1995
DOI: 10.1016/0006-8993(95)00783-m
|View full text |Cite
|
Sign up to set email alerts
|

Region-specific alterations of calbindin-D28k immunoreactivity in the rat hippocampus following adrenalectomy and corticosterone treatment

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

0
12
1

Year Published

1996
1996
2013
2013

Publication Types

Select...
6
1

Relationship

1
6

Authors

Journals

citations
Cited by 22 publications
(13 citation statements)
references
References 28 publications
0
12
1
Order By: Relevance
“…In contrast, the absence of calbindin from superficial pyramidal cells in spite of a pronounced condensation of the cell layer suggests an independent development of these characteristics in the sengi, guinea pig and rabbit CA1. Mechanisms related to age- (Poitier et al, 1994; Villa et al, 1994; de Jong et al, 1996), activity- (Lowenstein et al, 1991; Maglóczky et al, 1997), or hormone-dependent (Krugers et al, 1995; Trejo et al, 2000) changes of calbindin content in hippocampal principal cells may mediate species-specific expression patterns. Deep calbindin+ pyramidal cells are present in CA1 of fox and primates and in the distal and temporal CA1 of mouse and rat.…”
Section: Discussionmentioning
confidence: 99%
“…In contrast, the absence of calbindin from superficial pyramidal cells in spite of a pronounced condensation of the cell layer suggests an independent development of these characteristics in the sengi, guinea pig and rabbit CA1. Mechanisms related to age- (Poitier et al, 1994; Villa et al, 1994; de Jong et al, 1996), activity- (Lowenstein et al, 1991; Maglóczky et al, 1997), or hormone-dependent (Krugers et al, 1995; Trejo et al, 2000) changes of calbindin content in hippocampal principal cells may mediate species-specific expression patterns. Deep calbindin+ pyramidal cells are present in CA1 of fox and primates and in the distal and temporal CA1 of mouse and rat.…”
Section: Discussionmentioning
confidence: 99%
“…Animals that were exposed to this stress-paradigm displayed increased Calbindin-D28k immunoreactivity exclusively in the hippocampal CA1 pyramidal cell layer whereas PV immunoreactivity in the hippocampus was not altered by the stress. Previously we observed that prolonged exposure to high levels of corticosterone was associated with increased CB-immunoreactivity exclusively in the hippocampal CA1 pyramidal cell layer [14,15] which probably reflects increased protein levels of Calbindin-D28k [11]. Since the stress used at present transiently elevates plasma corticosterone levels (unpublished results) one might speculate that (1) corticosterone mediates the increased Calbindin-D28k immunoreactivity following prolonged stress, and (2) the increased immunoreactivity following stress reflects increased protein levels.…”
mentioning
confidence: 81%
“…Fax: + 31 (20) 525-7709. corticosteroids increase the capacity to maintain neuronal Ca 2+ homeostasis. High levels of corticosteroids increase the immunoreactivity [14,15], protein levels, and mRNA levels [11] of Calbindin-D28k (CB) which can act as intraneuronal Ca 2+ buffer [16,19,20,27]. In the present study we firstly investigated whether elevation of plasma steroid levels by physiological rather than pharmaceutical treatment alters the immunoreactivity of the calcium binding protein CB and Parvalbumin (PV).…”
mentioning
confidence: 99%
“…Several lines of evidence indicate that the level of brain calcium‐binding protein calbindin‐D28k (CB) expression can be elevated by social stressful experiences. In fact, hippocampal neurons of juvenile or adult animals submitted to maternal separation (Lephart and Watson, 1999), social challenges (Krugers et al, 1996) or treated directly with corticosterone (Iacopino and Christakos, 1990; Krugers et al, 1995) showed significant increases in CB expression. This CB up‐regulation probably occurs because glucocorticoids (GCs), released by stress‐induced activation of the hypothalamic–pituitary–adrenal axis, can promote Ca 2+ influx through either voltage‐dependent Ca 2+ channels (Zhou et al, 2000) or N ‐methyl‐ d ‐aspartate (NMDA) glutamate receptors (Stein‐Behrens et al, 1994).…”
Section: Methodsmentioning
confidence: 99%