author_facet Naumann, T.
Straube, A.
Frotscher, M.
Naumann, T.
Straube, A.
Frotscher, M.
author Naumann, T.
Straube, A.
Frotscher, M.
spellingShingle Naumann, T.
Straube, A.
Frotscher, M.
European Journal of Neuroscience
Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
General Neuroscience
author_sort naumann, t.
spelling Naumann, T. Straube, A. Frotscher, M. 0953-816X 1460-9568 Wiley General Neuroscience http://dx.doi.org/10.1111/j.1460-9568.1997.tb01488.x <jats:title>Abstract</jats:title><jats:p>Previous studies have suggested that target‐derived nerve growth factor (NGF) is essential for the survival of cholinergic basal forebrain neurons. Thus, axotomy of septohippocampal neurons in adult rats resulting in the withdrawal of target‐derived NGF caused a dramatic loss of choline acetyltransferase (ChAT)‐immunoreactive neurons in the medial septum‐diagonal band complex. We have recently shown that this loss of immunolabelled neurons does not indicate cell death, since many septohippocampal cholinergic neurons recover their immunoreactivity for ChAT after a long survival time despite disconnection from target‐derived neurotrophins. One possibility would be that these surviving ChAT‐immunoreactive neurons have gained access to other, probably local, NGF sources. Here we provide evidence that the recovery of ChAT immunoreactivity after axotomy is not accompanied by a similar recovery of NGF receptor expression in these neurons. <jats:italic>In situ</jats:italic> hybridization for p75<jats:sup>NTR</jats:sup> mRNA and trkA mRNA 6 months after bilateral fimbria‐fornix transection revealed a substantial loss of labelled cells. In addition, there was a persisting loss of p75<jats:sup>NTR</jats:sup>‐immunoreactive and NGF‐immunoreactive medial septal neurons. Cholinergic neurons in controls did not express NGF mRNA, but were heavily immunostained for NGF protein due to receptor‐mediated uptake. These data suggest that at least some cholinergic septohippocampal neurons re‐express ChAT either independently of NGF or with a reduced need for NGF.</jats:p> Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression European Journal of Neuroscience
doi_str_mv 10.1111/j.1460-9568.1997.tb01488.x
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series European Journal of Neuroscience
source_id 49
title Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_unstemmed Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_full Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_fullStr Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_full_unstemmed Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_short Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_sort recovery of chat lmmunoreactivity in axotomized rat cholinergic septal neurons despite reduced ngf receptor expression
topic General Neuroscience
url http://dx.doi.org/10.1111/j.1460-9568.1997.tb01488.x
publishDate 1997
physical 1340-1349
description <jats:title>Abstract</jats:title><jats:p>Previous studies have suggested that target‐derived nerve growth factor (NGF) is essential for the survival of cholinergic basal forebrain neurons. Thus, axotomy of septohippocampal neurons in adult rats resulting in the withdrawal of target‐derived NGF caused a dramatic loss of choline acetyltransferase (ChAT)‐immunoreactive neurons in the medial septum‐diagonal band complex. We have recently shown that this loss of immunolabelled neurons does not indicate cell death, since many septohippocampal cholinergic neurons recover their immunoreactivity for ChAT after a long survival time despite disconnection from target‐derived neurotrophins. One possibility would be that these surviving ChAT‐immunoreactive neurons have gained access to other, probably local, NGF sources. Here we provide evidence that the recovery of ChAT immunoreactivity after axotomy is not accompanied by a similar recovery of NGF receptor expression in these neurons. <jats:italic>In situ</jats:italic> hybridization for p75<jats:sup>NTR</jats:sup> mRNA and trkA mRNA 6 months after bilateral fimbria‐fornix transection revealed a substantial loss of labelled cells. In addition, there was a persisting loss of p75<jats:sup>NTR</jats:sup>‐immunoreactive and NGF‐immunoreactive medial septal neurons. Cholinergic neurons in controls did not express NGF mRNA, but were heavily immunostained for NGF protein due to receptor‐mediated uptake. These data suggest that at least some cholinergic septohippocampal neurons re‐express ChAT either independently of NGF or with a reduced need for NGF.</jats:p>
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author Naumann, T., Straube, A., Frotscher, M.
