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Glutamate transporters play an essential role in terminating the excitatory glutamatergic signal at post-synaptic receptors and in protecting neurones from excitotoxic effects, as well as replenishing the neurotransmitter supply at glutamatergic synapses. The distribution and density of glutamate transporters may be important determinants of vulnerability to glutamate-mediated injury. There is emerging evidence that glutamate transporter dysfunction may be present in motor neurone disease (MND). In this study, a monoclonal antibody, suitable for immunohistochemistry (IHC) in human post-mortem tissue, was produced to the human astrocytic glutamate transporter EAAT2 (excitatory amino acid transporter 2). Western blotting of homogenates of human cortical tissue with the EAAT2 antibody produced a discrete band at 66 kDa. Detailed IHC analysis of the expression of the EAAT2 protein in the human CNS was undertaken. EAAT2 was exclusively localised to astrocytes, with preferential expression in the caudate nucleus, nucleus basalis of Meynert, spinal ventral horn, cerebral cortex and hippocampus, but with lower levels of expression throughout many other CNS regions. Motor neurone groups vulnerable to neurodegeneration in MND appeared distinctive in being surrounded by extensive, coarse, strongly immunoreactive perisomatic glial profiles. Motor neurone groups which tend to be spared in MND, such as those present in the oculomotor nucleus, showed a lower expression of EAAT2, with fewer perisomatic profiles. The EAAT2 antibody will provide a useful tool for increasing our understanding of the role of EAAT2 in excitatory neurotransmission in health and disease states.
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
January 2007,
The Journal of biological chemistry,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
January 2009,
American journal of physiology. Gastrointestinal and liver physiology,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
September 2002,
The European journal of neuroscience,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
May 2007,
Glia,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
December 2005,
Neurochemistry international,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
August 2013,
Neuroscience,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
August 2012,
Neurobiology of disease,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
April 2000,
The Journal of neuroscience : the official journal of the Society for Neuroscience,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
January 2004,
Glia,
I D Milton, and
S J Banner, and
P G Ince, and
N H Piggott, and
A E Fray, and
N Thatcher, and
C H Horne, and
P J Shaw
January 2002,
Neuroscience,
