Re‐expression of glia‐derived nexin/protease nexin 1 depends on mode of lesion‐induction or terminal degeneration: Observations after excitotoxin or 6‐hydroxydopamine lesions of rat substantia nigra

Re‐expression of glia‐derived nexin/protease nexin 1 depends on mode of lesion‐induction or... The serine protease inhibitor and neurite outgrowth promoter glia derived nexin (GDN) is expressed in the rat CNS during embryogenesis and persists in the olfactory system of the adult where receptor neurons are replaced throughout life. We investigated whether GDN‐immunoreactivity also appears in the adult at sites of synaptic rearrangement following nerve cell death and anterograde terminal degeneration in experimental models for Parkinson's disease. Rat substantia nigra was unilaterally lesioned by stereotaxic application of different toxins: 6‐hydroxydopamine, which selectively destroys dopaminergic neurons, the excitotoxic glutamate analog ibotenic acid, or the glutamate receptor agonists N‐methyl‐D‐aspartate and quisqualate, which cause circumscript lesions of the whole substantia nigra. Nerve cell death and astroglial reactivity were monitored by parallel cresyl staining and immunocytochemistry for glial fibrillary acidic protein, at survival times ranging from 2 to 100 days. Sustained de novo synthesis of GDN occurred in the dopamine depleted caudate putamen following excitotoxin or 6‐hydroxydopamine induced degeneration of the substantia nigra and of the nigrostriatal pathway provided that the lesions were nearly complete. This is consistent with compensatory changes occurring in deafferented caudate putamen and suggests a permissive role of GDN in neuronal plasticity. In the substantia nigra astroglia exhibited GDN‐immunoreactivity following excitotoxin injection but not after application of 6‐hydroxydopamine. Thus differences in action mechanisms of neurotoxins may have distinct consequences on the astrocyte mediated response of the same affected brain region. © 1994 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Research Wiley

Re‐expression of glia‐derived nexin/protease nexin 1 depends on mode of lesion‐induction or terminal degeneration: Observations after excitotoxin or 6‐hydroxydopamine lesions of rat substantia nigra

Loading next page...
 
/lp/wiley/re-expression-of-glia-derived-nexin-protease-nexin-1-depends-on-mode-EpIHJcRSD6
Publisher site
See Article on Publisher Site

Abstract

The serine protease inhibitor and neurite outgrowth promoter glia derived nexin (GDN) is expressed in the rat CNS during embryogenesis and persists in the olfactory system of the adult where receptor neurons are replaced throughout life. We investigated whether GDN‐immunoreactivity also appears in the adult at sites of synaptic rearrangement following nerve cell death and anterograde terminal degeneration in experimental models for Parkinson's disease. Rat substantia nigra was unilaterally lesioned by stereotaxic application of different toxins: 6‐hydroxydopamine, which selectively destroys dopaminergic neurons, the excitotoxic glutamate analog ibotenic acid, or the glutamate receptor agonists N‐methyl‐D‐aspartate and quisqualate, which cause circumscript lesions of the whole substantia nigra. Nerve cell death and astroglial reactivity were monitored by parallel cresyl staining and immunocytochemistry for glial fibrillary acidic protein, at survival times ranging from 2 to 100 days. Sustained de novo synthesis of GDN occurred in the dopamine depleted caudate putamen following excitotoxin or 6‐hydroxydopamine induced degeneration of the substantia nigra and of the nigrostriatal pathway provided that the lesions were nearly complete. This is consistent with compensatory changes occurring in deafferented caudate putamen and suggests a permissive role of GDN in neuronal plasticity. In the substantia nigra astroglia exhibited GDN‐immunoreactivity following excitotoxin injection but not after application of 6‐hydroxydopamine. Thus differences in action mechanisms of neurotoxins may have distinct consequences on the astrocyte mediated response of the same affected brain region. © 1994 Wiley‐Liss, Inc.

Journal

Journal of Neuroscience ResearchWiley

Published: Feb 1, 1994

References

  • The functional anatomy of basal ganglia disorders
    Albin, Albin; Young, Young; Penney, Penney
  • The excitatory neurotransmitter glutamate causes filopodia formation in cultured hippocampal astrocytes
    Cornell‐Bell, Cornell‐Bell; Thomas, Thomas; Smith, Smith
  • The neostriatal mosaic: Multiple levels of compartmental organization
    Gerfen, Gerfen
  • Inhibition of mononuclear phagocytes reduces ischemic injury in the spinal cord
    Giulian, Giulian; Robertson, Robertson
  • Astroglia in CNS injury
    Hatten, Hatten; Liem, Liem; Shelanski, Shelanski; Mason, Mason
  • Chemical neurotoxins as denervation tools in neurobiology
    Jonsson, Jonsson

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off