This diagram of a NMDA receptor shows the binding points for a diverse array of molecules which can affect the receptor function. Legend: 1. Cell membrane 2.<unk>  by Mg2+ at the block site (3) 3. Block site by Mg2+ 4. Hallucinogen compounds binding site 5. Binding site for Zn2+ 6. Binding site for agonists(glutamate) and/or antagonist ligands(APV) 7. Glycosylation sites 8. Proton binding sites 9. Glycine binding sites 10. Polyamines binding site 11. Extracellular space 12. Intracellular space Receptor antagonist<unk> s are antagonists for the respective ion channels. Many channels have binding spots for regulatory elements which can promote or repress normal function depending on the requirements within the cell and organism. The normal function of agonist binding is the generation of cellular changes leading to various downstream effects; these effects range from altering membrane potential to initiation of signaling cascades. Conversely, when open<unk> s bind to the cell they prevent the normal function of agonist binding. For example, voltage-gated channels open and close based on membrane potential and are critical in the generation of action potentials by their allowance of ions to flow down established gradients. However, open<unk> s can bind to these channels to prevent ions from flowing, thus inhibiting the initiation of an action potential. Specificity of molecules Many different organic compounds can act as<unk> s despite channel specificity. Channels have evolved structures that, due to their membrane spanning regions, can discriminate between various ions or compounds. For example, some objects are too large for to fit into channels that are structurally specified to transport smaller objects, such as a potassium ion attempting to fit into a sodium channel. Conversely, some objects are too small to be properly stabilized by certain channel pores, such as a sodium ion attempting to pass through a potassium channel. In both cases, channel flux is not permitted. However, as long as a particular compound possesses adequate chemical affinity to a channel, that compound may be able to bind and block the channel pore. For example, TTX can bind and inactivate voltage-gated sodium channels, despite the fact that TTX is much larger and chemically different than sodium ions. Given the disparities in size and chemical properties between TTX and a sodium ion, this is an example of structure being used to block usually specific channels. Kinetics=== A channel block can be induced by many different types of organic compounds as long as they can bind to some portion of the target channel's pore. The kinetics of<unk> s are primarily understood though their use as anesthetics. Local anesthetics work by inducing a phasic block state in the targeted neurons. Initially, open<unk> s do not effectively prevent action potentials, as few channels are blocked and the blocker itself can be released from the channel either quickly or slowly depending on its characteristics. However, phasic blocks occur as repeated depolarization increases blockers’ affinity for channels in the neuron. The combination of an increase in available channels and the change in channel conformation to increase blocker binding affinity are responsible for this action.
Channel blocker
Channel opener
Channel modulator
Chloride channel opener
Calcium channel blocker
Beta-adrenergic agonist
Muscle relaxant
GABA analogue