Developmentally Regulated Expression of HDNF/NT‐3 mRNA in Rat Spinal Cord Motoneurons and Expression of BDNF mRNA in Embryonic Dorsal Root Ganglion

Ernfors, Patrik; Persson, Håkan

doi:10.1111/j.1460-9568.1991.tb00031.x

Cited by 138 publications

(57 citation statements)

References 65 publications

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“…N T-3 is retrogradely transported by large, myelinated mechanoceptive and proprioceptive fibers to large-diameter cell bodies of the DRG, which do not normally contain peptides and terminate in laminae III-V I of the spinal cord (DiStefano et al, 1992;Koliatsos et al, 1993). mRNA for NT-3 has been localized in rat muscle and motor neurones (Ernfors and Persson, 1991). NT-3 binding sites have been shown to be present throughout the rat spinal cord (Zhou and Rush, 1994), and immunoreactivity for the NT-3 receptor, trkC, has also been reported in the superficial dorsal horn of the monkey spinal cord (Ardvisson et al, 1994).…”

mentioning

confidence: 99%

Nerve Growth Factor- and Neurotrophin-3-Induced Changes in Nociceptive Threshold and the Release of Substance P from the Rat Isolated Spinal Cord

et al. 1997

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Acute superfusion of nerve growth factor (NGF; 1-100 ng/ml) through a naive rat spinal cord preparation did not alter basal or electrically evoked release of substance P-like immunoreactivity (SP-LI). In contrast, neurotrophin-3 (NT-3; 1-100 ng/ml), although not modifying SP-LI basal outflow, dose-dependently inhibited the electrically evoked, but not capsaicin (10 nM)-induced, release of the peptide. This NT-3 (10 ng/ml)-induced inhibition persisted even in the presence of 100 ng/ml NGF in the perfusion fluid and was still significant when the evoked release of SP-LI was enhanced by a prolonged in vivo treatment with NGF. Co-superfusion with naloxone (0.1 M), but not CGP 36742 (100 M), a GABA B antagonist, prevented NT-3 (10 ng/ ml) inhibition of SP-LI release. Basal and electrically evoked release of SP-LI from the rat spinal cord in vitro was not modified 24 hr after single systemic injection of either NGF (1 mg/kg) or NT-3 (10 mg/kg). At these time intervals from administration, NGF had induced thermal and mechanical hyperalgesia in the rat hindpaw, and NT-3 had induced mechanical, but not thermal, hypoalgesia. NT-3 administered six times over a 2 week period (at 1 mg/kg) did not alter thermal threshold but significantly reduced electrically evoked release of SP-LI from the spinal cord. An identical treatment regimen with 1 mg/kg NGF induced a significant increase in evoked release of SP-LI. However, this was not associated with a significant hyperalgesia. Although finding that NGF-induced hyperalgesia does not clearly correlate with changes in the release of SP-LI in the spinal cord, this study shows that NT-3 is an inhibitor of SP-LI release and suggests that this mechanism may be responsible for NT-3-induced antinociception.

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confidence: 99%

Nerve Growth Factor- and Neurotrophin-3-Induced Changes in Nociceptive Threshold and the Release of Substance P from the Rat Isolated Spinal Cord

et al. 1997

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“…The neurotrophic factor Ntf3 is specifically and strongly expressed in the motoneuron column of the embryonic spinal cord (Fig. 4A,C) (Ernfors and Persson, 1991). As Ntf3 expression was not observed in the ventral spinal cord of Olig2 KO mice, we analyzed the role of motoneuron-derived Ntf3 on sensory neuron development by generating Ntf3 cKO mice.…”

Section: Discussionmentioning

confidence: 99%

“…focused on Ntf3, because it is specifically and strongly expressed in the motor column within the ventral spinal cord of heterozygote embryos at E10.5 and E13.5 (Fig. 4A,C) (Ernfors and Persson, 1991;Fariñas et al, 1996) and Ntf3 expression in the Olig2 KO spinal cord is below detection level (Fig. 4B,D).…”

