Biochemical Pharmacology. Lecture Notes by MichaelPalmer

By MichaelPalmer

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Na+ and K+ fluxes during the action potential. 6. Experimental evocation and detection of action potentials. a: Detection of action potential propagation. Top: Schematic of the experimental setup to trigger and detect action potential. Below: Trace of an action potential passing the detection electrodes. The numbers refer to phases 1-4 as explained in the text b: Local stimulation, and the firing level. If a patch of nerve cell membrane is partially depolarized to a level of ~-55 mV, Na+ channels will start to open, and an all-out action potential will be triggered.

If the concentration of agonist is sufficiently high, the entire receptor population will be arrested in the active state. Analogously, an antagonist will preferentially bind the inactive conformation and therefore, at saturating concentrations, convert the entire receptor population to the inactive state. 12) and therefore bring about any appreciable receptor activation at all. 12. 6. Partial agonism and the two-state model of receptor activation The expression that that quantitatively describes the active fraction as a function of the ligand concentrationcan quite easily be derived using the equilibrium equations, together with the two equations above: K A = [Ractive][L] / [Ractive L] 35 being used in applications requiring something intermediate in strength between morphine and basic pain killers such as aspirin.

K is inversely related to the affinity; the higher it is, the lower the binding affinity. e. 1a). You will recognize the formal similarity to Michaelis-Menten enzyme kinetics. 1b, top). Shown are three curves, differing in their respective values for K. The bottom panel shows that plotting the same numbers on a logarithmic scale for the ligand yields nice sigmoidal plots, which are now distinguished solely by their parallel offsets along the x-axis. From these plots, K can be determined as the ligand concentration of half-maximal receptor occupancy.

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