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Hippocampal prosaposin changes during stress: A glucocorticoid‐independent event
Author(s) -
Scaccianoce Sergio,
Mattei Vincenzo,
Del Bianco Paola,
Gizzi Chiara,
Sorice Maurizio,
Hiraiwa Masao,
Misasi Roberta
Publication year - 2004
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.10192
Subject(s) - hippocampal formation , corticosterone , glucocorticoid , hippocampus , endocrinology , stimulus (psychology) , medicine , neuroprotection , endogeny , neuroscience , chemistry , neurotrophic factors , hormone , psychology , receptor , psychotherapist
Several studies indicate that stress can produce remarkable effects on neurotrophic factors. In this regard, hippocampus is the most interesting structure of the brain because of its broad involvement in behavioral and neuroendocrine phenomena. In the present study, we investigated the effect of stress on hippocampal prosaposin, which is known to act as a neurotrophic and neuroprotective factor. Rats subjected to restraint stress (120 min) had a significant and transient reduction of hippocampal, but not hypothalamic, prosaposin full‐length protein. Indeed, when this stressful stimulus was applied daily for 3 days, no differences were detected in comparison with naive rats. To investigate the role of glucocorticoids in the stress‐induced decrease in hippocampal prosaposin, adrenalectomized and corticosterone‐treated rats were studied. The results indicate that adrenalectomized rats behave as intact animals. This finding indicates that the absence of endogenous corticosterone does not prevent a decrease in hippocampal prosaposin. When an increase of corticosterone was achieved through exogenous administration, hippocampal prosaposin concentrations were unchanged in comparison with vehicle‐injected (sesame oil) rats. These results led to the conclusion that stress, not via an increase of glucocorticoid hormone, transiently reduces hippocampal prosaposin levels. This phenomenon is followed by rapid recovery of the neurotrophin level, even when the stress stimulus persists. © 2004 Wiley‐Liss, Inc.