BDNF attenuates the effects of intrastriatal injection of 6-hydroxydopamine

Shults, Clifford W.; Kimber, Teresa; Altar, Anthony

doi:10.1097/00001756-199505300-00009

Cited by 82 publications

(11 citation statements)

References 5 publications

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“…27 BDNF prevents the spontaneous death of dopaminergic neurons in rat primary mesencephalic cultures 31,32 and protects TH-immunoreactive neurons from the selective toxin MPP þ (1-methyl-4-phenylpyridinium). 29 Repeated intrastriatal injections of BDNF protect from damage induced by intrastriatal administration of 6-OHDA, 33 with moderate preserving of striatal dopaminergic nerve endings around the injection site. Likewise, direct nigral infusion of BDNF protects against reductions in striatal dopamine content induced by neurotoxins in the mouse.…”

Section: Bdnf Gives Trophic Support To a Variety Of Cns Neuronsmentioning

confidence: 99%

BDNF in schizophrenia, depression and corresponding animal models

2005

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Understanding the etiology and pathogenesis schizophrenia and depression is a major challenge facing psychiatry. One hypothesis is that these disorders are secondary to a malfunction of neurotrophic factors. Inappropriate neurotrophic support during brain development could lead to structural disorganisation in which neuronal networks are established in a nonoptimal manner. Inadequate neurotrophic support in adult individuals could ultimately be an underlying mechanism leading to decreased capacity of brain to adaptive changes and increased vulnerability to neurotoxic damage. Brain-derived neurotrophic factor (BDNF) is a mediator involved in neuronal survival and plasticity of dopaminergic, cholinergic, and serotonergic neurons in the central nervous system (CNS). In this review, we summarize findings regarding altered BDNF in schizophrenia and depression and animal models, as well as the effects of antipsychotic and antidepressive treatments on the expression of BDNF. Molecular Psychiatry (2005) 10, 345-352.

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Section: Bdnf Gives Trophic Support To a Variety Of Cns Neuronsmentioning

confidence: 99%

BDNF in schizophrenia, depression and corresponding animal models

2005

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“…In culture experiments, BDNF has been found to promote the survival and differentiation of mesencephalic DA neurons (Hyman et al, 1991;Feng et al, 1999). In vitro and in vivo, BDNF protects DA neurons from the toxic effects of low levels of the neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6Ј-OHDA (Levivier et al, 1995;Shults et al, 1995;Hung and Lee, 1996; for review, see Murer et al, 2001). BDNF stimulates dopamine activity and turnover in vitro and in vivo and is hypothesized to play a role in the mechanisms that allow the surviving DA neurons in early stage PD patients to compensate for cell losses (Blochl and Sirrenberg, 1996;Murer et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Is Required for the Establishment of the Proper Number of Dopaminergic Neurons in the Substantia Nigra Pars Compacta

Baquet¹,

Bickford²,

Jones³

2005

J. Neurosci.

270

190

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Brain-derived neurotrophic factor (BDNF) has been implicated in regulating neuronal survival, differentiation, and synaptic plasticity. Reduced expression of BDNF within the substantia nigra accompanies the deterioration of dopaminergic neurons in Parkinson's disease (PD) patients. Analysis of the effects of long-term BDNF absence from the CNS has been difficult because of the early postnatal lethality of BDNF Ϫ/Ϫ mice. Mice with a floxed BDNF allele were bred with Wnt1-Cre mice to generate Wnt-BDNF KO mice that lack BDNF from the midbrain-hindbrain (MHB). These mice are viable but exhibit hindlimb clutching and poor rotarod performance. Tyrosine hydroxylase (TH)-positive neuron numbers in the substantia nigra pars compacta (SNC) were estimated using stereological methods, revealing a persistent ϳ23% reduction of these cells at postnatal day 21 (P21) in Wnt-BDNF KO mice compared with controls. The diminishment of TH-expressing neurons was present at birth and continued through P120. This deficit appears selective for the dopaminergic population, because at P21, total neuron number within the SNC, defined as neuronal nuclei protein-positive cells, was not significantly reduced. Interestingly, and similar to observations in PD patients, SNC neuron subpopulations are not equally affected. Calbindin-and calretininexpressing SNC populations show no significant difference between Wnt-BDNF KO mice and controls. Thus, BDNF depletion from the MHB selectively leads to reduced TH expression in a subpopulation of neurons, but it remains unclear whether these cells are lost.

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“…We found that expression of TrkB mRNA (encoded by the Ntrk2 gene), but not Bdnf itself, was significantly reduced in SNpc DA neurons from old animals, although no change in TrkB was observed in the striatum. Previous studies have shown that changes in Bdnf expression or lack of TrkB expression increases the susceptibility of SN DA neurons to cytotoxic injury (Ding et al, 2011;Hung and Lee, 1996;Levivier et al, 1995;Shults et al, 1995;Fletcher-Turner, 2000, 2001). Furthermore, deprivation of Bdnf or TrkB has been shown to exacerbate motor dysfunction and impair DA uptake and neuronal survival in aged animals (Baydyuk et al, 2011;Boger et al, 2011;Porritt et al, 2005;Saylor et al, 2006), suggesting that the combination of ageing and TrkB deprivation are detrimental to SN neuronal survival.…”

Section: Discussionmentioning

confidence: 98%