<unk> s are a diverse group of medications that work through a variety of chemical pathways;<unk>  medications work through four main mechanisms to stimulate respiration.<unk> s can act as potassium channel blockers, ampakines, serotonin receptor agonists, and adenosine antagonists. Two common potassium channel blockers are doxapram and GAL-021. Both act on potassium channels in carotid bodies. These cells are responsible for sensing low concentrations of oxygen and transmitting information to the CNS, ultimately leading to an increase in respiration. Blocking the potassium channels on the membranes of these cells effectively depolarizes the membrane potential, which in turn leads to opening of voltage-gated calcium channels and neurotransmitter release. This begins the process of relaying the signal to the CNS. Doxapram blocks leaky potassium channels in the tandom pore domain family of potassium channels, while GAL-021 blocks BK channels, or big potassium channels, which are activated by a change in membrane electron potential or by an increase in internal calcium. AMPA Ampakines are the second common form of<unk> s, which elicit a different mechanism for an<unk>  response. They bind to AMPA receptors, or alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors, within the pre-Bötzinger complex. The pre-Bötzinger complex is part of the ventral respiratory group and the induction of long-term potentials in the postsynaptic membrane of these neurons leads to an increased respiratory rate. The endogenous AMPA receptor ligand is glutamate and ampakines mirror glutamate's interaction with the receptors. Ligand binding causes AMPA receptors to open and allow for sodium ions to flow into the cell, leading to depolarization and signal transduction. At this time, CX717 is the most successful ampakine in human trials and has very few side effects. The third common mechanism of which<unk> s take advantage is to act as serotonin receptor agonists. Buspirone and Mosapride successfully increased respiration in animals by binding to serotonin receptors which are G protein coupled receptors which, upon activation, induce a secondary messenger cascade and in this case that cascade leads to an<unk>  response. With respect to breathing, caffeine acts as a competitive adenosine antagonist. Researchers discovered this by administering adenosine or its derivatives are finding that the effects were opposite to that of caffeine. Increased adenosine levels are known to cause depression of spontaneous electrical activity of the neurons, inhibition of neurotransmission, and decreased release of neurotransmitters. Adenosine inhibits respiratory drive by blocking the electrical activity of respiratory neurons. Caffeine, as an adenosine antagonist, stimulates these respiratory neurons causing enhancement of respiratory minute volume.
Analeptic
Neuroskeptic
Carcinoid
Chyme
Hematinic
Cathartic
Toxoid
Narcotic