title: Expression of nitric oxide synthase in hypothalamic nuclei following axonal injury or colchicine treatment.
abstract: Nitric oxide (NO) has recently gained much attention due to its apparently double-edged role in neuronal injury. This study was aimed at elucidating neuronal nitric oxide synthase (nNOS) expression in the brain after two types of injury, namely axonal transection and colchicine treatment. The neurosecretory hypothalamo-pituitary pathway served as a model for the reaction of central neurons to these two types of injury. Axonal transection, i.e., pituitary stalk section, resulted in a qualitative increase in NOS content in the supraoptic and paraventricular nuclei. In these nuclei, there was also an increase in the number of NOS-expressing neurons after the operation. Surprisingly, in the periventricular nucleus, a strong decrease in the number of NOS-positive magnocellular neurons was observed in the anterior part of the nucleus. Intracerebroventricular injection of colchicine resulted in an increase in the cell count in the paraventricular nucleus, while the other nuclei remained unchanged. Our results suggest that axonal injury results in an increase in nNOS expression in the major neurosecretory nuclei, while the periventricular nucleus shows the opposite reaction. Colchicine treatment has an effect similar to that of axotomy in the major neurosecretory nuclei, suggesting that an increase in NOS expression may be induced by interrupted axonal transport. In the periventricular nucleus, the decrease in the number of NOS-containing neurons suggests differences among hypothalamic NOS-containing neuron groups in response to neuronal injury.
authors.affiliation: Department of Anatomy, Children's Castle Hospital, Helsinki, Finland.
authors.forename: A
authors.initials: A
authors.lastname: Lumme
authors.forename: S
authors.initials: S
authors.lastname: Vanhatalo
authors.forename: M
authors.initials: M
authors.lastname: Sadeniemi
authors.forename: S
authors.initials: S
authors.lastname: Soinila
mesh_terms: D000818:Animals; D001369:Axons; D002452:Cell Count; D003078:Colchicine / Q000633:toxicity*; D003714:Denervation; D004790:Enzyme Induction; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism; D007031:Hypothalamus / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism / Q000473:pathology; D009252:NADPH Dehydrogenase / Q000032:analysis; D009419:Nerve Tissue Proteins / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D009569:Nitric Oxide / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000096:biosynthesis* / Q000235:genetics; D009928:Organ Specificity; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D010902:Pituitary Gland / Q000293:injuries; D051381:Rats; D017208:Rats, Wistar; D013495:Supraoptic Nucleus / Q000187:drug effects / Q000201:enzymology / Q000473:pathology
chemical_list: D009419:Nerve Tissue Proteins; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D009252:NADPH Dehydrogenase; D003078:Colchicine