Nitric Oxide Synthase Expression in the Cerebral Cortex of Patients with Epilepsy

• Published in: Epilepsia (Copenhagen) Vol. 41; no. 10; pp. 1259 - 1268
• Main Authors: González‐Hernández, Tomás, García‐Marín, Victor, Perez‐Delgado, María del Mar, González‐González, María Ligia, Rancel‐Torres, Nélida, González‐Feria, Luis
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.10.2000; Blackwell
• Subjects: Adolescent; Adult; Biological and medical sciences; Biopsy; Cerebral cortex; Cerebral Cortex - chemistry; Cerebral Cortex - enzymology; Child; Endothelium - enzymology; Epilepsy; Epilepsy - enzymology; Female; GABAergic neurons; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Immunohistochemistry; Immunohistochemis‐try; Male; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Neurons - enzymology; Nitric oxide; Nitric Oxide Synthase - analysis; Nitric Oxide Synthase - metabolism; Protein Isoforms; Human; Immunohistochemistry; Nervous system diseases; Cerebral cortex; Pathophysiology; Enzyme; Epilepsy; Gene expression; Gabaergic neurone; Nitric-oxide synthase; Cerebral disorder; Pathology; Central nervous system disease; Oxidoreductases; Brain (vertebrata)
• ISSN: 0013-9580; 1528-1167
• DOI: 10.1111/j.1528-1157.2000.tb04603.x

Summary Purpose: Nitric oxide (NO), a short‐lived radical synthesized from L‐arginine by activation of the enzyme nitric oxide synthase (NOS), has been implicated in the pathophysiology of epilepsy by some investigators. However, the current data about NO and NOS in epilepsy are controversial and are derived only from animal models of epilepsy. In this study we investigated possible changes in NOS expression in the cerebral cortex of patients with epilepsy. Methods: Qualitative and quantitative parameters of the im‐munolabeling pattern of the neuronal, endothelial, and inducible isoforms of NOS were analyzed in biopsy material obtained from patients with short and long seizure history and from patients without epilepsy. Results: The comparative study showed that in the cerebral cortex of patients with epilepsy, particularly in those with a long seizure history, the number and labeling intensity of NOS‐positive neurons increased, and that a subpopulation of nonpy‐ramidal GABAergic neurons (type H NOS neurons) was responsible for this phenomenon. Conclusions: The fact that NOS upregulation is more evident in patients with a long seizure history suggests that this is a consequence of seizures, acting probably as an adaptative response to the sustained release of excitatory amino acids.