A glutamate-sensitive neuronal system originating from the area postrema terminates in and transports acetylcholinesterase to the nucleus of the solitary tract

Sarolta Karcsú, G. Jancsó, Georg W. Kreutzberg, Lajos Tóth, Elizabeth Király, Ernö Bácsy, F. László

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The possible cellular mechanism of action of systemically administered monosodium-l-glutamate and the projections of glutamate-sensitive area postrema neurons have been studied in rats. Parenteral administration of monosodium-l-glutamate induced a selective degeneration of a particular population of AChE-containing area postrema neurons. Electron microscopic cytochemistry and X-ray microanalysis revealed the presence of calcium-containing electron-dense deposits in the mitochondria of degenerating area postrema neurons indicating the possible pathogenetic role of an enhanced intracellular calcium level in the mechanism of monosodium-l-glutamate-induced nerve cell degeneration. Degeneration of area postrema neurons was followed by the appearance of degenerating axon terminals in a well-defined region of the nucleus of the solitary tract, the area subpostrema. Degenerating area postrema neurons and axon terminals were rapidly engulfed by phagocytes predominantly of microglial character. AChE activity, localized to the basal lamina of the capillaries of the area subpostrema under normal conditions, could no longer be detected in rats treated with monosodium-l-glutamate 3-4 weeks previously. These findings provide evidence for the existence of a particular population of glutamate-sensitive, AChE-containing area postrema neurons which project and transport AChE to the nucleus of the solitary tract. This specific neuronal pathway connecting the area postrema with the nucleus of the solitary tract may play an important role in some of the functions attributed to the area postrema. The results also strengthen the hypothesis that brain capillary AChE activity may be of neuronal origin.

Original languageEnglish
Pages (from-to)563-578
Number of pages16
JournalJournal of Neurocytology
Volume14
Issue number4
DOIs
Publication statusPublished - Aug 1985

Fingerprint

Area Postrema
Solitary Nucleus
Acetylcholinesterase
Glutamic Acid
Sodium Glutamate
Neurons
Presynaptic Terminals
Calcium
Electron Probe Microanalysis
Nerve Degeneration
Histocytochemistry
Vulnerable Populations
Phagocytes
Basement Membrane
Mitochondria
Electrons

ASJC Scopus subject areas

  • Neuroscience(all)
  • Histology
  • Anatomy
  • Cell Biology

Cite this

A glutamate-sensitive neuronal system originating from the area postrema terminates in and transports acetylcholinesterase to the nucleus of the solitary tract. / Karcsú, Sarolta; Jancsó, G.; Kreutzberg, Georg W.; Tóth, Lajos; Király, Elizabeth; Bácsy, Ernö; László, F.

In: Journal of Neurocytology, Vol. 14, No. 4, 08.1985, p. 563-578.

Research output: Contribution to journalArticle

@article{4edd6dd2629048d8accb2f5d6e3091fe,
title = "A glutamate-sensitive neuronal system originating from the area postrema terminates in and transports acetylcholinesterase to the nucleus of the solitary tract",
abstract = "The possible cellular mechanism of action of systemically administered monosodium-l-glutamate and the projections of glutamate-sensitive area postrema neurons have been studied in rats. Parenteral administration of monosodium-l-glutamate induced a selective degeneration of a particular population of AChE-containing area postrema neurons. Electron microscopic cytochemistry and X-ray microanalysis revealed the presence of calcium-containing electron-dense deposits in the mitochondria of degenerating area postrema neurons indicating the possible pathogenetic role of an enhanced intracellular calcium level in the mechanism of monosodium-l-glutamate-induced nerve cell degeneration. Degeneration of area postrema neurons was followed by the appearance of degenerating axon terminals in a well-defined region of the nucleus of the solitary tract, the area subpostrema. Degenerating area postrema neurons and axon terminals were rapidly engulfed by phagocytes predominantly of microglial character. AChE activity, localized to the basal lamina of the capillaries of the area subpostrema under normal conditions, could no longer be detected in rats treated with monosodium-l-glutamate 3-4 weeks previously. These findings provide evidence for the existence of a particular population of glutamate-sensitive, AChE-containing area postrema neurons which project and transport AChE to the nucleus of the solitary tract. This specific neuronal pathway connecting the area postrema with the nucleus of the solitary tract may play an important role in some of the functions attributed to the area postrema. The results also strengthen the hypothesis that brain capillary AChE activity may be of neuronal origin.",
author = "Sarolta Karcs{\'u} and G. Jancs{\'o} and Kreutzberg, {Georg W.} and Lajos T{\'o}th and Elizabeth Kir{\'a}ly and Ern{\"o} B{\'a}csy and F. L{\'a}szl{\'o}",
year = "1985",
month = "8",
doi = "10.1007/BF01200798",
language = "English",
volume = "14",
pages = "563--578",
journal = "Journal of Neurocytology",
issn = "0300-4864",
publisher = "Kluwer Academic Publishers",
number = "4",

