2009
DOI: 10.1016/j.fct.2008.10.012
|View full text |Cite
|
Sign up to set email alerts
|

Effects of adult-onset choline deprivation on the activities of acetylcholinesterase, (Na+,K+)- and Mg2+-ATPase in crucial rat brain regions

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

0
5
0
3

Year Published

2010
2010
2020
2020

Publication Types

Select...
6
1

Relationship

0
7

Authors

Journals

citations
Cited by 9 publications
(8 citation statements)
references
References 35 publications
0
5
0
3
Order By: Relevance
“…Thus, activation of different PKC isoforms may either activate or inhibit Na + K + activation (Xia et al, 1995). In the same trend, Liapi et al (2009) observed that the differentially affected activities of AchE and Na + K + ATPase could result in modulation of cholinergic neurotransmission, neural excitability, metabolic energy production, Mg +2 homeostasis and protein synthesis in crucial rat brain regions.…”
Section: Discussionmentioning
confidence: 84%
“…Thus, activation of different PKC isoforms may either activate or inhibit Na + K + activation (Xia et al, 1995). In the same trend, Liapi et al (2009) observed that the differentially affected activities of AchE and Na + K + ATPase could result in modulation of cholinergic neurotransmission, neural excitability, metabolic energy production, Mg +2 homeostasis and protein synthesis in crucial rat brain regions.…”
Section: Discussionmentioning
confidence: 84%
“…On the other hand, choline-deficient diets induced deficits of this precursor both in cell membranes and in the ACh synthesizing compartment [186]. Lack of membrane integrity could cause the impairment of energy production in brain mitochondria, leading to increased vulnerability of cholinergic neurons to neurodegenerative signals along with appearance of behavioral deficits [186, 187].…”
Section: Cholinementioning
confidence: 99%
“…Lack of membrane integrity could cause the impairment of energy production in brain mitochondria, leading to increased vulnerability of cholinergic neurons to neurodegenerative signals along with appearance of behavioral deficits [186, 187]. Such reciprocal interactions between aberrant acetyl-CoA/energy and choline metabolisms may trigger vicious cycle of early deterioration of cholinergic neurons under various neurodegenerative conditions.…”
Section: Cholinementioning
confidence: 99%
“…For example, tetramers of the "tailed" variant (AChE-T), constitute the main form of AChE in the mammalian brain, while in the mouse brain, stress and anticholinesterase inhibitors induce the expression of unspliced "readthrough" variant (AChE-R) mRNA which produces a monomeric form (Perrier et al 2005). Choline deficiency caused the increase of AChE expression in crucial rat brain regions (hippocampus, hypothalamus, frontal cortex and pons) to a diverse extent (Liapi et al 2009). Taking these facts into consideration, results of our study may be the consequence of competition between AChE variants and their homologs for interactions with the corresponding protein partner in investigated tissues.…”
Section: Discussionmentioning
confidence: 99%