Blocking, hindering or mimicking the<unk> tion of<unk>  has many uses in medicine. Drugs<unk> ting on the<unk>  system are either agonists to the receptors, stimulating the system, or antagonists, inhibiting it.<unk>  receptor agonists and antagonists can either have an effect directly on the receptors or exert their effects indirectly, e.g., by affecting the enzyme<unk> sterase, which degrades the receptor ligand. Agonists increase the level of receptor<unk> tivation, antagonists reduce it.<unk>  itself does not have therapeutic value as a drug for intravenous administration because of its multi-faceted<unk> tion (non-selective) and rapid inactivation by cholinesterase. However, it is used in the form of eye drops to cause constriction of the pupil during cataract surgery, which facilitates quick post-operational recovery. Nicotinic receptors Nicotine binds to and<unk> tivates nicotinic<unk>  receptors, mimicking the effect of<unk>  at these receptors.<unk>  opens a Na+ channel upon binding so that Na+ flows into the cell. This causes a depolarization, and results in an excitatory post-synaptic potential. Thus,<unk>  is excitatory on skeletal muscle; the electrical response is fast and short-lived. Curares are arrow poisons, which<unk> t at nicotinic receptors and have been used to develop clinically useful therapies. Muscarinic receptors Muscarinic receptors form G protein-coupled receptor complexes in the cell membranes of neurons and other cells. Atropine is a non-selective competitive antagonist with<unk>  at muscarinic receptors. Cholinesterase inhibitors Many<unk>  receptor agonists work indirectly by inhibiting the enzyme<unk> sterase. The resulting<unk> cumulation of<unk>  causes continuous stimulation of the muscles, glands, and central nervous system, which can result in fatal convulsions if the dose is high. They are examples of enzyme inhibitors, and increase the<unk> tion of<unk>  by delaying its degradation; some have been used as nerve agents (Sarin and VX nerve gas) or pesticides (organophosphates and the carbamates). Many toxins and venoms produced by plants and animals also contain cholinesterase inhibitors. In clinical use, they are administered in low doses to reverse the<unk> tion of muscle relaxants, to treat myasthenia gravis, and to treat symptoms of Alzheimer's disease (rivastigmine, which increases cholinergic<unk> tivity in the brain). Synthesis inhibitors Organic mercurial compounds, such as methylmercury, have a high affinity for sulfhydryl groups, which causes dysfunction of the enzyme choline<unk> etyltransferase. This inhibition may lead to<unk>  deficiency, and can have consequences on motor function. Release inhibitors Botulinum toxin (Botox)<unk> ts by suppressing the release of<unk> , whereas the venom from a black widow spider (alpha-latrotoxin) has the reverse effect.<unk>  inhibition causes paralysis. When bitten by a black widow spider, one experiences the wastage of<unk>  supplies and the muscles begin to contract. If and when the supply is depleted, paralysis occurs.
Acetylcholine
Serotonin
N-Acetylserotonin
Neuropil
Beta-Endorphin
Opioid peptide
Gluten exorphin
Glutamate 