Abstract:
:Chronic exposure to stress amplifies locomotor deficits and exacerbates dopamine neuron loss in an animal model for Parkinson's disease. The release of neurotrophic factors such as glial cell-line derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3) following neuronal injury attenuates exacerbated degeneration of these neurons. In this study, the neurotoxin 6-hydroxydopamine (6-OHDA) was injected unilaterally into the medial forebrain bundle of male Sprague Dawley rats. A subset of these rats was subjected to post-lesion restraint stress after which the effect of exposure to stress on locomotor activity (forelimb akinesia test), neurotrophic factor (GDNF and NT-3) and corticosterone concentration was assessed. Exposure to post-lesion stress resulted in increased preference to use the unimpaired forelimb (forelimb ipsilateral to the lesioned hemisphere) in the forelimb akinesia test. The expected increase in both GDNF and NT-3 concentration following injury was not present in the stressed animals. However, both the non-stressed and stressed lesioned groups had decreased neurotrophic factor concentration at one and two weeks post lesion. This decrease was exaggerated in the stressed rats. The decrease in neurotrophic factor concentration was accompanied by an increase in corticosterone concentration in the stressed rats. These findings demonstrate that exposure to post-6-OHDA lesion stress exaggerates dopamine neurodegeneration and enhance motor impairment. This suggests that conditions that result in a hyper-activated hypothalamic-pituitary-adrenal axis such as depression which is concomitant to a Parkinson's disease diagnosis may be responsible for enhanced dopamine depletion by attenuating neurotrophic factor concentration elevation in the nigrostriatal pathway following neuronal injury.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Ngema PN,Mabandla MVdoi
10.1007/s11011-017-9988-1subject
Has Abstractpub_date
2017-08-01 00:00:00pages
1061-1067issue
4eissn
0885-7490issn
1573-7365pii
10.1007/s11011-017-9988-1journal_volume
32pub_type
杂志文章abstract::Hyperammonemia is necessary for development of the cerebral complications to liver disease including hepatic encephalopathy and cerebral edema but the mechanisms are unclear. Ammonia is taken up by the brain in proportion to its arterial concentration. The flux into the brain is most likely by both diffusion of NH3 an...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-014-9494-7
更新日期:2014-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-0071-8
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-012-9334-6
更新日期:2012-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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更新日期:2017-04-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 已发布勘误
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更新日期:2020-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-010-9218-6
更新日期:2010-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF01996074
更新日期:1994-03-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-015-9678-9
更新日期:2015-10-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
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更新日期:2017-10-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020609213664
更新日期:1998-06-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9921-z
更新日期:2017-04-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-019-00496-z
更新日期:2020-01-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-006-9023-4
更新日期:2006-09-01 00:00:00
abstract::The availability of an animal model is crucial in studying the pathophysiological mechanisms of disease and to test possible therapies. Now, there are several models for the study of liver diseases, but there still remains a lack of a satisfactory animal model of chronic liver disease with hepatic encephalopathy (HE) ...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-005-7925-1
更新日期:2005-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9816-z
更新日期:2016-08-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-009-9150-9
更新日期:2009-09-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9581-9
更新日期:2015-02-01 00:00:00
abstract::Oxidative stress is strongly implicated in the pathogenesis of stroke. Strategies using antioxidants to improve neurological functions after stroke have, thus, gained significant attention. Ocimum basilicum L. is used traditionally to treat CNS disorders. Its antioxidant capacity is well established. Our laboratory ha...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0215-5
更新日期:2018-08-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9492-9
更新日期:2014-06-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-013-9399-x
更新日期:2013-09-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/BF01001350
更新日期:1988-03-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 临床试验,杂志文章
doi:
更新日期:1997-06-01 00:00:00
abstract::Long-term or excessive application of morphine leads to tolerance and addiction, which hindered its conventional applications as a drug. Although tremendous progress has been made on the mechanisms of morphine, crucial evidence elaborating the neurobiological basis of tolerance and dependence is still lacking. To furt...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9638-9
更新日期:2015-06-01 00:00:00
abstract::Maple syrup urine disease (MSUD) or branched-chain alpha-keto aciduria (BCKA) is an inherited disorder caused by a deficiency of the branched-chain alpha-keto acid dehydrogenase complex (BCKAD) activity. The blockage of this pathway leads to tissue accumulation of the branched-chain amino acids (BCAA) leucine, isoleuc...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-006-9030-5
更新日期:2006-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF01000160
更新日期:1992-09-01 00:00:00
abstract::Methamphetamine (METH) is a highly addictive psycho-stimulant that induces behavioral changes due to high level of METH-induced dopamine in the brain. Nucleus accumbens (NAc) plays an important role in these changes, especially in drug addiction. However, little is known about the underlying molecular mechanisms of ME...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-0061-x
更新日期:2017-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-019-00471-8
更新日期:2019-12-01 00:00:00
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journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF01000244
更新日期:1992-12-01 00:00:00
abstract::The present study analyses the potential role of MTHFR gene polymorphism, folate supplementation and dietary pattern among the mothers of NTD neonates and controls in heterogeneous populations of North India, with the special focus on their ethnic labels. Results indicated significant increased risk for neural tube de...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-011-9256-8
更新日期:2011-09-01 00:00:00