Any thoughts on how to get this cystine/glutamate antiporter process working more effectively? Or if it is problematic for some of us?
This was an additional edit I made back on my post about the SLC1a1 genewhich encodes for the EAAT1 enzyme. This article has some very good information about glutamate transport as a potential player in the pathology of OCD, as well as information in regarding the antiporter and glutathione production. (and other illnesses).
"I found out why NAC helps people with ocd and how it modulates glutamate in this article.
http://www.ocd.yale.edu/researchers/329_114509_Pittenger et al (2011) Glutamate abnormalities in OCD.pdf
"Indeed, excess glutamate has long been known to lead to neuronal death, a phenomenon known as excitotoxicity (Olney, 1969). Glutamate concentration is therefore tightly regulated. The principal mode of regulation is through high-affinity glutamate transporters, which efficiently remove glutamate from the perisynaptic and extrasynaptic spaces (Danbolt, 2001). Quantitatively, glutamate transporters on glial cells – principally astrocytes – are responsible for the majority of glutamate removal; these astrocytic glutamate transporters are a target of the glutamate-modulating drug riluzole, which has shown promise in the treatment of refractory OCD (Pittenger et al., 2008a). A smaller fraction of glutamate is removed by the neuronal glutamate transporter, EAAC1/EAAT3; as reviewed below, polymorphisms in the gene encoding this transporter have been repeatedly associated with OCD in recent studies (Arnold et al.,2006; Dickel et al., 2006; Stewart et al., 2007; Shugart et al., 2009). Finally,
glutamate is also transported into glial cells in exchange for the oxidized amino acid cystine via the glutamate-cystine antiporter; undersome circumstances the activity of this antiporter, which is influenced by the drug N-acetylcysteine, may be the principal determinant of baseline levels of extrasynaptic glutamate (Kalivas, 2009)"