Inhibition and inactivation of presynaptic cholinergic markers using redox-reactive choline analogs

1993 ◽  
Vol 36 (13) ◽  
pp. 1893-1901 ◽  
Author(s):  
Phenil J. Patel ◽  
William S. Messer ◽  
Richard A. Hudson
2021 ◽  
Vol 22 (11) ◽  
pp. 5499
Author(s):  
Veronica Corsetti ◽  
Carla Perrone-Capano ◽  
Michael Sebastian Salazar Intriago ◽  
Elisabetta Botticelli ◽  
Giancarlo Poiana ◽  
...  

Dorsal root ganglia (DRG) neurons synthesize acetylcholine (ACh), in addition to their peptidergic nature. They also release ACh and are cholinoceptive, as they express cholinergic receptors. During gangliogenesis, ACh plays an important role in neuronal differentiation, modulating neuritic outgrowth and neurospecific gene expression. Starting from these data, we studied the expression of choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) expression in rat DRG neurons. ChAT and VAChT genes are arranged in a “cholinergic locus”, and several splice variants have been described. Using selective primers, we characterized splice variants of these cholinergic markers, demonstrating that rat DRGs express R1, R2, M, and N variants for ChAT and V1, V2, R1, and R2 splice variants for VAChT. Moreover, by RT-PCR analysis, we observed a progressive decrease in ChAT and VAChT transcripts from the late embryonic developmental stage (E18) to postnatal P2 and P15 and in the adult DRG. Interestingly, Western blot analyses and activity assays demonstrated that ChAT levels significantly increased during DRG ontogenesis. The modulated expression of different ChAT and VAChT splice variants during development suggests a possible differential regulation of cholinergic marker expression in sensory neurons and confirms multiple roles for ACh in DRG neurons, both in the embryo stage and postnatally.


2013 ◽  
Vol 33 (3) ◽  
pp. 767-773 ◽  
Author(s):  
Maria Luisa Rocco ◽  
Andrea Pristerà ◽  
Luana Pistillo ◽  
Luigi Aloe ◽  
Nadia Canu ◽  
...  

1990 ◽  
Vol 52 ◽  
pp. 74
Author(s):  
Toru Egashira ◽  
Fumie Murayama ◽  
Yoshihira Kimba ◽  
Yasumitsu Yamanaka

2008 ◽  
Vol 26 (5) ◽  
pp. 467-475 ◽  
Author(s):  
Caiping Mao ◽  
Xin Yuan ◽  
Hong Zhang ◽  
Juanxiu Lv ◽  
Junchang Guan ◽  
...  

2008 ◽  
Vol 1246 ◽  
pp. 167-177 ◽  
Author(s):  
Cornelius K. Donat ◽  
Martin U. Schuhmann ◽  
Cornelia Voigt ◽  
Karen Nieber ◽  
Winnie Deuther-Conrad ◽  
...  

1986 ◽  
Vol 64 (3) ◽  
pp. 369-375 ◽  
Author(s):  
S. R. El-Defrawy ◽  
R. J. Boegman ◽  
K. Jhamandas ◽  
R. J. Beninger

Excitotoxins such as kainic acid, ibotenic acid, and quinolinic acid are a group of molecules structurally related to glutamate or aspartate. They are capable of exciting neurons and producing axon sparing neuronal degeneration. Quinolinic acid (QUIN), an endogenous metabolite of the amino acid, tryptophan, has been detected in brain and its concentration increases with age. The content of QUIN in the brain and the activity of the enzymes involved in its synthesis and metabolism show a regional distribution. The neuroexcitatory action of QUIN is antagonized by magnesium (Mg2+) and the aminophosphonates, proposed N-methyl-D-aspartate (NMDA) receptor antagonists, suggesting that QUIN acts at the Mg2+-sensitive NMDA receptor. Like its excitatory effects, QUIN's neurotoxic actions in the striatum are antagonized by the aminophosphonates. This suggests that QUIN neurotoxicity involves the NMDA receptor and (or) another receptor sensitive to the aminophosphonates. The neuroexcitatory and neurotoxic effects of QUIN are antagonized by kynurenic acid (KYN), another metabolite of tryptophan. QUIN toxicity is dependent on excitatory amino acid afferents and shows a regional variation in the brain. Local injection of QUIN into the nucleus basalis magnocellularis (NBM) results in a dose-dependent reduction in cortical cholinergic markers including the evoked release of acetylcholine. A significant reduction in cortical cholinergic function is maintained over a 3-month period. Coinjection of an equimolar ratio of QUIN and KYN into the NBM results in complete protection against QUIN-induced neurodegeneration and decreases in cortical cholinergic markers. In contrast, focal injections of QUIN into the frontoparietal cortex do not alter cortical cholinergic function. Animals showing central cholinergic hypofunction induced by QUIN could serve as experimental models for testing pharmacological agents aimed at improving the function of damaged cholinergic neurons.


2005 ◽  
Vol 46 (5) ◽  
pp. 409-422 ◽  
Author(s):  
Debby Van Dam ◽  
Bart Marescau ◽  
Sebastiaan Engelborghs ◽  
Thomas Cremers ◽  
Jan Mulder ◽  
...  

2005 ◽  
Vol 30 (12) ◽  
pp. 1511-1520 ◽  
Author(s):  
Kristin Huse Haug ◽  
Inger Lise Bogen ◽  
Harald Osmundsen ◽  
Ivar Walaas ◽  
Frode Fonnum

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