A. Lumme et al., EXPRESSION OF NITRIC-OXIDE SYNTHASE IN HYPOTHALAMIC NUCLEI FOLLOWING AXONAL INJURY OR COLCHICINE TREATMENT, Experimental neurology, 144(2), 1997, pp. 248-257
Nitric oxide (NO) has recently gained much attention due to its appare
ntly double-edged role in neuronal injury. This study was aimed at elu
cidating neuronal nitric oxide synthase (nNOS) expression in the brain
after two types of injury, namely axonal transection and colchicine t
reatment, The neurosecretory hypothalamo-pituitary pathway served as a
model for the reaction of central neurons to these two types of injur
y, Axonal transection, i.e., pituitary stalk section, resulted in a qu
alitative increase in NOS content in the supraoptic and paraventricula
r nuclei. In these nuclei, there was also an increase in the number of
NOS-expressing neurons after the operation, Surprisingly, in the peri
ventricular nucleus, a strong decrease in the number of NOS-positive m
agnocellular neurons was observed in the anterior part of the nucleus.
Intracere-broventricular injection of colchicine resulted in an incre
ase in the cell. count in the paraventricular nucleus, while the other
nuclei remained unchanged, Our results suggest that axonal injury res
ults in an increase in nNOS expression in the major neurosecretory nuc
lei, while the periventricular nucleus shows the opposite reaction, Co
lchicine treatment has an effect similar to that of axotomy in the maj
or neurosecretory nuclei, suggesting that an increase in NOS expressio
n may be induced by interrupted axonal transport, In the periventricul
ar nucleus, the decrease in the number of NOS-containing neurons sugge
sts differences among hypothalamic NOS-containing neuron groups in res
ponse to neuronal injury. (C) 1997 Academic Press.