Artane is a selective muscarinic receptor antagonist. It has a high affinity for the M1 (neuronal) muscarinic receptor, and does not target other muscarinic receptors, like in the heart.

That's why a tiny amount of artane helps me feel better, and a large amount of another anticholinergic that I take does nothing for my PD symptoms. Artane is mainly targeted to the brain which is where I need it!

Some PET scan evidence:

Effects of trihexyphenidyl and L-dopa on brain muscarinic cholinergic receptor binding measured by positron emission tomography

Received: 17 March 1993 Accepted: 13 September 1993


Summary

The effects of pharmacological intervention on brain muscarinic cholinergic receptor (mAChR) binding were assessed in seven patients with Parkinson's disease by positron emission tomography and carbon-11 labelled N-methyl-4-piperidyl benzilate ([11C]NMPB). [11C]NMPB was injected twice, approximately 2 hours apart, in each patient, to assess the effect of single doses of 4 mg of trihexyphenidyl (n=5) or 400 mg of L-dopa with 57 mg of benserazide (n=2) on the binding parameter of mAChRs (K3).

There was a mean 28% inhibition of K3 values in the brain in the presence of trihexyphenidyl, which was assumed to reflect mAChR occupancy.

No significant change in K3 was observed in the presence of L-dopa. This study demonstrates the feasibility of measuring mAChR occupancy by an anticholinergic medication with PET.

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By the way, I take doxepin, a tricyclic antidepressant and antihistamine that targets the histamine H1 receptor. One of the main reasons I take it is for itching, and joint pain. Interesting how these anticholinergics differ. Doxepin works better than many antihistamines.

I stand corrected
 

Zuchinni, of course you are right.

The state of knowledge I aluded to, belonged to the time up to the writing of the referenced book and the "google it" was a complete, unwarranted goof up.
Apologize.

On another subject, I found an interesting comment on page 624:

"Birkmayer attempted to stimulate tyrosinase activity by supplying p-tyrosine (200mg i.v.) and the cofactor for the enzime, nicotinamide adenine dinucleotide diphosphate (NADH; 20mg i.v.); the combination produced a kinetic effect in some patients comparable with that of L-Dopa/4-4602(benserazide), supporting Birkmayer's suspicion that the conversion of tyrosine to L-Dopa was defficient in parkinsonism. This therapeutic approach, however, was not further pursued at this stage."

http://deposit.d-nb.de/cgi-bin/dokse...=96446392x.pdf