Age-Dependent vasopressinergic modulation of Noc/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury.
This study was designed to characterize the role of vasopressin in nociceptin/orphanin FQ (NOC/oFQ)-induced impairment of NMDA cerebrovasodilation after fluid percussion brain injury (FPI) as a function of age in newborn (1-5 days old) and juvenile (3-4 weeks old) pigs equipped with a closed cranial window. Previous studies have observed that NOC/oFQ is released into CSF and contributes to impaired NMDA induced pial artery dilation following FPI to a greater extent in newborn versus juvenile pigs. Topical vasopressin (40 pg/mL), a concentration approximating that observed in CSF following FPI in the newborn, increased CSF NOC/oFQ from 69 +/- 3 to 102 +/- 8 pg/mol under non-FPI conditions. CSF NOC/oFQ was elevated within 60 min of FPI (70 +/- 3 to 444 +/- 51 pg/mL), but release was attenuated by MEAVP, a vasopressin antagonist, in the newborn (71 +/- 3 to 146 +/- 11 pg/mL). CSF vasopressin and NOC/oFQ were not elevated as greatly in the juvenile following FPI and MEAVP correspondingly did not attenuate CSF NOC/oFQ release as much as in the newborn. Under noninjury conditions, vasopressin (40 pg/mL) coadministered with NMDA (10(-8), 10(-6) M) attenuated pial dilation to this excitatory amino acid (9 +/- 1% and 16 +/- 1% vs. 3 +/- 1% and 5 +/- 2%). Following FPI in the newborn, NMDA-induced pial artery dilation was reversed to vasoconstriction, and both NOC/oFQ and vasopressin receptor antagonists partially prevented these alterations (9 +/- 1%) and 16 +/- 1%, sham control; -7 +/- 1% and -12 +/- 1%, FPI; -2 +/- 1% and -3 +/- 1%, FPI-NOC/oFQ antagonist; and 1 +/- 1% and 4 +/- 1%, FPI-vasopressin antagonist). NMDA-induced pial dilation was only attenuated following FPI in the juvenile and modestly restored by NOC/oFQ and vasopressin receptor antagonists. These data show that vasopressin, in concentrations present in CSF following FPI, contributes to the release of CSF NOC/oFQ following such an insult. The greater release of vasopressin following FPI in the newborn contributes to the corresponding greater release of NOC/oFQ in the newborn versus the juvenile. Moreover, vasopressin also contributes to the impairment of NMDA cerebrovasodilation after brain injury to a greater extent in newborn versus juveniles. These data suggest that vasopressin modulates NOC/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury in an age-dependent manner.[1]References
- Age-Dependent vasopressinergic modulation of Noc/oFQ-induced impairment of NMDA cerebrovasodilation after brain injury. Armstead, W.M. J. Neurotrauma (2001) [Pubmed]
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