Summary
Nicotine is a toxic substance which because of its lipid solubility can cross the blood brain barrier. It has several different actions in the CNS; one of which is neuroexcitation, where it can result in seizure activity. Based on the observations that nicotine pretreatment ameliorated blood flow and glucose utilisation in caudate putamen on rats whose mesostriatal dopamine system had been cut and that nicotine pretreatment rendered animals less susceptible to nicotine induced seizures than saline administered controls, we conducted this set of experiments where we investigated the protective effect of nicotine pretreatment on the BBB permeability in nicotine induced seizures. Administration of saline or subseizure producing dose of nicotine (1 mg/kg i.p.) was followed by seizure producing doses of nicotine (2, 5 or 8 mg/kg, i. p.). Intravenous technique was used to calculate the unidirectional blood to brain transfer constant (Kin) for six different brain regions, with [3H] œ-AIB as a tracer. Mean Kin in brains of all acute nicotine groups (2, 5 or 8 mg/kg) increased by 83.94%, 182.6% and 265% respectively. Twenty one days chronic nicotine pretreatment prevented the rise in Kin AIB to 2 mg/kg acute nicotine and partially ameliorated the disturbed BBB to 5 and 8 mg/kg.
Résumé
La nicotine est une substance toxique qui, du fait de son caractère lipophile, peut traverser la barrière hémato-encéphalique. Elle a différents effets au niveau du système nerveux central, dont la neuroexcitation pouvant conduire à un état de choc. Des études montrent que chez des rats, dont le sytème dopaminergique mésostriatal est lésé, un prétraitement avec de la nicotine augmente le flux sanguin et le métabolisme du glucose dans le caude putamen. De même, un prétraitement à la nicotine rend les animaux moins sensibles à l’effet de choc dû à cette substance que des animaux témoins prétraités avec du sérum physiologique. Nous avons étudié l’influence de cet effet protecteur de la nicotine sur la perméabilité de la barrière hémato-encéphalique au cours des états de choc provoqués par la nicotine. L’administration d’une solution saline de doses de nicotine inférieures à celles produisant un effet de choc (1 mg/kg, i.p.), ou de doses conduisant à l’apparition d’états de choc (2, 5 et 8 mg/kg) a été réalisée. La technique d’injection intraveineuse a été utilisée pour calculer la constante de transfert du sang vers le cerveau (Kin) du traceur 3H AIB dans 6 régions différentes du cerveau. Le Kin moyen pour les groupes d’animaux traités avec 2,5 et 8 mg/kg de nicotine augmentait respectivement de 83.94, 182.6 et 265%. Un prétraitement de 21 jours par la nicotine prévient totalement l’augmentation du Kin apres injection de 2mg/kg de nicotine et partiellement pour les doses de 5 et 8 mg/kg.
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Diler, A.S., Üzüm, G., Lefauconnier, J.M., Ziylan, Y.Z. (1996). The Effect of Nicotine Pretreatment on the Blood-Brain Barrier Permeability in Nicotine-Induced Seizures. In: Couraud, PO., Scherman, D. (eds) Biology and Physiology of the Blood-Brain Barrier. Advances in Behavioral Biology, vol 46. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9489-2_54
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DOI: https://doi.org/10.1007/978-1-4757-9489-2_54
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