Volume 14, Number 6
2004
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Nitric oxide synthase and arginase expression changes in the rat perirhinal
and entorhinal cortices following unilateral vestibular damage: A link to
deficits in object recognition?
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pp. 411 - 417
Ping Liu, Catherine M. Gliddon, Libby Lindsay, Cynthia L. Darlington, Paul F. Smith
Previous studies have shown that peripheral vestibular damage
causes long-term neurochemical changes in the hippocampus
which may be related to spatial memory deficits. Since recent
studies have also demonstrated deficits in non-spatial object
recognition memory following vestibular lesions, the aim of the present
study was to extend these investigations into the perirhinal cortex (PRC), which
is known to be important for object recognition, and the related entorhinal cortex
(EC). We examined the effects of unilateral vestibular deafferentation (UVD) on
the expression of four enzymes associated with neuronal plasticity, neuronal nitric
oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), arginase I and
arginase II (AI and II), in the rat EC and PRC using Western blotting. Tissue was
collected at 10 hs, 50 hs and 2 weeks post-UVD. In the EC and PRC, nNOS protein
expression decreased on the contralateral side at 2 weeks post-UVD but not
before. At the same time, eNOS protein expression increased in both regions on the
contralateral side. In the EC, AII protein expression increased on the ipsilateral
side at 2 weeks post-UVD. In the PRC, AI increased and decreased on the contralateral
and ipsilateral sides (respectively) at 2 weeks post-UVD. AII showed a bilateral
increase in the PRC at 2 weeks post-UVD. These results demonstrate changes in NOS
and arginase protein expression in the PRC and EC following UVD, which are unlikely
to be due to the initial severity of the vestibular syndrome because they develop well
after vestibular compensation has taken place. Neurochemical changes in these regions
of the medial temporal lobe may be implicated in the development of object recognition
deficits that contribute to cognitive dysfunction following peripheral vestibular damage.
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