We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
NMDA-evoked [Ca2+]i increase in salamander retinal ganglion cells: Modulation by PKA and adrenergic receptors.
- Authors
HAN, YI; WU, SAMUEL M.
- Abstract
Application of NMDA induces a depolarization and increase of intracellular calcium concentration ([Ca2+]i) in retinal ganglion cells, which cause ganglion cell death in models of glaucoma. In the present study, we investigated the pharmacological mechanism of how NMDA-evoked increase in calcium could be modulated in dissociated retinal ganglion cells from tiger salamander. In these neurons, protein kinase A (PKA) up-regulated the NMDA-evoked [Ca2+]i increase. In the presence of 8-bromo-cAMP or forskolin to stimulate PKA, the elevation level of [Ca2+]i induced by NMDA became even higher; In the presence of H-89, a PKA inhibitor, the NMDA-evoked [Ca2+]i increase was attenuated. In addition, applications of adrenergic compounds were also found to influence the NMDA-evoked [Ca2+]i increase. UK-14,304, a selective ±2 agonist, reduced the elevation level of [Ca2+]i caused by NMDA. In contrast, isoproterenol, a ² agonist, augmented the NMDA-evoked [Ca2+]i increase. These adrenergic regulations were due to direct activation of adrenoceptors, since modulations of both UK-14,304 and isoproterenol on the NMDA-evoked [Ca2+]i increase were abolished by their respective antagonists. Furthermore, adrenergic regulations were mediated through a PKA-related pathway since PKA inhibitor blocked adrenergic regulations. The possible modulatory site(s) by PKA was also discussed.
- Publication
Visual Neuroscience, 2002, Vol 19, Issue 3, p249
- ISSN
0952-5238
- Publication type
Article
- DOI
10.1017/S0952523802192029