Abstract
Tyrosine is unable to cross the blood-brain barrier and is therefore unable to improve the status of brain dopamine (DA) and to provide relief for patients with Parkinson's disease (PD) or other DA-insufficient disorders. We report the creation of an amide bond molecule [N-(α-linolenoyl)tyrosine (NLT)] that combines tyrosine with a fatty acid mixture. NLT significantly improves the rotational behavior of rats [following unilateral striatal lesions (as a model for Parkinson's)] and overcomes the exaggerated eye-blinking induced by a potent DA-depleting agent (as a model for essential blepharospasm). These results are supported by the finding that NLT's mode of action, in striatum, is the same as the mode of action of D-amphetamine. They both induce an increase in the DA level, DA turnover and release.
| Original language | English |
|---|---|
| Pages (from-to) | 7-11 |
| Number of pages | 5 |
| Journal | Pharmacology Biochemistry and Behavior |
| Volume | 72 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - May 2002 |
Keywords
- Amide bond
- Animal model
- Dopamine
- Parkinson's disease
- Tyrosine
- α-Linolenic acid
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