}

TY - JOUR

T1 - A glutamate-sensitive neuronal system originating from the area postrema terminates in and transports acetylcholinesterase to the nucleus of the solitary tract

AU - Karcsú, Sarolta

AU - Jancsó, G.

AU - Kreutzberg, Georg W.

AU - Tóth, Lajos

AU - Király, Elizabeth

AU - Bácsy, Ernö

AU - László, F.

PY - 1985/8

Y1 - 1985/8

N2 - The possible cellular mechanism of action of systemically administered monosodium-l-glutamate and the projections of glutamate-sensitive area postrema neurons have been studied in rats. Parenteral administration of monosodium-l-glutamate induced a selective degeneration of a particular population of AChE-containing area postrema neurons. Electron microscopic cytochemistry and X-ray microanalysis revealed the presence of calcium-containing electron-dense deposits in the mitochondria of degenerating area postrema neurons indicating the possible pathogenetic role of an enhanced intracellular calcium level in the mechanism of monosodium-l-glutamate-induced nerve cell degeneration. Degeneration of area postrema neurons was followed by the appearance of degenerating axon terminals in a well-defined region of the nucleus of the solitary tract, the area subpostrema. Degenerating area postrema neurons and axon terminals were rapidly engulfed by phagocytes predominantly of microglial character. AChE activity, localized to the basal lamina of the capillaries of the area subpostrema under normal conditions, could no longer be detected in rats treated with monosodium-l-glutamate 3-4 weeks previously. These findings provide evidence for the existence of a particular population of glutamate-sensitive, AChE-containing area postrema neurons which project and transport AChE to the nucleus of the solitary tract. This specific neuronal pathway connecting the area postrema with the nucleus of the solitary tract may play an important role in some of the functions attributed to the area postrema. The results also strengthen the hypothesis that brain capillary AChE activity may be of neuronal origin.

AB - The possible cellular mechanism of action of systemically administered monosodium-l-glutamate and the projections of glutamate-sensitive area postrema neurons have been studied in rats. Parenteral administration of monosodium-l-glutamate induced a selective degeneration of a particular population of AChE-containing area postrema neurons. Electron microscopic cytochemistry and X-ray microanalysis revealed the presence of calcium-containing electron-dense deposits in the mitochondria of degenerating area postrema neurons indicating the possible pathogenetic role of an enhanced intracellular calcium level in the mechanism of monosodium-l-glutamate-induced nerve cell degeneration. Degeneration of area postrema neurons was followed by the appearance of degenerating axon terminals in a well-defined region of the nucleus of the solitary tract, the area subpostrema. Degenerating area postrema neurons and axon terminals were rapidly engulfed by phagocytes predominantly of microglial character. AChE activity, localized to the basal lamina of the capillaries of the area subpostrema under normal conditions, could no longer be detected in rats treated with monosodium-l-glutamate 3-4 weeks previously. These findings provide evidence for the existence of a particular population of glutamate-sensitive, AChE-containing area postrema neurons which project and transport AChE to the nucleus of the solitary tract. This specific neuronal pathway connecting the area postrema with the nucleus of the solitary tract may play an important role in some of the functions attributed to the area postrema. The results also strengthen the hypothesis that brain capillary AChE activity may be of neuronal origin.

UR - http://www.scopus.com/inward/record.url?scp=0021885968&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021885968&partnerID=8YFLogxK

U2 - 10.1007/BF01200798

DO - 10.1007/BF01200798

M3 - Article

C2 - 2415686

AN - SCOPUS:0021885968

VL - 14

SP - 563

EP - 578

JO - Journal of Neurocytology

JF - Journal of Neurocytology

SN - 0300-4864

IS - 4

ER -