Identification of cells in rat brain and peripheral tissues expressing mRNA for members of the nerve growth factor family

Ernfors, Patrik; Wetmore, Cynthia; Olson, Lar̀s; Persson, Håkan

doi:10.1016/0896-6273(90)90090-3

Cited by 772 publications

(368 citation statements)

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“…Thus, exogenous BDNF appears to be capable of augmenting functional as well as structural aspects of serotonergic neurons. The ability of BDNF to induce the sprouting of intact serotonergic fibers and prevent the PCA-induced loss of 5HT axons is of particular interest, inasmuch as BDNF mRNA levels are particularly abundant in the neocortex (Ernfors et al, 1990). Thus, cortical BDNF levels or trkB receptor activation may regulate the individual susceptibility of serotonergic axons to 5HT neurotoxins such as PCA, MDA, MDMA, and fenfluramine.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain

et al. 1995

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A pathology of brain serotonergic (5-HT) systems has been found in psychiatric disturbances, normal aging and in neurodegenerative disorders including Alzheimer's and Parkinson's disease. Despite the clinical importance of 5-HT, little is known about the endogenous factors that have neurotrophic influences upon 5-HT neurons. The present study examined whether chronic pain parenchymal administration of the neurotrophins brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) or NGF could prevent the severe degenerative loss of serotonergic axons normally caused by the selective 5-HT neurotoxin p-chloroamphetamine (PCA). The neurotrophins (5–12 micrograms/d) or the control substances (cytochrome c or PBS vehicle) were continuously infused into the rat frontoparietal cortex using an osmotic minipump. One week later, rats were subcutaneously administered PCA (10 mg/kg) or vehicle, and the 5-HT innervation was evaluated after two more weeks of neurotrophin infusion. As revealed with 5-HT immunocytochemistry, BDNF infusions into the neocortex of intact (non-PCA-lesioned) rats caused a substantial increase in 5-HT axon density in a 3 mm diameter region surrounding the cannula tip. In PCA-lesioned rats, intracortical infusions of BDNF completely prevented the severe neurotoxin-induced loss of 5-HT axons near the infusion cannula. In contrast, cortical infusions of vehicle or the control protein cytochrome c did not alter the density of serotonergic axons in intact animals, nor did control infusions prevent the loss of 5-HT axons in PCA-treated rats. NT-3 caused only a modest sparing of the 5-HT innervation in PCA-treated rats, and NGF failed to prevent the loss of 5-HT axon density. The immunocytochemical data were supported by neurochemical evaluations which showed that BDNF attenuated the PCA-induced loss of 5-HT and 5- HIAA contents and 3H-5-HT uptake near the infusion cannula. Thus, BDNF can promote the sprouting of mature, uninjured serotonergic axons and dramatically enhance the survival or sprouting of 5-HT axons normally damaged by the serotonergic neurotoxin PCA.

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Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain

et al. 1995

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“…The NTRK2 receptor for NT4 and BDNF is strongly expressed in granulosa cells of primordial and early developing follicles in humans, with some expression in oocytes (Harel et al 2006). NT3 expression has been previously detected in the granulosa cells of growing follicles in rats (Ernfors et al 1990). In humans, and NTRK3 was detected in oocytes (Seifer et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Neurotrophin Nt3 Promotes Ovarian Primordial to Primary Follicle Transition.

Nilsson

Dole²,

Skinner³

2009

Biology of Reproduction

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Neurotrophins are growth factors that are known to have a role in promoting cell survival and differentiation. The focus of the current study is to examine the role of neurotrophins in regulating ovarian primordial follicle development. Ovaries from 4-day old rats were placed into organ culture and cultured for 10 days in the absence or presence of neurotrophin-3 (NT3), brain-derived neurotrophic factor (BDNF), or nerve growth factor (NGF). Treatment of ovaries with NT3 resulted in a significant (P<0.01) increase in primordial follicle development (i.e. primordial to primary follicle transition). Treatment with BDNF at high doses of 100-250 ng/ml also significantly (P<0.01) increased primordial follicle development, but NGF had no effect. Immunohistochemical studies determined that NT3 was present in granulosa cells, interstitial tissue, and in the oocytes of primordial and primary follicles. The NT3 receptor NTRK3 was present in oocytes at all stages of development. Analysis of ovaries that contain predominantly primordial follicles demonstrated the transcripts for NT3, NTRK3, NGF, and the BDNF/ neurotrophin-4 (NT4) receptor NTRK2 are expressed, while BDNF, NT4, and the NGF receptor NTRK1 are not detectable. Inhibition of the NTRK3 receptor with the tyrphostin AG 879 resulted in oocyte death and a significant (P<0.01) reduction in follicle pool size. Inhibition of the NTRK receptors with K252a slowed primordial to primary follicle transition. A microarray analysis demonstrated that a small number of genes were differentially expressed after NT3 treatment. Observations indicate that the neurotrophin NT3, acting through the NTRK3 receptor in oocytes, promotes the primordial to primary follicle transition.

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“…20,21 This neurotrophin plays an important role in regulating the survival and differentiation of selective populations of neurons during development 22,23 and is an important mediator of neuronal adaptive responses. [12][13][14] The expression of BDNF is regulated by neuronal activity, shows marked and transient changes in response to a number of neuronal insults, including ischemia, hypoglycemia, epileptic activity, immobilization stress and trauma 17,[24][25][26][27][28] and its modulation involves a complex interplay between different neurotransmitter systems.…”

Section: Introductionmentioning

confidence: 99%

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

Molteni

Lipska²,

Weinberger³

et al. 2001

Mol Psychiatry

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The neonatal (PND 7) lesion of the ventral hippocampus (VH) with ibotenic acid represents a well-established experimental paradigm that recapitulates many schizophrenia-like phenomena. In order to investigate molecular changes that could contribute to long lasting consequences on brain function, we have investigated the effects of the VH lesion on the expression for the trophic factors FGF-2 and BDNF. We used RNase protection assay to measure their mRNA levels in cortical regions of prepubertal (PND 35) and young adult (PND 56) animals, both under basal condition as well as in response to an acute restraint stress. The expression of BDNF was not altered by the VH lesion in prefrontal (PFC) and frontal cortex (FC) of PND 35 or PND 56 rats. An acute restraint stress at PND 35 produced a significant increase of the neurotrophin expression in PFC of sham as well as lesioned animals. However in young adult animals a significant elevation of BDNF expression was observed only in sham rats. We also found that the VH lesion produced a significant reduction of basal BDNF mRNA levels in the cingulate cortex of young adult, but not prepubertal rats. This effect was not accompanied by changes in the acute modulation of the neurotrophin, which was up-regulated by stress in both experimental groups. Conversely the expression of FGF-2 at PND 35 and PND 56 was not altered by early postnatal VH lesion, and there were no major differences between sham and lesioned animals in response to the acute stress. The changes in trophic factor expression may be relevant for the long-term effects of VH lesion on synaptic plasticity and may determine an increased vulnerability of the brain under challenging situations. Molecular Psychiatry (2001) 6, 285-292.

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Identification of cells in rat brain and peripheral tissues expressing mRNA for members of the nerve growth factor family

Cited by 772 publications

References 50 publications

Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain

Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain

Neurotrophin Nt3 Promotes Ovarian Primordial to Primary Follicle Transition.

Developmental and stress-related changes of neurotrophic factor gene expression in an animal model of schizophrenia

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