Age-related changes in levels of brain-derived neurotrophic factor in selected brain regions of rats, normal mice and senescence-accelerated mice: a comparison to those of nerve growth factor and neurotrophin-3

Katoh‐Semba, Ritsuko; Semba, Reiji; Takeuchi, Ikuo; Kato, Kanefusa

doi:10.1016/s0168-0102(98)00040-6

Cited by 155 publications

(108 citation statements)

References 40 publications

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“…The presence of NT-3 mRNA has been a point of contention. Some earlier studies have failed to locate NT-3 mRNA in the olfactory bulb [14,26] yet others have detected NT-3 protein by ELISA [29]. Taken together with the results of this study, it is clear that NT-3 is indeed expressed in the olfactory bulb.…”

Section: Discussionsupporting

confidence: 76%

Cultured olfactory ensheathing cells express nerve growth factor, brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor and their receptors

Woodhall

West

Chuah

2001

Molecular Brain Research

307

209

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In the primary olfactory pathway axons of olfactory neurons (ONs) are accompanied by ensheathing cells (ECs) as the fibres course towards the olfactory bulb. Ensheathing cells are thought to play an important role in promoting and guiding olfactory axons to their appropriate target. In recent years, studies have shown that transplants of ECs into lesions in the central nervous system (CNS) are able to stimulate the growth ofaxons and in some cases restore functional connections. In an attempt to identify a possible mechanism underlying EC support for olfactory nerve growth and CNS axonal regeneration, this study investigated the production of growth factors and expression of corresponding receptors by these cells. Three techniques immunohistochemistry, enzyme linked immunosorbent assay (ELISA) and reverse transcriptase-polymerase chain reaction (RT-PCR) were used to assess growth factor expression in cultured ECs. Immunohistochemistry showed that ECs expressed nerve growth factor (NGF), brain derived neurotrophic factor (BDNF) and glial cell-line derived neurotrophic factor (GDNF). ELISA confirmed the intracellular presence of NGF and BDNF and showed that, compared to BDNF, about seven times as much NGF was secreted by ECs. RT-PCR analysis demonstrated expression of mRNA for NGF, BDNF, GDNF and neurturin (NTN). In addition, ECs also expressed the receptors trkB, GFRa-1 and GFRa-2. The results of the experiments show that ECs express a number of growth factors and that BDNF in particular could act both in a paracrine and autocrine manner.

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Section: Discussionsupporting

confidence: 76%

Cultured olfactory ensheathing cells express nerve growth factor, brain-derived neurotrophic factor, glia cell line-derived neurotrophic factor and their receptors

Woodhall

West

Chuah

2001

Molecular Brain Research

307

209

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“…Also the loss of contrast sensitivity in amblyopia 5,47 is reminiscent of our observations in TrkB.T1-EGFP transgenic mice. Interestingly, reduction of TrkB/BDNF-signaling 7,8,9 and reduced synaptic strength 48 have also been observed under these conditions and may thus have a causal role. This suggests that the search for therapeutic strategies for these deficiencies should include strategies that increase TrkB/BDNF signaling in the visual cortex.…”

Section: Normalization Model Reliably Matches Experimental Datamentioning

confidence: 91%

“…It is believed to be caused by deficient processing in the visual cortex 5 , but the mechanisms underlying the dissociations of retinal and cortical acuity in amblyopia and in the healthy aging and developing brain are unclear. Interestingly, there is a good match between changes in the cortical expression level of brain-derived neurotrophic factor (BDNF) and changes in visual acuity.During development, acuity and BDNF levels rise 6 , while both slowly decrease with age 4,7 . This relationship between BDNF and acuity also holds for experimentally induced amblyopia.…”

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confidence: 99%

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Contrast gain control and cortical TrkB signaling shape visual acuity

Heimel¹,

Saiepour²,

Chakravarthy³

et al. 2010

Nat Neurosci

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2The limits of visual acuity and contrast sensitivity are set by the eye, but what we perceive is determined by the visual cortex 1 . In healthy, mature people and animals, the visual acuities of the retina and the cortex are well-matched 2 , but this match is neither automatic nor unbreakable. Differences between cortical and retinal acuity are most apparent during development, when cortical acuity continues to rise after retinal development is completed 3 , and during aging, when behavioral acuity falls even without obvious changes in the eye or the thalamus 4 . Differences also occur as a result of cortical injury or erroneous development. This is the case with amblyopia, the most prevalent (2-4%) visual impairment in young people. Amblyopia is a reduced psychophysical acuity in one or both eyes. It is believed to be caused by deficient processing in the visual cortex 5 , but the mechanisms underlying the dissociations of retinal and cortical acuity in amblyopia and in the healthy aging and developing brain are unclear. Interestingly, there is a good match between changes in the cortical expression level of brain-derived neurotrophic factor (BDNF) and changes in visual acuity.During development, acuity and BDNF levels rise 6 , while both slowly decrease with age 4,7 . This relationship between BDNF and acuity also holds for experimentally induced amblyopia. BDNF mRNA and protein levels 8,9 and acuity 10 in the primary visual cortex (V1) responding to a monocularly deprived eye are all below normal. In amblyopic rats receiving environmental enrichment 11 or antidepressant treatment 12 , increased BDNF expression in the cortex was seen in parallel to the restoration of visual acuity. Moreover, transgenic mice overexpressing BDNF in the forebrain show a faster rise of cortical acuity 6 even when reared in darkness 13 . Although there is a wealth of data on the involvement of BDNF and its main receptor TrkB in neuronal development 14 , synaptic efficacy 15 , -morphology 16 and -plasticity 17,18 , it has remained unknown how BDNF promotes visual acuity at the coding level and whether BDNF signaling plays a role in acuity in the mature cortex. For these reasons we studied visual acuity in adult transgenic mice where, after normal development is completed, cortical TrkB/BDNF signaling is impaired. We found a loss of acuity, caused by a reduction in apparent contrast. Using a combination of experiments and modeling, we show the involvement of cortical gain control in the selective loss of responses to visual stimuli with high spatial frequencies and the maintenance of responses to low spatial frequencies. RESULTS Genetic inhibition of TrkB signaling in the adult cortexTo investigate the role of TrkB signaling in cortical acuity in the mature animal we overexpressed a dominant negative TrkB.T1-EGFP fusion protein 19 in a large proportion of pyramidal cells after the maturation of cortical acuity. This was achieved by crossing mice carrying a Cre-dependent TrkB.T1-EGFP-transgene under the control of the Thy-1 promoter ...

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“…The blockade of the glutamate receptors and/or stimulation of the GABAergic system reduces NGF mRNAs in hippocampus and NGF protein in hippocampus and septum [9]. The level of NGF in the nervous system and cerebrospinal fluid has been found to decrease with age [10,11]. During the fetal and early post-natal periods, neurons are NGF-dependent; however, at later stages, they become NGF-sensitive.…”

Section: Nerve Growth Factor and The Nervous Systemmentioning

confidence: 99%