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Re: H1 antagonists vs H3 antagonists » DSCH

Posted by Larry Hoover on August 12, 2003, at 8:28:40

In reply to H1 antagonists vs H3 antagonists, posted by DSCH on August 11, 2003, at 12:53:20

> > Every drug you mentioned in this thread is an antagonist, a substance that negates the effect of histamine. You'd need less, not more. However, I think that's a simplistic explanation, in any case (just like the serotonin imbalance explanation for depression).
>
> Don't confuse the action of H1 and H3 antagonists. H3 antagonists are not "antihistamines" and cause *more* histamine to be released into the synpases, especially in the posterior hypothalamus. Take a peak at the abstracts you get if you run a search on "H3 antagonist". Activating effects rather than the classic sedation of antihistamines that cross the BBB.

That's not what this one says:

Ann Pharm Fr. 2003 May;61(3):173-84.

[The histamine H(3) receptor: a target for new drugs]

[Article in French]

Arrang JM.

Unite de neurobiologie et pharmacologie moleculaire, INSERM U573, Centre Paul Broca, 2ter, rue d'Alesia, F 75014 Paris.

The histamine H3 receptor has been identified in the rat brain as a presynaptic autoreceptor inhibiting histamine synthesis and release. Following its recent cloning, more than fifteen years later, the existence of isoforms, species pharmacological differences and the high constitutive activity of the receptor were established. All these molecular findings have to be taken into account for the optimization of the ligands aiming at a clinical use. They show the interest of antagonists/inverse agonists in the symptomatic treatment of schizophrenia and cognitive and attentional deficits.


I didn't post that to quibble. When I look at histaminic neurotransmission as a system, I find major contradictions and conditional activities. Check out this abstract (and the final sentence, in particular):

J Pharmacol Exp Ther. 2001 Dec;299(3):908-14.

Constitutive activity of histamine h(3) receptors stably expressed in SK-N-MC cells: display of agonism and inverse agonism by H(3) antagonists.

Wieland K, Bongers G, Yamamoto Y, Hashimoto T, Yamatodani A, Menge WM, Timmerman H, Lovenberg TW, Leurs R.

Leiden/Amsterdam Center for Drug Research, Division of Medicinal Chemistry, Vrije Universiteit, Division of Chemistry, Amsterdam, The Netherlands.

Agonist-independent activity of G-protein-coupled receptor, also referred to as constitutive activity, is a well-documented phenomenon and has been reported recently for both the histamine H(1) and H(2) receptors. Using SK-N-MC cell lines stably expressing the human and rat H(3) receptors at physiological receptor densities (500-600 fmol/mg of protein), we show that both the rat and human H(3) receptors show a high degree of constitutive activity. The forskolin-mediated cAMP production in SK-N-MC cells is inhibited strongly upon expression of the G(i)-coupled H(3) receptor. The cAMP production can be further inhibited upon agonist stimulation of the H(3) receptor and can be enhanced by a variety of H(3) antagonists acting as inverse agonists at the H(3) receptor. Thioperamide, clobenpropit, and iodophenpropit raise the cAMP levels in SK-N-MC cells with potencies that match their receptor binding affinities. Surprisingly, impentamine and burimamide act as effective H(3) agonists. Modification of the amine group of impentamine dramatically affected the pharmacological activity of the ligand. Receptor affinity was reduced slightly for most impentamine analogs, but the functional activity of the ligands varied from agonist to neutral antagonist and inverse agonist, indicating that subtle changes in the chemical structures of impentamine analogs have major impact on the (de)activation steps of the H(3) receptor. In conclusion, upon stable expression of the rat and human H(3) receptor in SK-N-MC cells constitutive receptor activity is detected. In this experimental system, H(3) receptors ligands, previously identified as H(3) antagonists, cover the whole spectrum of pharmacological activities, ranging from full inverse agonists to agonists.


So, I have recently decided to steer clear of mechanisms. They seem to be post hoc rationalizations, and may be nothing more than the scientific equivalent to "The blind men and the elephant". All mechanistic explanations are inherently simplistic, IMHO, despite the complexity that is so obvious to us.

Lar

 

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poster:Larry Hoover thread:249973
URL: http://www.dr-bob.org/babble/20030812/msgs/250204.html