Convulsant

A convulsant is a drug which induces convulsions and/or epileptic seizures, the opposite of an anticonvulsant. These drugs generally act as stimulants at low doses, but are not used for this purpose due to the risk of convulsions and consequent excitotoxicity. Most convulsants are antagonists (or inverse agonists) at either the GABAA or glycine receptors, or ionotropic glutamate receptor agonists. Many other drugs may cause convulsions as a side effect at high doses (e.g. bupropion, tramadol, pethidine, dextropropoxyphene, clomipramine) but only drugs whose primary action is to cause convulsions are known as convulsants. Nerve agents such as sarin, which were developed as chemical weapons, produce convulsions as a major part of their toxidrome, but also produce a number of other effects in the body and are usually classified separately.[1][2][3][4]

Uses

Some convulsants such as pentetrazol and flurothyl were previously used in shock therapy in psychiatric medicine, as an alternative to electroconvulsive therapy. Others such as strychnine and tetramethylenedisulfotetramine are used as poisons for exterminating pests. Bemegride and flumazenil are used to treat drug overdoses (of barbiturates and benzodiazepines respectively), but may cause convulsions if the dose is too high. Convulsants are also widely used in scientific research, for instance in the testing of new anticonvulsant drugs. Convulsions are induced in captive animals, then high doses of anticonvulsant drugs are administered.[5][6][7]

Examples
GABAA receptor antagonists, inverse agonists or negative allosteric modulators
GABA synthesis inhibitors
Glycine receptor antagonists
Ionotropic glutamate receptor agonists
Acetylcholine receptor agonists

References
  1. Mares P, Folbergrová J, Kubová H. "Excitatory aminoacids and epileptic seizures in immature brain". Physiological Research. 53 Suppl 1: S115-24. PMID 15119942.
  2. Calabrese EJ. "Modulation of the epileptic seizure threshold: implications of biphasic dose responses". Critical Reviews in Toxicology. 38 (6): 543–56. doi:10.1080/10408440802014261. PMID 18615309.
  3. Johnston GA (May 2013). "Advantages of an antagonist: bicuculline and other GABA antagonists". British Journal of Pharmacology. 169 (2): 328–36. doi:10.1111/bph.12127. PMC 3651659. PMID 23425285.
  4. de Araujo Furtado M, Rossetti F, Chanda S, Yourick D (December 2012). "Exposure to nerve agents: from status epilepticus to neuroinflammation, brain damage, neurogenesis and epilepsy". Neurotoxicology. 33 (6): 1476–1490. doi:10.1016/j.neuro.2012.09.001. PMID 23000013.
  5. Löscher W (June 2002). "Animal models of epilepsy for the development of antiepileptogenic and disease-modifying drugs. A comparison of the pharmacology of kindling and post-status epilepticus models of temporal lobe epilepsy". Epilepsy Research. 50 (1–2): 105–23. doi:10.1016/s0920-1211(02)00073-6. PMID 12151122.
  6. Löscher W (May 2009). "Preclinical assessment of proconvulsant drug activity and its relevance for predicting adverse events in humans". European Journal of Pharmacology. 610 (1–3): 1–11. doi:10.1016/j.ejphar.2009.03.025. PMID 19292981.
  7. Rubio C, Rubio-Osornio M, Retana-Márquez S, Verónica Custodio ML, Paz C (December 2010). "In vivo experimental models of epilepsy". Central Nervous System Agents in Medicinal Chemistry. 10 (4): 298–309. doi:10.2174/187152410793429746. PMID 20868357.
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