Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

Jamal, Mostofa; Ameno, Kiyoshi; Miki, Takanori; Tanaka, Naoko; Ohkubo, Eriko; Kojima, Hiroshi

doi:10.1007/s11064-010-0155-x

Cited by 9 publications

(5 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These complex behaviors allow for adaptation in response to changes in the environment and are modulated by various neurotransmitters, including the cholinergic system (Logue and Gould 2014 ). Acute ethanol injection shows a dose-dependent effect on ACh release in PFC (Stancampiano et al 2004 ): low intraperitoneal doses of ethanol (0.5 g/kg) increase, while higher doses (1 g/kg) reduce ACh release in the rat PFC (Stancampiano et al 2004 ; Jamal et al 2010 ). These biphasic changes of ACh transmission in the PFC may be of relevance for the bidirectional modulation of working memory by ethanol (Rossetti et al 2002 ; Stancampiano et al 2004 ).…”

Section: Introductionmentioning

confidence: 99%

Cholinesterase inhibitors, donepezil and rivastigmine, attenuate spatial memory and cognitive flexibility impairment induced by acute ethanol in the Barnes maze task in rats

Gaweł

Labuz

Gibuła-Bruzda

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

Central cholinergic dysfunction contributes to acute spatial memory deficits produced by ethanol administration. Donepezil and rivastigmine elevate acetylcholine levels in the synaptic cleft through the inhibition of cholinesterases—enzymes involved in acetylcholine degradation. The aim of our study was to reveal whether donepezil (acetylcholinesterase inhibitor) and rivastigmine (also butyrylcholinesterase inhibitor) attenuate spatial memory impairment as induced by acute ethanol administration in the Barnes maze task (primary latency and number of errors in finding the escape box) in rats. Additionally, we compared the influence of these drugs on ethanol-disturbed memory. In the first experiment, the dose of ethanol (1.75 g/kg, i.p.) was selected that impaired spatial memory, but did not induce motor impairment. Next, we studied the influence of donepezil (1 and 3 mg/kg, i.p.), as well as rivastigmine (0.5 and 1 mg/kg, i.p.), given either before the probe trial or the reversal learning on ethanol-induced memory impairment. Our study demonstrated that these drugs, when given before the probe trial, were equally effective in attenuating ethanol-induced impairment in both test situations, whereas rivastigmine, at both doses (0.5 and 1 mg/kg, i.p.), and donepezil only at a higher dose (3 mg/kg, i.p.) given prior the reversal learning, attenuated the ethanol-induced impairment in cognitive flexibility. Thus, rivastigmine appears to exert more beneficial effect than donepezil in reversing ethanol-induced cognitive impairments—probably due to its wider spectrum of activity. In conclusion, the ethanol-induced spatial memory impairment may be attenuated by pharmacological manipulation of central cholinergic neurotransmission.

show abstract

Section: Introductionmentioning

confidence: 99%

Cholinesterase inhibitors, donepezil and rivastigmine, attenuate spatial memory and cognitive flexibility impairment induced by acute ethanol in the Barnes maze task in rats

Gaweł

Labuz

Gibuła-Bruzda

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

show abstract

“…In contrast, the CTS 100 and CTS 200 groups had reduced enzymatic activity of 88.36% and 59.72%, respectively. Many studies indicated that dysfunction of learning and memory was caused by the degeneration of cholinergic nervous system, and increased AChE activity in the brain could elevate the risk of cognitive disorders (Cohen et al, 2007;Jamal et al, 2010;Srikumar et al, 2004). Tiwari et al (2009) demonstrated that enhanced AChE activity in cerebral cortex and hippocampus of EtOH-treated rats is involved in cognitive deficit.…”

Section: Resultsmentioning

confidence: 99%

Protective effect of Carthamus tinctorius L. seed on oxidative stress and cognitive impairment induced by chronic alcohol consumption in mice

Choi

Lee

Park

et al. 2018

Food Sci Biotechnol

View full text Add to dashboard Cite

Chronic alcohol consumption induces damage to the brain that can cause various forms of dementia. An abundance of acetaldehyde is produced by excessive alcohol consumption and accumulates in the body to induce oxidative stress, apoptosis, and inflammation in neuronal cells, which results in learning and cognitive decline. In the present study, C57BL/N mice were orally administered alcohol (16%) and Carthamus tinctorius L. seed (CTS) (100 and 200 mg/kg/day). Behavioral experiments showed that memory and cognitive abilities were significantly higher in the CTS groups than the alcoholtreated control group in the T-maze test, novel object recognition test, and Morris water maze test. In addition, CTS inhibited alcohol-induced lipid peroxidation and nitric oxide production in the brain, kidney, and liver. Moreover, alcohol increased acetylcholinesterase activity in the brain, but this was significantly decreased by the administration of CTS. Therefore, CTS may play role in the prevention of alcohol-related dementia.

show abstract

“… Karadsheh, Kussie, and Linthicum (1991 ) reported that caffeine inhibited AChE through binding of the N-methyl group of the pyrrolidine ring to AChE. Moreover, it was found that nicotine alone decreased AChE mRNA expression ( Jamal et al, 2010 ). Thus, the oxidative stress, binding of the enzyme, and reduced synthesis may all contribute to the decreased AChE activity induced by caffeine and nicotine, in the present study, thereby augmenting cholinergic activity.…”

Section: Discussionmentioning

confidence: 99%

A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats

Mourad

Noor

Mohammed

et al. 2021

BCN

View full text Add to dashboard Cite

Objective: Caffeine and nicotine are the most consumed psychostimulants worldwide. Although the effects of each drug alone on the central nervous system (CNS) were studied extensively, the literature on the neurochemical and electrophysiological effects of their combined treatments is scarce. The present study investigates the cortical electrophysiological and neurochemical alterations induced by acute administration of caffeine and nicotine in rats. Methods: Rats received caffeine and nicotine with 1h interval between the two treatments. Results: Caffeine and nicotine administration resulted in a significant decrease in the concentrations of cortical amino acid neurotransmitters namely glutamate, aspartate, glycine and taurine while γ-aminobutyric acid (GABA) was significantly increased. An increased cortical lipid peroxidation and decreased reduced glutathione and nitric oxide levels and acetylcholinesterase and Na+, K+-ATPase activities were also observed. The electroencephalogram (EEG) showed an increase in delta frequency power band while theta, beta-1 and beta-2 were decreased after caffeine and nicotine treatment. These findings suggest that caffeine and nicotine adversely exacerbate their stimulant effects. This was manifested by the EEG changes and mediated by increasing cholinergic transmission, disturbing the balance between the excitatory and inhibitory amino acids leading to oxidative stress.

show abstract

Effects of Systemic Nicotine, Alcohol or Their Combination on Cholinergic Markers in the Frontal Cortex and Hippocampus of Rat

Cited by 9 publications

References 42 publications

Cholinesterase inhibitors, donepezil and rivastigmine, attenuate spatial memory and cognitive flexibility impairment induced by acute ethanol in the Barnes maze task in rats

Cholinesterase inhibitors, donepezil and rivastigmine, attenuate spatial memory and cognitive flexibility impairment induced by acute ethanol in the Barnes maze task in rats

Protective effect of Carthamus tinctorius L. seed on oxidative stress and cognitive impairment induced by chronic alcohol consumption in mice

A Neurochemical and Electrophysiological Study on the Combined Effects of Caffeine and Nicotine in the Cortex of Rats

Contact Info

Product

Resources

About