Effect of the acetylcholinesterase inhibitor galanthamine on
learning and memory in prolonged alcohol intake rat model of
acetylcholine deficit

Iliev, Alexandar; Traykov,; Prodanov, Dimiter; Mantchev, G; Yakimova, K; Krushkov, I; Boyadjieva, Nadka

doi:10.1358/mf.1999.21.4.538182

Cited by 27 publications

(12 citation statements)

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“…Galantamine reduced alcohol intake without decreasing food consumption and total fluid intake. Subsequently, galantamine has also shown to improve the speed of learning, short-term memory and spatial orientation in rats after prolonged (16 weeks) alcohol intake [291]. This last observation is consistent with the hypothesis that prolonged alcohol intake could lead to an acetylcholine deficit and to an impairment of many brain functions.…”

Section: Acetylcholinesterase Inhibitorssupporting

confidence: 81%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

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Treating alcohol use disorders represents a main goal in public health, but the effect of current medications is modest. Thus, in the last few years, research has been focusing on identifying new neuropharmacological targets for alcohol dependence. This review will summarize recent research, which has identified new targets to treat alcohol dependence. A variety of systems have been investigated, such as the endocannabinoid system, modulators of glutamatergic transmission, corticotropin-releasing factor (CRF), neuropeptide Y (NPY), nociceptin, glial cell line-derived neurotrophic factor (GDNF), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha-adrenergic receptor, and many others. Compared to preclinical studies, only a few clinical studies have been conducted so far. Thus, there is a critical need to translate successful preclinical results into human clinical trials. However, since some clinical studies have failed to replicate preclinical findings, future research will have not only to identify more efficacious medications, but also delineate the best match between a particular pharmacotherapy with a specific alcoholic subtype.

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Section: Acetylcholinesterase Inhibitorssupporting

confidence: 81%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

View full text Add to dashboard Cite

show abstract

“…Treatment with galantamine reversed learning impairments in passive avoidance and Morris water maze tasks resulting from lesions of the nucleus basalis magnocellularis (Sweeney et al 1988(Sweeney et al , 1990, and radial arm maze learning impaired by alcohol-induced cholinergic dysfunction (Iliev et al 1999). Galantamine is proposed to function in two ways.…”

Section: Cholinergic Modulation and Learningmentioning

confidence: 99%

Galantamine Facilitates Acquisition of Hippocampus-Dependent Trace Eyeblink Conditioning in Aged Rabbits

Weible¹,

Oh²,

Lee³

et al. 2004

Learn. Mem.

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Cholinergic systems are critical to the neural mechanisms mediating learning. Reduced nicotinic cholinergic receptor (nAChR) binding is a hallmark of normal aging. These reductions are markedly more severe in some dementias, such as Alzheimer's disease. Pharmacological central nervous system therapies are a means to ameliorate the cognitive deficits associated with normal aging and aging-related dementias. Trace eyeblink conditioning (EBC), a hippocampusand forebrain-dependent learning paradigm, is impaired in both aged rabbits and aged humans, attributable in part to cholinergic dysfunction. In the present study, we examined the effects of galantamine (3 mg/kg), a cholinesterase inhibitor and nAChR allosteric potentiating ligand, on the acquisition of trace EBC in aged (30-33 months) and young (2-3 months) female rabbits. Trace EBC involves the association of a conditioned stimulus (CS) with an unconditioned stimulus (US), separated by a stimulus-free trace interval. Repeated CS-US pairings results in the development of the conditioned eyeblink response (CR) prior to US onset. Aged rabbits receiving daily injections of galantamine (Aged/Gal) exhibited significant improvements compared with age-matched controls in trials to eight CRs in 10 trial block criterion (P = 0.0402) as well as performance across 20 d of training [F(1,21) = 5.114, P = 0.0345]. Mean onset and peak latency of CRs exhibited by Aged/Gal rabbits also differed significantly [F (1,21) = 6.120/6.582, P = 0.0220/0.0180, respectively] compared with age-matched controls, resembling more closely CR timing of young drug and control rabbits. Galantamine did not improve acquisition rates in young rabbits compared with age-matched controls. These data indicate that by enhancing nicotinic and muscarinic transmission, galantamine is effective in offsetting the learning deficits associated with decreased cholinergic transmission in the aging brain.

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“…In addition, prolonged withdrawal from chronic ethanol consumption is associated with a decrease in β 2 -subunit containing nicotinic receptor availability in nonhuman primates (88). Iliev et al (89) showed that administration of galantamine (2.5 mg/kg) to prolonged alcohol intake rats improved the speed of learning and short-term memory in the shuttle box test and the passive avoidance memory in the eight-arm radial maze.…”

Section: Alcohol Addiction (Preference/memory Im Pairment)mentioning

confidence: 99%

Pharmacological Aspects of the Acetylcholinesterase Inhibitor Galantamine

et al. 2011

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Abstract. Several lines of evidence suggest that cholinergic deficits may contribute to the pathophysiology of psychiatric disorders as well as Alzheimer's disease. There is growing clinical evidence that galantamine, currently used for the treatment of Alzheimer's disease, may improve cognitive dysfunction and psychiatric illness in schizophrenia, major depression, bipolar disorder, and alcohol abuse. Since galantamine is a rather weak acetylcholinesterase inhibitor, but has additional allosteric potentiating effects at nicotinic receptors, it affects not only cholinergic transmission but also other neurotransmitter systems such as monoamines, glutamate, and γ-aminobutyric acid (GABA) through its allosteric mechanism. It is likely that these effects may result in more beneficial effects. To understand the underlying mechanism for the clinical effectiveness of galantamine, neuropharmacological studies have been performed in animal models of several psychiatric disorders. These studies suggest that not only the nicotinic receptor-modulating properties but also the muscarinic receptor activation contribute to the antipsychotic effect and improvement of cognitive dysfunction by galantamine. This review summaries the current status on the pharmacology of galantamine, focusing on its effect on neurotransmitter release and pharmacological studies in animal models of psychiatric disorders.

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Effect of the acetylcholinesterase inhibitor galanthamine on learning and memory in prolonged alcohol intake rat model of acetylcholine deficit

Cited by 27 publications

References 0 publications

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Galantamine Facilitates Acquisition of Hippocampus-Dependent Trace Eyeblink Conditioning in Aged Rabbits

Pharmacological Aspects of the Acetylcholinesterase Inhibitor Galantamine

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