2006
DOI: 10.1016/j.brainres.2006.04.056
|View full text |Cite
|
Sign up to set email alerts
|

Role of cellular prion protein on LTP expression in aged mice

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

2
30
1

Year Published

2007
2007
2023
2023

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 40 publications
(33 citation statements)
references
References 47 publications
2
30
1
Order By: Relevance
“…A defect in nitric oxide signaling (Keshet et al, 1999), which is required for mossy fiber-granule cell LTP (Maffei et al, 2003), could explain the absence of presynaptic changes needed to generate EPSC potentiation (Sola et al, 2004). Therefore, PrP knock-out may directly affect the LTP mechanism, as originally proposed for hippocampal synapses (Collinge et al, 1994;Curtis et al, 2003;Maglio et al, 2004Maglio et al, , 2006 (but see Lledo et al, 1996).…”
Section: Discussionmentioning
confidence: 95%
See 1 more Smart Citation
“…A defect in nitric oxide signaling (Keshet et al, 1999), which is required for mossy fiber-granule cell LTP (Maffei et al, 2003), could explain the absence of presynaptic changes needed to generate EPSC potentiation (Sola et al, 2004). Therefore, PrP knock-out may directly affect the LTP mechanism, as originally proposed for hippocampal synapses (Collinge et al, 1994;Curtis et al, 2003;Maglio et al, 2004Maglio et al, , 2006 (but see Lledo et al, 1996).…”
Section: Discussionmentioning
confidence: 95%
“…However, subsequent analysis revealed several motor, cognitive, and emotional abnormalities (Roesler et al, 1999;Criado et al, 2005) and increased susceptibility to seizures . Recordings from brain slices of PrP 0/0 mice showed reduced synaptic inhibition and long-term potentiation (LTP) (a neural correlate of learning) (Bliss and Collingridge, 1993) in the hippocampus (Collinge et al, 1994;Curtis et al, 2003;Maglio et al, 2004Maglio et al, , 2006, but this observation was not confirmed (Lledo et al, 1996). Several abnormalities have been observed in PrP 0/0 neurons in culture, including reduced Ca 2ϩ -dependent K ϩ currents (Colling et al, 1996;Herms et al, 2001;Mallucci et al, 2002) and cytoplasmic Ca 2ϩ levels (Herms et al, 2000).…”
Section: Introductionmentioning
confidence: 99%
“…Mitochondrial dysfunction is thought to be a key factor in agerelated diseases of humans [19] and should therefore be investigated in the cattle. Biological relationships between aging and PrP C , including antioxidant-like activity [2], synaptic transmission [15], and the expression of PrP C in brain homogenates after PK treatment. The samples after PK treatment were separated by SDS-PAGE, transferred onto PVDF membranes and reacted with mAb 44B1.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, PrP c , by Cu 2+ binding, may participate in the control of calcium flux and redox stage of the presynaptic terminal (Vassallo and Herms, 2003). Lastly, pioneering electrophysiological studies (using PrP c knockout slices) by Collinge established that PrP c participates in long-term potentiation (Collinge et al, 1994;Curtis et al, 2003;Maglio et al, 2006). More recently, it has been shown that the absence of PrP c alters the expression of several neurotransmitter receptors (see (Maglio et al, 2004;Rangel et al, 2007) for examples).…”
Section: Introductionmentioning
confidence: 99%