title: [Cytokines and the nervous system: the relationship between seizures and epilepsy].
abstract: INTRODUCTION. The immune system and the peripheral and central nervous system are in constant communication by means of messengers and signalling molecules released, such as cytokines, neuropeptides, neurohormones and neurotransmitters, among others. Seizures are defined as the transitory appearance of signs and symptoms that trigger an abnormally excessive neuronal activity in the brain. Following seizures the generation of a neuroinflammatory process has been observed to occur, with the consequent release of proinflammatory cytokines and inflammation-mediating molecules, which make the patient more prone to epilepsy. AIM. To offer evidence suggesting and supporting the role of cytokines in the appearance of seizures and in epilepsy, since these molecules have proven to have dual properties. DEVELOPMENT. The central nervous system, by means of the blood-brain barrier, restricts the flow of activated cells and inflammation mediators released from the peripheral system towards the brain parenchyma. Moreover, there is also another series of mechanisms that contributes to the 'selective and modified' immunity of the central nervous system. The purpose of all this series of events is to limit the responses of the immune system at central level, although it has been shown that in the central nervous system they are permanently under the control and regulation of the immune system. CONCLUSIONS. Cytokines in epilepsy play a dual role with pro- and anti-convulsive properties. Seizures do not induce the expression of cytokines only inside the brain, but also peripherally.
authors.affiliation: Centro de Investigacion Biomedica de Occidente IMSS, Guadalajara, Mexico.
authors.forename: S F
authors.initials: SF
authors.lastname: Velasco-Ramirez
authors.forename: L Y
authors.initials: LY
authors.lastname: Rosales-Rivera
authors.forename: A C
authors.initials: AC
authors.lastname: Ramirez-Anguiano
authors.forename: O K
authors.initials: OK
authors.lastname: Bitzer-Quintero
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier; D002490:Central Nervous System / Q000503:physiopathology*; D003292:Convulsants / Q000633:toxicity; D016207:Cytokines / Q000502:physiology*; D004827:Epilepsy / Q000503:physiopathology*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007107:Immune System / Q000503:physiopathology*; D007239:Infections / Q000150:complications / Q000503:physiopathology; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; D007696:Kindling, Neurologic / Q000187:drug effects / Q000502:physiology; D051379:Mice; D015213:Neuroimmunomodulation / Q000502:physiology*; D009479:Neuropeptides / Q000502:physiology; D009490:Neurosecretory Systems / Q000503:physiopathology; D018377:Neurotransmitter Agents / Q000502:physiology; D017933:Peripheral Nervous System / Q000503:physiopathology*; D012640:Seizures / Q000503:physiopathology*; D003294:Seizures, Febrile / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D003292:Convulsants; D016207:Cytokines; D018836:Inflammation Mediators; D009479:Neuropeptides; D018377:Neurotransmitter Agents; D014409:Tumor Necrosis Factor-alpha