrations of DA and dihydroxyphenylacetic acid (DOPAC), as well as the expression of brain-derived neurotrophic factor (BDNF), were analyzed in corpus striatum ipsilateral and contralateral to the lesioning. No significant differences in these parameters were noted in the contralateral striatum between saline- and CGP 56999A-treated subjects. In contrast, as compared to animals receiving saline only, daily treatment with the GABA(B) receptor antagonist significantly attenuated the 6-hydroxydopamine-induced decline in DA and increased the expression of BDNF in the ipsilateral striatum. The results indicate that CGP 56999A enhances BDNF gene expression in the rat corpus striatum and prevents the decline in DA content that is a characteristic sequela of 6-hydroxydopapmine lesions of the nigrostraital dopamine pathway. These findings suggest that GABA(B) receptor antagonists may be of value in the treatment of Parkinson's disease and other conditions that would benefit from an enhanced production of neurotrophic factors in brain.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Enna SJ,Reisman SA,Stanford JAdoi
10.1016/j.neulet.2006.07.004subject
Has Abstractpub_date
2006-10-02 00:00:00pages
102-6issue
1-2eissn
0304-3940issn
1872-7972pii
S0304-3940(06)00713-0journal_volume
406pub_type
杂志文章abstract::The death of neurons after brain ischaemia may be associated with activation of cyclin-dependent kinases (CDKs) and upregulation of cyclins, reflecting aberrant entry of neurons into the cell cycle. Little has been published on the expression of cell cycle proteins after brain ischaemia in man. Well-characterized anti...
journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
pub_type: 杂志文章
doi:10.1016/0304-3940(86)90043-1
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
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pub_type: 杂志文章
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journal_title:Neuroscience letters
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journal_title:Neuroscience letters
pub_type: 杂志文章
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journal_title:Neuroscience letters
pub_type: 杂志文章
doi:10.1016/j.neulet.2017.03.034
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