Distribution of neuronal receptors for nerve growth factor in the rat

Richardson, P. M.; Issa, V. M. K.; Riopelle, R. J.

doi:10.1523/jneurosci.06-08-02312.1986

Cited by 387 publications

(153 citation statements)

References 42 publications

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“…Similar findings were obtained when NGF receptors were visualized using iodinated NGF in receptor autoradiography (Richardson et al, 1986;Raivich and Kreutzberg, 1987). Direct evidence for the exclusive localization of NGF-R molecules in cholinergic neurons was obtained in the human brain where NGF-R and AChE were found to be located within the same cells .…”

Section: Selectivity For Cholinergic Neuronssupporting

confidence: 70%

“…The fact that NGF is synthesized by target tissues of forebrain cholinergic neurons (Korsching et al, 1985;Goedert et al, 1986;Shelton and Reichardt, 1986;Whittemore et al, 1986) and the selective localization of NGF-R on cholinergic neurons Richardson et al, 1986;Hefti and Mash, 1988;Raivich and Kreutzberg, 1987;Springer et al, 1987) strongly suggest that NGF is involved in the function of these neurons in the adult brain. However, such a physiological role has not been clearly established since its unequivocal demonstration would require "removal" of NGF from the brain.…”

Section: Physiological Role Of Ngf In the Adult Brainmentioning

confidence: 99%

“…Levels of NGF and mRNANGF in the adult striatum are very low compared with hippocampal and cortical levels (Korsching et al, 1985;Shelton and Reichardt, 1986;Whittemore et al, 1986). Raivich and Kreutzberg (1987) and Richardson et al (1986) reported visualization of NGF-R in the striatum by receptor autoradiography. However, immunohistochemical procedures using 2 different antibodies failed to visualize NGF-R in both rat and human striatum Hefti and Mash, 1987;Montero and Hefti, unpublished observations).…”

Section: Physiological Role Of Ngf In the Adult Brainmentioning

confidence: 99%

“…In adult rats, levels of NGF mRNANGF correlate with the anatomical distribution of basal forebrain cholinergic neurons (Crutcher and Collins, 1982;Korsching et al, 1985;Goedert et al, 1986;Shelton and Reichardt, 1986;Whittemore et al, 1986). NGF receptors (NGF-R) were demonstrated in the adult brain by crosslinking iodinated NGF (Taniuchi et al, 1986b) and were visualized on forebrain cholinergic neurons in rat and human brains using autoradiographic and immunohistochemical techniques Richardson et al, 1986;Raivich and Kreutzberg, 1987;Springer et al, 1987). These receptors mediate internalization and retrograde transport of NGF by cholinergic neurons (Schwab et al, 1979;Seiler and Schwab, 1984).…”

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Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment

Hefti

1988

J. Neurosci.

205

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We earlier reported that chronic intraventricular injections of NGF into adult rats with partial transection of the fimbria prevent the lesion-induced disappearance of cholinergic neurons in the medial septal nucleus and the diagonal band of Broca (Hefti, 1986). The present study assessed the specificity and treatment requirements of this effect of NGF. Immunohistochemical visualization of NGF receptors (NGF-R) revealed that these molecules are selectively located in forebrain cholinergic neurons of unlesioned brains. Fimbrial transection resulted in transient accumulation of NGF-R in proximal stumps of lesioned axons but failed to induce the expression of NGF-R by other cells in the septal area or near the lesion. Two to three weeks after lesioning, the number of septal neurons expressing NGF-R was reduced by approximately 50% in parallel with the reduction of the number of neurons expressing cholinergic marker enzymes. Repeated intraventricular NGF injections during 4 weeks prevented the disappearance of these cells. Fimbrial transections also reduced the number of septal GABAergic neurons visualized by glutamate decarboxylase immunohistochemistry. The loss of GABAergic neurons was not prevented by NGF. These findings suggest that NGF prevents the lesion-induced degeneration of cholinergic neurons by directly acting on NGF-R expressed by cholinergic cells and that NGF does not affect any neuron with an axonal lesion. Delayed start of the NGF treatment failed to prevent the disappearance of lesioned cholinergic neurons, providing evidence that NGF treatment indeed promotes the survival of these cells rather than simply upregulating the expression of transmitter-specific enzymes. A single injection of NGF at the time of the lesion was not sufficient to prevent the lesion-induced degeneration of cholinergic neurons. Furthermore, termination of chronic NGF treatment after 4 weeks was followed by loss of septal cholinergic neurons after an additional 4 weeks. These findings suggest that the continuous presence of NGF during more than 4 weeks is required to prevent the degeneration of cholinergic cells. The data are discussed in the context of a possible physiological role of NGF in the function of adult forebrain cholinergic neurons.

