A single pulse of nerve growth factor triggers long-term neuronal excitability through sodium channel gene induction

Toledo‐Aral, Juan José; Brehm, Paul; Halegoua, Simon; Mandel, Gail

doi:10.1016/0896-6273(95)90317-8

Cited by 158 publications

(122 citation statements)

References 30 publications

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“…Studying action potential firing in transfected neurons can only be undertaken after 424 h in culture to allow adequate expression of recombinant channels. We found that supplementing the culture media with nerve growth factor (NGF) and glial cell-line-derived neurotrophic factor (GDNF) (see Experimental Design) was necessary to reproducibly record action potentials in transfected DRG neurons, which is consistent with the published data that NGF and GDNF are necessary to maintain the expression of Na v 1.8 and Na v 1.9 channels in cultured DRG neurons 16,17 , and NGF also regulates the expression of Na v 1.7 channel 32,33 .…”

Section: Box 1 | Glossarysupporting

confidence: 78%

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

et al. 2009

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We provide here detailed electrophysiological protocols to study voltage-gated sodium channels and to investigate how wild-type and mutant channels influence firing properties of transfected mammalian dorsal root ganglion (DRG) neurons. Whole-cell voltage-clamp recordings permit us to analyze kinetic and voltage-dependence properties of ion channels and to determine the effect and mode of action of pharmaceuticals on specific channel isoforms. They also permit us to analyze the role of individual sodium channels and their mutant derivatives in regulating firing of DRG neurons. Five to ten cells can be recorded daily, depending on the extent of analysis that is required. Because of different internal solutions that are used in voltage-clamp and current-clamp recordings, only limited information can be obtained from recording the same neuron in both modes. These electrophysiological studies help to elucidate the role of specific channels in setting threshold and suprathreshold responses of neurons, under normal and pathological conditions.

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Section: Box 1 | Glossarysupporting

confidence: 78%

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

et al. 2009

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“…We cannot comment, on the basis of the present results, on the mechanisms that determine whether a given axon will express Na v 1.6 or Na v 1.2; neurotrophic factors play a role in regulating neuronal sodiumchannel expression (54)(55)(56), but other factors may also be involved. Irrespective of this, our results provide a demonstration of molecular plasticity along demyelinated axons in the human CNS in MS, in which the pattern of sodium-channel expression is altered compared with normal myelinated axons.…”

Section: Discussionmentioning

confidence: 76%

Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Na _v 1.2 and Na _v 1.6 sodium channels and Na ⁺ /Ca ² + exchanger

Craner

Newcombe

Black

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

423

305

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Although voltage-gated sodium channels are known to be deployed along experimentally demyelinated axons, the molecular identities of the sodium channels expressed along axons in human demyelinating diseases such as multiple sclerosis (MS) have not been determined. Here we demonstrate changes in the expression of sodium channels in demyelinated axons in MS, with Nav1.6 confined to nodes of Ranvier in controls but with diffuse distribution of Nav1.2 and Nav1.6 along extensive regions of demyelinated axons within acute MS plaques. Using triple-labeled fluorescent immunocytochemistry, we also show that Nav1.6, which is known to produce a persistent sodium current, and the Na ؉ ͞Ca 2؉ exchanger, which can be driven by persistent sodium current to import damaging levels of calcium into axons, are colocalized with ␤-amyloid precursor protein, a marker of axonal injury, in acute MS lesions. Our results demonstrate the molecular identities of the sodium channels expressed along demyelinated and degenerating axons in MS and suggest that coexpression of Nav1.6 and Na ؉ ͞Ca 2؉ exchanger is associated with axonal degeneration in MS.demyelinating diseases ͉ action potential conduction ͉ axonal degeneration

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“…Induction of the expression of ion channels, which are closely associated with the transmitter release, by neurotrophins have also been reported (Mandel eta!., 1988;Toledo-Aral et al, 1995). Thus, there is a possibility that the induction of ion channels by BDNF in this culture system may also play important roles in up-regulation of regulated release.…”

Section: Discussionmentioning

confidence: 87%

Brain‐Derived Neurotrophic Factor Increases the Stimulation‐Evoked Release of Glutamate and the Levels of Exocytosis‐Associated Proteins in Cultured Cortical Neurons from Embryonic Rats

Takei

Sasaoka

Inoue

et al. 1997

Journal of Neurochemistry

143

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Differentiation and survival of neurons induced by neurotrophins have been widely investigated, but little has been reported about the long-term effect of brainderived neurotrophic factor (BDNF) on synaptic transmission. Among many steps of neurotransmission, one important step is regulated release of transmitters. Therefore, the release of glutamate and GABA from cortical neurons cultured for several days with or without BDNF was measured by an HPLC-fluorescence method. Although BDNF had little effect on the basal release of glutamate, high K + -evoked release was greatly increased by BDNF. BDNF also tended to increase evoked release of GABA. Recently, several proteins involved in the step of "regulated release" have been identified. Thus, the effect of BDNF on the levels of these proteins was then investigated. Neurons were cultivated with or without BDNF, collected, and electrophoresed for western blotting. BDNF increased levels of synaptotagmin, synaptobrevin, synaptophysin, and rab3A, which were known as vesicle protein. Levels of syntaxin, SNAP-25, and /3-SNAP were also increased by BDNF. In addition, the numbers of cored and clear vesicles in nerve terminals or varicosities were also increased by BDNF. These results raise the possibility that BDNF increases regulated release of neurotransmitters through the up-regulation of secretory mechanisms. Key Words: Brain-derived neurotrophic factor-Neurotrophin-3-Neurotrophin-Exocytosis-Synaptic vesicle-Transmitter release.

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A single pulse of nerve growth factor triggers long-term neuronal excitability through sodium channel gene induction

Cited by 158 publications

References 30 publications

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Na _v 1.2 and Na _v 1.6 sodium channels and Na ⁺ /Ca ² + exchanger

Brain‐Derived Neurotrophic Factor Increases the Stimulation‐Evoked Release of Glutamate and the Levels of Exocytosis‐Associated Proteins in Cultured Cortical Neurons from Embryonic Rats

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A single pulse of nerve growth factor triggers long-term neuronal excitability through sodium channel gene induction

Cited by 158 publications

References 30 publications

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Voltage-clamp and current-clamp recordings from mammalian DRG neurons

Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Na v 1.2 and Na v 1.6 sodium channels and Na + /Ca 2 + exchanger

Brain‐Derived Neurotrophic Factor Increases the Stimulation‐Evoked Release of Glutamate and the Levels of Exocytosis‐Associated Proteins in Cultured Cortical Neurons from Embryonic Rats

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Molecular changes in neurons in multiple sclerosis: Altered axonal expression of Na _v 1.2 and Na _v 1.6 sodium channels and Na ⁺ /Ca ² + exchanger