Literature DB >> 2306615

Basal forebrain cell loss following fimbria/fornix transection.

M H Tuszynski1, D M Armstrong, F H Gage.   

Abstract

Following fimbria/fornix transection, cells in the medial septum appear to undergo retrograde degeneration as shown by Nissl and acetylcholine esterase (AChE) staining. Recent studies using immunocytochemical techniques have also demonstrated loss of choline acetyltransferase (ChAT) and nerve growth factor receptor (NGFr) labeling of neurons in this region. Whether the apparent loss of ChAT- and NGFr-positive neurons is the result of the actual death of these neurons, or is instead a loss of ChAT enzyme or NGFr expression below levels detectable by immunocytochemical methods, remains an unresolved issue. In order to address this question, rhodamine-labeled fluorescent latex microspheres were injected into the hippocampus where they retrogradely transported to the cell bodies of the medial septum. Five days later these animals received either unilateral or bilateral fimbria/fornix lesions and were allowed to survive an additional 4 weeks. Compared to unlesioned control animals, unilaterally lesioned animals showed a 91% loss of fluorescently labeled cells and bilaterally lesioned animals showed a 93% loss. The inability to detect the fluorescent microspheres in the medial septum suggests that the majority of medial septal cells die after fimbria/fornix transection. ChAT and NGFr immunohistochemical staining were also performed. Cells stained for ChAT were reduced in number by 92% in animals with unilateral lesions and by 75% in animals with bilateral lesions, while NGFr-stained cells were reduced in number by 75% in animals with unilateral lesions and by 68% in animals with bilateral lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1990        PMID: 2306615     DOI: 10.1016/0006-8993(90)90402-w

Source DB:  PubMed          Journal:  Brain Res        ISSN: 0006-8993            Impact factor:   3.252


  7 in total

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Review 3.  Maintaining the neuronal phenotype after injury in the adult CNS. Neurotrophic factors, axonal growth substrates, and gene therapy.

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Authors:  C A Lucidi-Phillipi; D O Clary; L F Reichardt; F H Gage
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5.  Functional blockade of tyrosine kinase A in the rat basal forebrain by a novel antagonistic anti-receptor monoclonal antibody.

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6.  Ciliary neurotrophic factor prevents retrograde neuronal death in the adult central nervous system.

Authors:  R E Clatterbuck; D L Price; V E Koliatsos
Journal:  Proc Natl Acad Sci U S A       Date:  1993-03-15       Impact factor: 11.205

7.  Nerve growth factor is primarily produced by GABAergic neurons of the adult rat cortex.

Authors:  Jeremy Biane; James M Conner; Mark H Tuszynski
Journal:  Front Cell Neurosci       Date:  2014-08-07       Impact factor: 5.505

  7 in total

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