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Section: Selectivity For Cholinergic Neuronssupporting

confidence: 70%

Section: Physiological Role Of Ngf In the Adult Brainmentioning

confidence: 99%

Section: Physiological Role Of Ngf In the Adult Brainmentioning

confidence: 99%

mentioning

confidence: 99%

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Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment

Hefti

1988

J. Neurosci.

205

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“…In contrast to nodose neurons in chick, which do not have high-affinity NGF receptors (Lindsay andRohrer, 1986) Mandelzys et al (1990) showed that neonatal rat nodose neurons express high-affinity NGF receptors in culture in the absence of satellite cells, and Richardson et al (1986) showed that, in adult rat, some nodose neurons have high-affinity NGF receptor. As it has been recently shown that the proto-oncogene product trk is involved in high-affinity NGF binding (Kaplan et al,199 l), one might expect that nodose neurons in rodents express trk mRNA.…”

Section: Discussionmentioning

confidence: 99%

NGF induces neonatal rat sensory neurons to extend dendrites in culture after removal of satellite cells

1993

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Vertebrate sensory neurons have a pseudo-unipolar morphology; their somata are covered by satellite cells and lack dendrites or synaptic contacts. However, when neonatal rat sensory neurons from the nodose ganglia develop in culture in absence of satellite cells and with NGF, they form synapses among themselves. In this study, we investigated whether neonatal rat nodose neurons express dendrites under the same culture conditions. We show by Lucifer yellow injection that nodose neurons remain typically unipolar when cocultured with their ganglionic satellite cells. However, when these neurons are cultured without satellite cells, virtually all neurons acquire a multipolar morphology. Moreover, when NGF is added to satellite cell-free cultures, several neurons extend dendrites; these processes stain positively for microtubule-associated protein-2. NGF induces a 17-fold increase in dendritic outgrowth after 3 weeks but has little effect on axon number. In addition, we find that the ability of nodose neurons to extend dendrites is developmentally regulated. Furthermore, in a combined morphological and electrophysiological study, using whole-cell voltage- clamp technique with Lucifer yellow in the recording solution, we demonstrate a positive correlation between the extent of dendritic outgrowth and the density of ACh currents, suggesting that these dendrites have ACh receptors. Our results indicate that neonatal rat nodose neurons are capable of extending dendrites and that extrinsic factors can induce or suppress their extension. In addition, the results suggest that these dendrites may act as principal post-synaptic structures for synapse formation that occurs in these cultures.

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Phenotype of intraadrenal ganglion neurons during postnatal development in rat

1996

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The postnatal development of intraadrenal ganglion neurons was studied in rat by using indirect immunohistochemistry and in situ hybridization. The large neuropeptide tyrosine (NPY)-expressing ganglion neurons (type I ganglion neurons) matured postnatally, with marked increases in acetylcholinesterase (AChE)-, neurofilament 10 (NF10)-, and tyrosine hydroxylase (TH)-like immunoreactivities (LIs) paralleled by increasing levels of mRNAs encoding NPY, low-affinity neurotrophin receptor (LANR), and tropomyosin kinase receptor (trk). The smaller vasoactive intestinal polypeptide (VIP)-immunoreactive (IR) ganglion neurons (type II ganglion neurons) expressed increasing levels of VIP mRNA postnatally and also contained immunoreactive nitric oxide synthase (NOS) and its mRNA. These type II ganglion neurons appeared to be relatively mature already at postnatal day (P2) and did not express detectable levels of LANR or trk mRNAs. The cell size of both the type I and type II ganglion neurons increased about 2.5-fold postnatally. The type I ganglion neurons formed more densely packed clusters with increasing age, whereas the type II ganglion neurons were spread out in small groups or individually, mainly in the peripheral parts of the medulla, and appeared to fulfill their migration into the medulla and/or to the inner regions of the cortex early postnatally, possibly after establishing contact with their cortical targets. We suggest that the type I ganglion neurons represent sympathetic ganglion neurons of the same origin as the chromaffin cells and that they mature mainly postnatally. The development of the type II (VIP/NOS) ganglion neurons takes place earlier; however, their phenotype remains more uncertain.

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Distribution of neuronal receptors for nerve growth factor in the rat

Cited by 387 publications

References 42 publications

Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment

Rescue of lesioned septal cholinergic neurons by nerve growth factor: specificity and requirement for chronic treatment

NGF induces neonatal rat sensory neurons to extend dendrites in culture after removal of satellite cells

Phenotype of intraadrenal ganglion neurons during postnatal development in rat

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