Section: Motoneuron-derived Ntf3 Is An Important Factor For Sensory Nmentioning

confidence: 99%

“…Here, we report abnormal phenotypes in the sensory neurons of Olig2 KO mice: first, the decreased number of sensory neurons and the increased number of apoptotic cells in the DRG; and second, the abnormal axonal projection of central and peripheral branches of DRG neurons. The neurotrophic factor neurotrophin 3 (Ntf3; previously NT-3) is specifically and strongly expressed in the motoneuron column of the embryonic spinal cord (Ernfors and Persson, 1991). As Ntf3 is not expressed in the ventral spinal cord of Olig2 KO embryos, we investigated the role of motoneuron-derived Ntf3 in suppression of apoptosis and in proper axonal projection of sensory neurons during development.…”

Section: Introductionmentioning

confidence: 99%

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Role of motoneuron-derived neurotrophin 3 in survival and axonal projection of sensory neurons during neural circuit formation

et al. 2012

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SUMMARYSensory neurons possess the central and peripheral branches and they form unique spinal neural circuits with motoneurons during development. Peripheral branches of sensory axons fasciculate with the motor axons that extend toward the peripheral muscles from the central nervous system (CNS), whereas the central branches of proprioceptive sensory neurons directly innervate motoneurons. Although anatomically well documented, the molecular mechanism underlying sensory-motor interaction during neural circuit formation is not fully understood. To investigate the role of motoneuron on sensory neuron development, we analyzed sensory neuron phenotypes in the dorsal root ganglia (DRG) of Olig2 knockout (KO) mouse embryos, which lack motoneurons. We found an increased number of apoptotic cells in the DRG of Olig2 KO embryos at embryonic day (E) 10.5. Furthermore, abnormal axonal projections of sensory neurons were observed in both the peripheral branches at E10.5 and central branches at E15.5. To understand the motoneuron-derived factor that regulates sensory neuron development, we focused on neurotrophin 3 (Ntf3; NT-3), because Ntf3 and its receptors (Trk) are strongly expressed in motoneurons and sensory neurons, respectively. The significance of motoneuron-derived Ntf3 was analyzed using Ntf3 conditional knockout (cKO) embryos, in which we observed increased apoptosis and abnormal projection of the central branch innervating motoneuron, the phenotypes being apparently comparable with that of Olig2 KO embryos. Taken together, we show that the motoneuron is a functional source of Ntf3 and motoneuron-derived Ntf3 is an essential pre-target neurotrophin for survival and axonal projection of sensory neurons.

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“…Recently, it has been reported by the same group that NT-3 mRNA is expressed by spinal motoneurons during embryonic development [26]. Highest levels were found from embryonic days [13][14][15][16].…”

Section: The Nerve-growth-factor Gene Family: Unresolved Functions Fomentioning

confidence: 99%

Workshop on Trophic Factors in the Peripheral Nervous System. Capri, October 1991

Sendtner

Kreutzberg²,

Jennekens³

1992

Neuromuscular Disorders

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Developmentally Regulated Expression of HDNF/NT‐3 mRNA in Rat Spinal Cord Motoneurons and Expression of BDNF mRNA in Embryonic Dorsal Root Ganglion

Cited by 138 publications

References 65 publications

Nerve Growth Factor- and Neurotrophin-3-Induced Changes in Nociceptive Threshold and the Release of Substance P from the Rat Isolated Spinal Cord

Nerve Growth Factor- and Neurotrophin-3-Induced Changes in Nociceptive Threshold and the Release of Substance P from the Rat Isolated Spinal Cord

Role of motoneuron-derived neurotrophin 3 in survival and axonal projection of sensory neurons during neural circuit formation

Workshop on Trophic Factors in the Peripheral Nervous System. Capri, October 1991

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