Literature DB >> 7812773

[3H]D-aspartate binding sites in the normal human spinal cord and changes in motor neuron disease: a quantitative autoradiographic study.

P J Shaw1, R M Chinnery, P G Ince.   

Abstract

The distribution and density of glutamate transporter sites was determined in human cervical and lumbar spinal cord, by quantitative autoradiography using [3H]D-aspartate. In the normal human spinal cord (n = 8) there was specific binding of [3H]D-aspartate throughout the spinal grey matter, with the highest levels observed in the substantia gelatinosa and central grey matter. In the ventral horns, particularly at the L5 level, focal hot spots of binding were observed in a distribution corresponding to that of lower motor neuron somata. Comparison of motor neuron disease (MND) cases (n = 12) with normal controls showed a reduction in the density of [3H]D-aspartate binding in the intermediate grey matter and the substantia gelatinosa of the lumbar cord. These changes were more marked in the amyotrophic lateral sclerosis (ALS) compared to the progressive muscular atrophy (PMA) subgroup, and may be due to loss of glutamatergic terminals of the corticospinal tract. The changes observed in the cervical cord were milder and did not reach statistical significance. No differences were found between [3H]D-aspartate binding in the spinal cords of the normal controls and a neurological disease control group (n = 6), suggesting that the changes observed in MND are disease specific. These findings provide further evidence in support of a disturbance of glutamatergic neurotransmission in MND.

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Year:  1994        PMID: 7812773     DOI: 10.1016/0006-8993(94)91614-4

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


  8 in total

1.  Disruption of glial glutamate transport by reactive oxygen species produced in motor neurons.

Authors:  Shyam D Rao; Hong Z Yin; John H Weiss
Journal:  J Neurosci       Date:  2003-04-01       Impact factor: 6.167

Review 2.  Glutamate, excitotoxicity and amyotrophic lateral sclerosis.

Authors:  P J Shaw; P G Ince
Journal:  J Neurol       Date:  1997-05       Impact factor: 4.849

3.  Nucleus Accumbens 1, a Pox virus and Zinc finger/Bric-a-brac Tramtrack Broad protein binds to TAR DNA-binding protein 43 and has a potential role in Amyotrophic Lateral Sclerosis.

Authors:  M D Scofield; L Korutla; T G Jackson; P W Kalivas; S A Mackler
Journal:  Neuroscience       Date:  2012-09-25       Impact factor: 3.590

4.  Astrocytes in amyotrophic lateral sclerosis: direct effects on motor neuron survival.

Authors:  K A Staats; L Van Den Bosch
Journal:  J Biol Phys       Date:  2009-03-21       Impact factor: 1.365

5.  Focal loss of the glutamate transporter EAAT2 in a transgenic rat model of SOD1 mutant-mediated amyotrophic lateral sclerosis (ALS).

Authors:  David S Howland; Jian Liu; Yijin She; Beth Goad; Nicholas J Maragakis; Benjamin Kim; Jamie Erickson; John Kulik; Lisa DeVito; George Psaltis; Louis J DeGennaro; Don W Cleveland; Jeffrey D Rothstein
Journal:  Proc Natl Acad Sci U S A       Date:  2002-01-29       Impact factor: 11.205

6.  Regional distribution of sodium-dependent excitatory amino acid transporters in rat spinal cord.

Authors:  Susan A Queen; J Patrick Kesslak; Richard J Bridges
Journal:  J Spinal Cord Med       Date:  2007       Impact factor: 1.985

Review 7.  Glutamate transporters and the excitotoxic path to motor neuron degeneration in amyotrophic lateral sclerosis.

Authors:  Emily Foran; Davide Trotti
Journal:  Antioxid Redox Signal       Date:  2009-07       Impact factor: 8.401

8.  Experimental models for the study of neurodegeneration in amyotrophic lateral sclerosis.

Authors:  Luis B Tovar-Y-Romo; Luz Diana Santa-Cruz; Ricardo Tapia
Journal:  Mol Neurodegener       Date:  2009-07-20       Impact factor: 14.195

  8 in total

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