2005
DOI: 10.1016/j.nbd.2005.05.023
|View full text |Cite
|
Sign up to set email alerts
|

Increased calbindin-D28k immunoreactivity in striatal projection neurons of R6/2 Huntington's disease transgenic mice

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

0
7
0

Year Published

2008
2008
2021
2021

Publication Types

Select...
8

Relationship

0
8

Authors

Journals

citations
Cited by 10 publications
(7 citation statements)
references
References 86 publications
0
7
0
Order By: Relevance
“…Early physiological changes in MSNs observed in animal models of HD are reminiscent of those observed in dopamine-depleted animals, including an increase in input resistance and a decrease in spine density (Klapstein et al, 2001), as well as increased expression of calcium binding proteins (Huang et al, 1995; Sun et al, 2005). While these changes may arise as a direct consequence of mutant htt expression in MSNs, another possibility is that they represent compensatory responses to increased excitatory drive from cortex.…”
Section: Basal Ganglia Circuit Function and Dysfunctionmentioning
confidence: 99%
“…Early physiological changes in MSNs observed in animal models of HD are reminiscent of those observed in dopamine-depleted animals, including an increase in input resistance and a decrease in spine density (Klapstein et al, 2001), as well as increased expression of calcium binding proteins (Huang et al, 1995; Sun et al, 2005). While these changes may arise as a direct consequence of mutant htt expression in MSNs, another possibility is that they represent compensatory responses to increased excitatory drive from cortex.…”
Section: Basal Ganglia Circuit Function and Dysfunctionmentioning
confidence: 99%
“…The consequences of CalDAG-GEFII dysregulation in HD models still need to be evaluated. Interestingly, in contrast to CalDAG-GEFI, another matrix-enriched calcium-binding protein, calbindin-D28K, is up-regulated in HD and HD animal models, and this change has been suggested to be protective against calcium-induced excitotoxicity (Huang et al, 1995; Sun et al, 2005). Most striatum-enriched genes are down-regulated in HD however (Desplats et al, 2006), which may be a compensatory response to the differential vulnerability of the MSN cell-type to mutant Htt expression.…”
Section: Striosomes Signaling and Diseasementioning
confidence: 99%
“…Moreover, in HD, increased expression of the calcium-binding proteins parvalbumin and calretinin is positively associated with interneuron survival [206]. Parvalbumin and calretinin exert calcium-buffering effects in response to excessive calcium-induced excitotoxicity and are thought to be neuroprotective and important for the survival of interneurons [207,208]. However, the enrichment of calcium-permeable AMPA receptors in parvalbumin interneurons may be a potential pathogenic mechanism [209].…”
Section: Striatal Pathologymentioning
confidence: 99%
“…In HD, increased expression of calcium-binding protein calbindin-D28K is positively associated with interneuron survival [206]. Calbindin-D28K is predominantly found in the matrix and thought to exert neuroprotective effects that promote calcium-buffering in response to excessive calcium-induced excitotoxicity [207,208]. Crittenden et al found that calcium diacylglycerol guanine nucleotide exchange factors (CalDAG-GEFs), which are striatum-enriched calcium and diacylglycerol binding proteins, are severely down-regulated in the R6/2 mouse model of HD and post-mortem striatal tissues from patients with HD [89].…”
Section: Striatal Pathologymentioning
confidence: 99%