Cell Signaling Technology

Product Pathways - Neuroscience

EAAT1 Antibody #4166

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Endogenous 58 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

EAAT1 Antibody detects endogenous levels of total EAAT1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human EAAT1. Antibodies are purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from human cerebellum, mouse and rat brain using EAAT1 Antibody.

Background

Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system. During neurotransmission, glutamate is released from vesicles of the pre-synaptic cell, and glutamate receptors (e.g. NMDA Receptor, AMPA Receptor) bind glutamate for activation at the opposing post-synaptic cell. Excitatory amino acid transporters (EAATs) regulate and maintain extracellular glutamate concentrations below excitotoxic levels. In addition, glutamate transporters may limit the duration of synaptic excitation by an electrogenic process in which the transmitter is cotransported with three sodium ions and one proton, followed by countertransport of a potassium ion. Five EAATs (EAAT1-5) are characterized: EAAT2 (GLT-1) is primarily expressed in astrocytes but is also expressed in neurons of the retina and during fetal development (1). Homozygous EAAT2 knockout mice have spontaneous, lethal seizures and an increased predisposition to acute cortical injury (2). PKC phosphorylates Ser113 of EAAT2 and coincides with glutamate transport (3).

EAAT2 accounts for up to 90% of the total glutamate transport in brain while EAAT1 contributes the remaining 5-10% (4). The contribution of EAAT1 in neurotransmission is unclear since EAAT2 is much more abundant. However, EAAT1 expression is upregulated by increasing concentrations of glutamate in the media of cultured primary astrocytes, potentially giving this glutamate transporter additional importance (5). EAAT1 has neuroprotective potential following ischemia since reactive astrocytes and activated microglia express EAAT1 but not EAAT2 (6).

  1. Amara, S.G. and Fontana, A.C. (2002) Neurochem Int 41, 313-8.
  2. Tanaka, K. et al. (1997) Science 276, 1699-702.
  3. Casado, M. et al. (1993) J Biol Chem 268, 27313-7.
  4. Hediger, M.A. (1999) Am J Physiol 277, F487-92.
  5. Gegelashvili, G. et al. (1996) Neuroreport 8, 261-5.
  6. Beschorner, R. et al. (2007) Histopathology 50, 897-910.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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