I have been using Sulbutiamine on an average of three times a week for about 4 months, and I have nothing but good things to say about my experience with this Nootropic. I have also noticed a very positive increase in my long term memory in combination with Choline Bitartrate (Precursor to AcetylCholine) over the time I’ve been taking it. This is supported by studies suggesting Cholinergic and Glutimate activity increase during activity of Sulbutiamine. Now here’s another interesting study on the neurological effects of both acute and chronic Sulbutiamine administration.

http://www.ncbi.nlm.nih.gov/pubmed/10996447

Here’s the Abstract>>

“Abstract:

Chronic treatment of rats by sulbutiamine induced no change in density of N-methyl-D-aspartate (NMDA) and (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors in the cingular cortex, but a significant decrease of the kainate binding sites, as measured by quantitative autoradiography. In the same treated animals, an increase of D1 dopaminergic (DA) binding sites was measured both in the prefrontal and the cingular cortex, while no modification of the D2 binding sites was detected. Furthermore, an acute sulbutiamine administration induced a decrease of kainate binding sites but no change of the density of D1 and D2 DA receptors. Acute sulbutiamine injection led to a decrease of the DA levels in the prefrontal cortex and 3,4-dihydroxyphenylacetic acid levels in both the cingular and the prefrontal cortex. These observations are discussed in terms of a modulatory effect of sulbutiamine on both dopaminergic and glutamatergic cortical transmissions.”

So basically, in terms of oral ingestion, this is saying that Sulbutiamine increases the sensitivity to D1 type dopamine long term , without significantly effecting the sensitivity to other types of Dopamine. This is interesting because a major brain-activity dropping effect of chronic Cocaine use is the DEsensitization to Dopamine. This means that, theoretically, Sulbutiamine increases the overall activity of the brain, and possibly even help repair damage in recovering cocaine addicts’ brains. The slight decrease in Kainate Glutimate receptors can be attributed to down regulation due to Sulbuitiamine’s Glutimatergic mode-of-action, meaning that the memory transcription boost of Sulbutiamine may be in part from this Kainate Glutimate activity.