Agonist high affinity form

However, if the agonist high affinity form of the receptor is labelled prior to solubilization by incubation of membranes with [3H]n-propylapomorphine then the agonist high affinity form of the receptor appears to be stable to solubilization (Table I). Shown in Table I are the results of three... 

A fourth important pharmacophoric element was established for the non-classical cannabinoid series in the form of a southern aliphatic hydroxyl group. Addition of this group to (192) resulted in the high-affinity CBi and CB2 receptor full agonist CP 55,940 (193) [129, 133], the tritiated form of which was used to first demonstrate specific cannabinoid binding sites in brain tissue [134]. Its enantiomer, CP 56,667 (194) has lower affinity for the CBi receptor (Table 6.17). 

Fig. 3 Potential subunit compositions of nAChRs expressed in dopaminergic nerve terminals. A combination of ligand binding ([ H]-epibatidine and [ I]-a-conotoxin Mil), immunoprecipita-tion, and dopamine release data have led to the conclusion that rodent brain expresses a minimum of five different nAChR subtypes. Three of these (the two forms of a4p2 and a4aSP2) do not bind a-conotoxin Mil with high affinity (a-conotoxin Mll-resistant). The three a6-containing subtypes bind a-conotoxin Mil with high affinity (conotoxin Mil-sensitive). In general, the conotoxin-sensitive nAChR subtypes are activated by lower concentrations of agonist than are required to activate the a-conotoxin Mll-resistant subtypes (Salminen et al. 2007)...

The 5-HT3 receptors, in the form of M-type serotonin receptors, represent one of the earliest investigated populations of 5-HT receptors. However, they were not identified in the mammalian brain until the late 1980s. Nevertheless, a plethora of very high-affinity and selective 5-HT3 antagonists quickly became available (e.g., ref. 43). What was lacking for the longest time was a useful 5-HT3 agonist. 

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