دورية أكاديمية
Nitric oxide (NO) is an endogenous anticonvulsant but not a mediator of the increase in cerebral blood flow accompanying bicuculline-induced seizures in rats
| العنوان: | Nitric oxide (NO) is an endogenous anticonvulsant but not a mediator of the increase in cerebral blood flow accompanying bicuculline-induced seizures in rats |
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| المؤلفون: | Wang, Q, Theard, M A, Pelligrino, D A, Baughman, V L, Hoffman, W E, Albrecht, R F, Cwik, M, Paulson, O B, Lassen, N A |
| المصدر: | Wang , Q , Theard , M A , Pelligrino , D A , Baughman , V L , Hoffman , W E , Albrecht , R F , Cwik , M , Paulson , O B & Lassen , N A 1994 , ' Nitric oxide (NO) is an endogenous anticonvulsant but not a mediator of the increase in cerebral blood flow accompanying bicuculline-induced seizures in rats ' , Brain Research , vol. 658 , no. 1-2 , pp. 192-8 . https://doi.org/10.1016/s0006-8993Test(09)90026-9 |
| سنة النشر: | 1994 |
| المجموعة: | University of Copenhagen: Research / Forskning ved Københavns Universitet |
| مصطلحات موضوعية: | Amino Acid Oxidoreductases/antagonists & inhibitors, Animals, Anticonvulsants/metabolism, Arginine/analogs & derivatives, Bicuculline, Cerebrovascular Circulation/drug effects, Male, Nitric Oxide/physiology, Nitric Oxide Synthase, Nitroarginine, Rats, Wistar, Seizures/chemically induced, Stereoisomerism |
| الوصف: | Neurons synthesize NO, which may act as a retrograde messenger, involved in either potentiating or depressing neuronal excitability. NO may also play a role in the cerebral vasodilatory response to increased neuronal activity (i.e., seizures). In this study, two questions were asked: (1) is NO an endogenous anticonvulsant or proconvulsant substance? and (2) is the cerebral blood flow (CBF) increase accompanying bicuculline (BC)-induced seizures mediated by NO? The experiments were performed in 300-400-g Wistar rats anesthetized with 0.6% halothane and 70% N2O/30% O2. CBF was measured using the intracarotid 133Xe clearance method or laser-Doppler flowmetry. EEG activity was recorded. Chronic treatment (4 days) with nitro-L-arginine (L-NA), a potent NO synthase (NOS) inhibitor (400 mg/kg total), suppressed brain NOS by > 97% and prolonged seizure duration from 6 +/- 1 (saline-treated controls) to 12 +/- 2 min. In the L-NA-treated group, the CBF increase was sustained as long as seizure activity remained, indicating that CBF was still tightly coupled to seizure activity. Interestingly, the supposed inactive enantiomer of L-NA, D-NA, also showed an inhibition of brain NOS activity, ranging from 87 to 100%. The duration of seizures in this group (average 8 +/- 2 min) corresponded directly to the magnitude of reduction in NOS activity (r = 0.83, P < 0.05). Specifically, the D-NA results indicated that NOS inhibition had to exceed 95% before any effect on seizure duration could be seen.(ABSTRACT TRUNCATED AT 250 WORDS) |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1016/s0006-8993(09)90026-9 |
| الإتاحة: | https://doi.org/10.1016/s0006-8993Test(09)90026-9 https://curis.ku.dk/portal/da/publications/nitric-oxide-no-is-an-endogenous-anticonvulsant-but-not-a-mediator-of-the-increase-in-cerebral-blood-flow-accompanying-bicucullineinduced-seizures-in-ratsTest(3572884e-ca1f-469f-8af1-e0f4991a44de).html |
| حقوق: | info:eu-repo/semantics/restrictedAccess |
| رقم الانضمام: | edsbas.76FDBC9D |
| قاعدة البيانات: | BASE |
| DOI: | 10.1016/s0006-8993(09)90026-9 |
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