Skip to main content
Log in

The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment

  • Psychiatry and Preclinical Psychiatric Studies - Review article
  • Published:
Journal of Neural Transmission Aims and scope Submit manuscript

Abstract

Glutamate is the major excitatory neurotransmitter in the brain and may be a key neurotransmitter involved in autism. Literature pertaining to glutamate and autism or related disorders (e.g., Fragile X syndrome) is reviewed in this article. Interest in glutamatergic dysfunction in autism is high due to increasing convergent evidence implicating the system in the disorder from peripheral biomarkers, neuroimaging, protein expression, genetics and animal models. Currently, there are no pharmaceutical interventions approved for autism that address glutamate deficits in the disorder. New treatments related to glutamatergic neurotransmission, however, are emerging. In addition, older glutamate-modulating medications with approved indications for use in other disorders are being investigated for re-tasking as treatments for autism. This review presents evidence in support of glutamate abnormalities in autism and the potential for translation into new treatments for the disorder.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Similar content being viewed by others

References

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Donald C. Rojas.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Rojas, D.C. The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment. J Neural Transm 121, 891–905 (2014). https://doi.org/10.1007/s00702-014-1216-0

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1007/s00702-014-1216-0

Keywords

Navigation