Cough suppression

Cough suppression refers to the reduction or inhibition of the cough reflex, typically as a therapeutic goal in respiratory medicine. This effect can be achieved pharmacologically via central or peripheral mechanisms. Central antitussives (e.g., codeine, dextromethorphan, gabapentin) reduce the sensitivity of the cough center in the brainstem, primarily by acting on the μ-opioid receptor or modulating neural transmission in pathways converging on the nucleus tractus solitarius[1][4][6]. Peripheral antitussive agents directly inhibit sensory afferents in the respiratory tract. The drug targets that mediate cough suppression include μ-opioid receptors, NMDA receptors, P2X3 receptors, and various sensory neuron receptors and channels[2][6][8]. However, "cough suppression" itself is not a molecular entity but a therapeutic effect mediated by these various targets.

Other names

Cough suppressantAntitussive effectCough suppression

Activation of μ-opioid receptor in CNS (for codeine, morphine). Inhibition of glutamatergic transmission in the nucleus tractus solitarius (codeine)[1]. Blockade of NMDA receptors (dextromethorphan). Blockade of peripheral C-fiber afferents (peripheral acting agents, e.g., benzonatate). P2X3 receptor antagonism (e.g., gefapixant, camlipixant)[2]. Modulation of GABAergic neurotransmission (gabapentin). Anxiolytic/central mechanisms (neuromodulators, some NK-1 antagonists)[2].