author_facet Naumann, T., Straube, A., Frotscher, M., Naumann, T., Straube, A., Frotscher, M.
author_sort naumann, t.
container_issue 7
container_start_page 1340
container_title European Journal of Neuroscience
container_volume 9
description <jats:title>Abstract</jats:title><jats:p>Previous studies have suggested that target‐derived nerve growth factor (NGF) is essential for the survival of cholinergic basal forebrain neurons. Thus, axotomy of septohippocampal neurons in adult rats resulting in the withdrawal of target‐derived NGF caused a dramatic loss of choline acetyltransferase (ChAT)‐immunoreactive neurons in the medial septum‐diagonal band complex. We have recently shown that this loss of immunolabelled neurons does not indicate cell death, since many septohippocampal cholinergic neurons recover their immunoreactivity for ChAT after a long survival time despite disconnection from target‐derived neurotrophins. One possibility would be that these surviving ChAT‐immunoreactive neurons have gained access to other, probably local, NGF sources. Here we provide evidence that the recovery of ChAT immunoreactivity after axotomy is not accompanied by a similar recovery of NGF receptor expression in these neurons. <jats:italic>In situ</jats:italic> hybridization for p75<jats:sup>NTR</jats:sup> mRNA and trkA mRNA 6 months after bilateral fimbria‐fornix transection revealed a substantial loss of labelled cells. In addition, there was a persisting loss of p75<jats:sup>NTR</jats:sup>‐immunoreactive and NGF‐immunoreactive medial septal neurons. Cholinergic neurons in controls did not express NGF mRNA, but were heavily immunostained for NGF protein due to receptor‐mediated uptake. These data suggest that at least some cholinergic septohippocampal neurons re‐express ChAT either independently of NGF or with a reduced need for NGF.</jats:p>
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spelling Naumann, T. Straube, A. Frotscher, M. 0953-816X 1460-9568 Wiley General Neuroscience http://dx.doi.org/10.1111/j.1460-9568.1997.tb01488.x <jats:title>Abstract</jats:title><jats:p>Previous studies have suggested that target‐derived nerve growth factor (NGF) is essential for the survival of cholinergic basal forebrain neurons. Thus, axotomy of septohippocampal neurons in adult rats resulting in the withdrawal of target‐derived NGF caused a dramatic loss of choline acetyltransferase (ChAT)‐immunoreactive neurons in the medial septum‐diagonal band complex. We have recently shown that this loss of immunolabelled neurons does not indicate cell death, since many septohippocampal cholinergic neurons recover their immunoreactivity for ChAT after a long survival time despite disconnection from target‐derived neurotrophins. One possibility would be that these surviving ChAT‐immunoreactive neurons have gained access to other, probably local, NGF sources. Here we provide evidence that the recovery of ChAT immunoreactivity after axotomy is not accompanied by a similar recovery of NGF receptor expression in these neurons. <jats:italic>In situ</jats:italic> hybridization for p75<jats:sup>NTR</jats:sup> mRNA and trkA mRNA 6 months after bilateral fimbria‐fornix transection revealed a substantial loss of labelled cells. In addition, there was a persisting loss of p75<jats:sup>NTR</jats:sup>‐immunoreactive and NGF‐immunoreactive medial septal neurons. Cholinergic neurons in controls did not express NGF mRNA, but were heavily immunostained for NGF protein due to receptor‐mediated uptake. These data suggest that at least some cholinergic septohippocampal neurons re‐express ChAT either independently of NGF or with a reduced need for NGF.</jats:p> Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression European Journal of Neuroscience
spellingShingle Naumann, T., Straube, A., Frotscher, M., European Journal of Neuroscience, Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression, General Neuroscience
title Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_full Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_fullStr Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_full_unstemmed Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_short Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
title_sort recovery of chat lmmunoreactivity in axotomized rat cholinergic septal neurons despite reduced ngf receptor expression
title_unstemmed Recovery of ChAT lmmunoreactivity in Axotomized Rat Cholinergic Septal Neurons Despite Reduced NGF Receptor Expression
topic General Neuroscience
url http://dx.doi.org/10.1111/j.1460-9568.1997.tb01488.x