The effects of cholinergic drugs and cholinergic-rich foetal neural transplants on alcohol-induced deficits in radial maze performance in rats

Hodges, Helen; Allen, Y.S.; Sinden, John D.; Mitchell, Stephen N.; Arendt, Thomas; Lantos, Peter L.; Gray, Jeffrey A.

doi:10.1016/s0166-4328(05)80048-8

Cited by 137 publications

(40 citation statements)

References 51 publications

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“…Cognitive defi cits induced by chronic ethanol intoxication in alcoholics are known to be associated with morphological, functional and biochemical alterations in the brain [35,36] . Chronic ethanol administration to experimental animals also induces neuroanatomic and neurochemical impairments resembling those occurring in alcoholics [37][38][39][40] .…”

Section: Discussionmentioning

confidence: 99%

Testosterone Reverses Ethanol-Induced Deficit in Spatial Reference Memory in Castrated Rats

Khalil

King²,

Soliman³

2005

Pharmacology

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The present study was designed to evaluate the effects of ethanol, testosterone and combination of ethanol and testosterone, on spatial reference memory and β-endorphin (β-EN) levels in castrated rats. Male Sprague-Dawley rats (120–150 g) were used in this study, Animals were castrated and ethanol, testosterone or combination of the drugs were administered to rats at 09:00 h. The drugs were administered after a training period of 5 days and spatial reference memory was evaluated for 7 days using the Morris water maze. One hour after the last injection, animals were sacrificed, their brains removed and dissected into cortex, hypothalamus, hippocampus and midbrain. The β-EN levels in these brain regions were determined by radioimmunoassay. The time to find the platform (latency period) was significantly increased in ethanol-treated rats, indicating that ethanol induces deficit in spatial reference memory. On the other hand, testosterone administration improved spatial reference memory by significantly decreasing the latency period. In addition, there was a significant decrease in latency period in the animals treated with combination of ethanol and testosterone. Results also indicate that administration of ethanol resulted in a significant increase in β-EN levels in the hippocampus and in the cortex while concurrent administration with testosterone abolished this increase. These findings clearly indicate that administration of testosterone did not only improve memory but also abolished the spatial memory deficit induced by ethanol in castrated rats.

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Section: Discussionmentioning

confidence: 99%

Testosterone Reverses Ethanol-Induced Deficit in Spatial Reference Memory in Castrated Rats

Khalil

King²,

Soliman³

2005

Pharmacology

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“…While as reviewed above, nicotinic agents have been shown to improve memory in normal rats, there is growing evidence that these agents can lead to improvement in laboratory models of memory and learning impairment. For instance, there is evidence that nicotine can counteract memory deficits induced by lesions of the forebrain cholinergic projection systems in a passive avoidance task, water maze task, or radial maze task Grigoryan et al 1994;Hodges et al 1991;Riekkinen et al 1993). Chronic nicotine infusion also has been shown to reverse working memory deficits due to lesions of fimbria medial basalocortical projection (Levin et al 1993b).…”

Section: Animal Studiesmentioning

confidence: 99%

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

2005

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Discovery of the behavioral, pharmacological, and anatomic specificity of nicotinic effects on learning, memory, and attention not only aids the understanding of nicotinic involvement in the basis of cognitive function, but also helps in the development of novel nicotinic treatments for cognitive dysfunction. Nicotinic treatments directed at specific receptor subtypes and nicotinic cotreatments with drugs affecting interacting transmitter systems may provide cognitive benefits most relevant to different syndromes of cognitive impairment such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder. Further research is necessary in order to determine the efficacy and safety of nicotinic treatments of these cognitive disorders.

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“…Moreover, the immunotoxin 192 IgG saporin, which depletes choline acetyltransferase by 95%, impairs attention; although this depends upon the cholinergic forebrain projection system lesioned (Torres et al 1994;Wenk et al 1994;Leanza et al 1996). It also evident from the literature that the effect on learning and memory of some manipulations of the cholinergic system may be interpreted as indirect effects resulting from changes in attention (Spencer et al 1985;Deacon 1991;Hodges et al 1991aHodges et al , 1991bPontercorvo et al 1991;Stanhope et al 1995).…”

Section: Introductionmentioning

confidence: 99%

The role of nicotinic and muscarinic acetylcholine receptors in attention

Mirza

Stolerman

2000

Psychopharmacology

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The effects of cholinergic drugs and cholinergic-rich foetal neural transplants on alcohol-induced deficits in radial maze performance in rats

Cited by 137 publications

References 51 publications

Testosterone Reverses Ethanol-Induced Deficit in Spatial Reference Memory in Castrated Rats

Testosterone Reverses Ethanol-Induced Deficit in Spatial Reference Memory in Castrated Rats

Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization

The role of nicotinic and muscarinic acetylcholine receptors in attention

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