B-50 GAP-43 PHOSPHORYLATION IN HIPPOCAMPAL SLICES FROM AGED RATS - EFFECTS OF PHOSPHATIDYLSERINE ADMINISTRATION/

Citation
C. Gianotti et al., B-50 GAP-43 PHOSPHORYLATION IN HIPPOCAMPAL SLICES FROM AGED RATS - EFFECTS OF PHOSPHATIDYLSERINE ADMINISTRATION/, Neurobiology of aging, 14(5), 1993, pp. 401-406
Citations number
47
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01974580
Volume
14
Issue
5
Year of publication
1993
Pages
401 - 406
Database
ISI
SICI code
0197-4580(1993)14:5<401:BGPIHS>2.0.ZU;2-M
Abstract
Phosphorylation of the presynaptic protein B-50/GAP-43, a substrate of protein kinase C (PKC), has been implicated in neuronal mechanisms re lated to learning and memory. We evaluated both basal (5 mM KCl) and s timulated (30 mM KCl) B-50/GAP-43 phosphorylation in P-32-prelabeled h ippocampal slices obtained from adult and senescent male Sprague-Dawle y rats. The in situ B-50/GAP-43 phosphorylation was assayed by quantit ative immunoprecipitation. There was no age-related difference in B-50 /GAP-43 basal phosphorylation. However, B-50/GAP-43 phosphorylation in depolarized slices from aged rats was significantly decreased relativ e to that of adult animals. Aged rats were treated with either tris bu ffer or sonicated suspension of phosphatidylserine (PS) in tris buffer (15 mg/kg IP for 7 and 17 days). PS did not affect basal and high K+- induced B-50/GAP-43 phosphorylation in the 7-day treatment. However, a fter 17 days, PS restored the K+-induced B-50/GAP-43 phosphorylation. It is proposed that repeated PS administrations might be beneficial to the age-induced deterioration of endogenous B-50/GAP-43 phosphorylati on by acting on Ca++ homeostatic mechanisms and/or PKC.