Ethidium bromide inhibits rat brain acetylcholinesterase activity in vitro

Mazzanti, Cinthia M.; Spanevello, Rosélia Maria; Obregón, Adriana; Pereira, Luciane Belmonte; Streher, Cristiane A.; Ahmed, Mushtaq; Mazzantí, Alexandre; Graça, Dominguita Lühers; Morsch, Vera Maria; Schetinger, Maria Rosa Chitolina

doi:10.1016/j.cbi.2006.05.013

Cited by 19 publications

(11 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2 and 3). These results are in accordance with a previous study from our laboratory demonstrating in vitro the inhibition of AChE by EB in the ST HP, CC and CB at various concentrations tested (Mazzanti et al, 2006b). We also carried out studies in vivo using EB as the demyelinating agent demonstrating that the AChE activity was inhibited on 7, 15 and 30 days after EB injection in the same brain structures as used in this study (Mazzanti et al, 2006a).…”

Section: Discussionsupporting

confidence: 93%

Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide

Mazzanti

Spanevello

Ahmed

et al. 2007

Intl J of Devlp Neuroscience

Self Cite

View full text Add to dashboard Cite

Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striatum, hippocampus, hypothalamus, cerebellum and pons of the rats experimentally demyelinated by ethidium bromide. Rats were divided into four groups: I control (injected with saline), II (treated with cyclosporine A), III (injected with 0.1% ethidium bromide) and IV (injected with 0.1% the ethidium bromide and treated with cyclosporine A). The results showed a significant inhibition (p<0.05) of acetylcholinesterase activity in the groups II, III and IV in all brain structures analyzed. In the striatum, hippocampus, hypothalamus and pons the inhibition was greater (p<0.005) when ethidium bromide was associated with cyclosporine A. In conclusion, the present investigation demonstrated that cyclosporine A is an inhibitor of acetylcholinesterase activity and this effect is increased after an event of toxic demyelination of the central nervous system.

show abstract

Section: Discussionsupporting

confidence: 93%

Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide

Mazzanti

Spanevello

Ahmed

et al. 2007

Intl J of Devlp Neuroscience

Self Cite

View full text Add to dashboard Cite

show abstract

“…In an attempt to explain the ameliorative effects of (PhSe) 2 in the scopolamine model, one can speculate that (PhSe) 2 acts on the cholinergic system by inhibiting acetylcholinesterase (AChE) activity. This hypothesis is supported by the fact that ebselen, another organoselenium compound, inhibited AChE activity in different brain regions (Mazzanti et al, 2009). This idea is also supported by the cholinergic hypothesis, in which many efforts have been made to reverse cognitive deficits by increasing brain cholinergic activity through AChE inhibitors, acetylcholine precursors, or cholinergic agonists (Giacobini, 1996).…”

Section: Discussionmentioning

confidence: 92%

Diphenyl diselenide improves scopolamine-induced memory impairment in mice

Souza

Brüning²,

Leite³

et al. 2010

Behavioural Pharmacology

View full text Add to dashboard Cite

This study was conducted to evaluate the effects of exposure to diphenyl diselenide (PhSe)2 on cognitive impairment induced by scopolamine, a muscarinic antagonist, using the Y-maze and Morris water maze tests in mice. One hour before the tests, mice were treated with (PhSe)2 (50 mg/kg, oral) and 30 min later memory impairment was induced by administration of scopolamine (1 mg/kg, intraperitoneal). (PhSe)2 (50 mg/kg, oral) significantly improved scopolamine-induced memory impairment in the Y-maze test. At the probe trial session in Morris water maze, (PhSe)2 (50 mg/kg, oral) significantly decreased the escape latency, increased the number of crossings in the platform local, and increased the time spent in the platform quadrant when compared with the scopolamine-treated group. General locomotor activity was similar in all groups. This study showed that (PhSe)2 ameliorated the impairments of spatial long-term memory and short-term memory, showed by the performance of mice in the Morris water maze and Y-maze tasks, respectively. These results suggest that (PhSe)2 may be useful for the treatment of cognitive impairment that may hold significant therapeutic value in alleviating certain memory deficits observed in Alzheimer's disease.

show abstract

“…Recently, was demonstrated by our laboratory that EB is a strong inhibitor of AChE activity in vitro, and that this inhibition was not homogeneous in all cerebral structures evaluated [46]. In relation to the treatment with IFN-b, it was observed that this compound associate with EB did not alter AChE activity, suggesting that IFN-b was not able to prevent the inhibitors effects of EB.…”

Section: Discussionmentioning

confidence: 95%

Acetylcholinesterase Activity in Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon Beta

et al. 2006

View full text Add to dashboard Cite

The ethidium bromide (EB) demyelinating model was associated with interferon beta (IFN-beta) to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC), cerebellum (CB), hypothalamus (HY), pons (PN) and synaptosomes from the CC. Rats were divided into four groups: I control (saline), II (IFN-beta), III (EB) and IV (EB and IFN-beta). After 7, 15 and 30 days rats (n = 6) were sacrificed, and the brain structures were removed for enzymatic assay. AChE activity was found to vary in all the brain structures in accordance with the day studied (7-15-30 days) (P < 0.05). In the group III, there was an inhibition of the AChE activity in the ST, CB, HY, HP and also in synaptosomes of the CC (P < 0.05). It was observed that IFN-beta per se was capable to significantly inhibit (P < 0.05) AChE activity in the ST, HP, HY and synaptosomes of the CC. Our results suggest that one of the mechanisms of action of IFN-beta is through the inhibition of AChE activity, and EB could be considered an inhibitor of AChE activity by interfering with cholinergic neurotransmission in the different brain regions.

show abstract

Ethidium bromide inhibits rat brain acetylcholinesterase activity in vitro

Cited by 19 publications

References 34 publications

Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide

Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide

Diphenyl diselenide improves scopolamine-induced memory impairment in mice

Acetylcholinesterase Activity in Rats Experimentally Demyelinated with Ethidium Bromide and Treated with Interferon Beta

Contact Info

Product

Resources

About