XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

Lectures
SPINAL CORD INJURY: PATHOGENESIS AND TREATMENT
Nadežda Lukáčová, Alexandra Dávidová, Ľudmila Capková and Andrea Kucharíková
Institute of Neurobiology, Slovak Academy of Sciences, Košice
Transversal spinal cord lesions interrupt a neuronal pathways which provide an inhibitory
effect on reflex activity. Subsequently, spasticity develops below the injury site. The aim of
this study was to find out whether neuronal degeneration correlates with up-regulation
of nitric oxide synthase (NOS) forming nitric oxide, and whether these neurons are protected
by parvalbumin (PV), buffering free intracellular calcium. Fluoro-Jade B was used
to detect dying neurons. 7 and 14 days after spinal cord injury both the level of nNOS
protein and nNOS mRNA level were significantly increased in segments below the site of
injury. We noted strong nNOS upregulation in motoneurons and in neurons of laminae
VII. However, a-motoneurons were not Fluoro-Jade B positive. While PV-IR was increased
in a number of small neurons in rat, rabbit’s a-motoneurons exhibited very strong PV
fluorescent staining. The results indicate the participation of PV in motor control. After
spinal injury the animals were treated with GABA B
receptor agonist Baclofen (3 µg/2 x
daily from 7th day), or with NNLA (an inhibitor of neuronal NOS dosed at 20 mg/b.w.)
independently, or combined together. Intrathecal treatment with Baclofen for three days
restored both the NO synthase and PV levels almost to control value. NNLA or Baclofen
decreased the level of nNOS mRNA in spinal cord, but combined use of both drugs was
not effective.
Acknowledgements: Supported by APVV 0314-06 and by VEGA 2/0015/08.
76 XXII. Biochemistry Congress, Martin