Your really not a very nice person, are you Smyth? I bet you never got "works and plays well with others" on your report card.
Anyway, what makes you think clonazepam is that different from other benzos? I'll just quote something I said in OD a couple months back, when someone basically asked "why do benzos all feel different".
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That is an epically complicated question. Basically, the differences are going to boil down to different affinities at the different GABA-A receptor subunit make ups.
Now I can't exactly remeber how many different subunit types there are, but I think, there are alpha 1 to 6, beta 1 to 3, gamma 1 to 3, delta, epsilon, theta and pi. Now all of those different benzos, will have different affinities has GABA-A receptors made up with different combination of 5 of those subtypes. So Thats actaully a huge number.
So instead of doing an actual week of research, I'll post this abstract
Doble A.
New insights into the mechanism of action of hypnotics.
J Psychopharmacol. 1999;13(4 Suppl 1):S11-20
Between 1987 and 1989, the different protein subunits that make up the receptor for the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) were identified. These make up the alpha, beta, gamma and delta families, for each of which exist several subtypes. This receptor is the molecular target of modern hypnotic drugs (i.e. benzodiazepines, zopiclone, zolpidem and zaleplon). In the 10 years that have followed this milestone, significant progress has been made in exploring the molecular mechanisms of hypnotic drug action. Receptor subtype specificity of hypnotics has been explained in terms of differential affinity for receptors containing different alpha subunits, which are expressed in different brain regions. Zolpidem and zaleplon bind preferentially to alpha1-containing receptors, whereas benzodiazepines and zopiclone are aspecific. Different sets of subunits are encoded in contiguous 'cassettes' on the genome, and the transcription of each set appears to be regulated coherently. The predominant GABA(A) receptor composition found in the brain is alpha1beta2gamma2, which are all encoded on human chromosome 5. Targeted gene disruption has provided clues to the physiological functions served by GABA(A) receptors containing different subunits. Receptors containing gamma2 appear to have a vital role in maintaining appropriate central inhibition, beta3-containing receptors may also be important determinants of excitability in certain brain regions, whereas a clear role for alpha5-, alpha6- and gamma3-containing receptors has not yet been established by these techniques. Site-directed mutagenesis has indicated that benzodiazepines bind to a cleft on the GABA(A) receptor surface at the interface between the alpha and gamma subunits. Other drugs (flumazenil, zopiclone, zolpidem) also bind to the a subunit, but interact with amino acids in different binding domains to the benzodiazepines. The molecular mechanism of hypnotic dependence has been explored, and seems to involve downregulation of transcription of the normally prevalent alpha1, beta2 and gamma2 subunits, and the reciprocal upregulation of the expression of rarer subunits. Chronic treatment with hypnotic drugs that may have less dependence potential, such as zopiclone and zolpidem, appears to produce more limited change in GABA(A) receptor subunit expression. These ideas will be important both for designing new hypnotic drugs with a better safety/efficacy profile, and for evaluating more appropriate ways of using the drugs available today.
They say the hypnotics are more specific for GABA-A channels that contain the alpha subunit, I'm not sure if thats correct;
but the difference in the subjective effect of benzos will be due to their subunit specificity.
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Also, the pharmacokinetics would modulate the effects somewhat, as faster absorbed and distributed benzos would probabyl be more enjoyable.