Cholinergic system and memory in the rat: Effects of chronic ethanol, embryonic basal forebrain brain transplants and excitotoxic lesions of cholinergic basal forebrain projection system

Arendt, Thomas; Allen, Y.S.; Marchbanks, R. M.; Schugens, Markus M.; Sinden, John D.; Lantos, Peter L.; Gray, Jeffrey A.

doi:10.1016/0306-4522(89)90397-7

Cited by 253 publications

(96 citation statements)

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“…Previous studies have shown that the effect of chronic alcohol consumption is associated with cholinergic neuronal damage in hippocampus (Arendt et al, 1989). Our study also show significantly decreased the cholinergic neurons densities in all areas of hippocampus in the ethanol treated group.…”

Section: Discussionsupporting

confidence: 80%

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<i>COSCINIUM FENESTRATUM</i> PROTECTS AGAINST ETHANOL-INDUCED NEURODEGENERATION IN ADULT RAT BRAIN

Phachonpai

Wannanon

Thipkaew

et al. 2012

American Journal of Pharmacology and Toxicology

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Alcoholism is a serious problem throughout the world. Despite intensive efforts to develop novel therapeutics for strategy efficacy against neuronal loss leading to memory impairment in alcoholism is still limited. In view of the pitfalls of psychological dependence and adverse behavioral effects of synthetic drugs, the development of low toxicity and high efficiency medicines derived from natural herbal antioxidants exhibits expansive market prospects. In this respect, Coscinium Fenestratum (C. Fenestratum; CF) could be an attractive candidate as a diet supplement for neuroprotactant against ethanol-induced neurodegeneration. Herein, we determined the neuroprotective effects of CF against ethanol-induced neuronal damage in both hippocampus and cerebral cortex. The stems of CF extract (No. HHP-2-462) were dried, refluxed with ethanoland evaporated with lyophilizer. Extract was gave a yield of 8.53%. The rats were pretreated with the extract at various doses ranging from 5, 10 and 20 mg kg −1 once daily per os, 30 min prior to ethanol administration at a dose of 1.8 g kg −1 via i.p for 14 consecutive days and were evaluated the densities of survival and cholinergic neurons in all areas as mention above by immune histological techniques. CF extract at a dose of 5 mg kg −1 showed the attenuation of the neurotoxicity in all brain areas just mentioned except in the temporal cortex. In addition, it also mitigated the degeneration of cholinergic neurons in all areas of hippocampus except in CA3 region. This study indicated that CF extract consumption may be served as a diet supplement protect against neuronal degeneration resulting from excessive continuous consumption of alcohol. However, further researches about possible active ingredients and pharmacokinetic of the extract are still required before moving forward to clinical trial study.

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Section: Discussionsupporting

confidence: 80%

“…Abundant evidence suggests that the memory impairment induced by chronic alcohol consumption was Science Publications AJPT reported to be associated with the decreased cholinergic neurons (Arendt et al, 1989;Nordberg et al, 1982). In addition, chronic alcoholism could also produce the neurode generation in hippocampus (Agartz et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

<i>COSCINIUM FENESTRATUM</i> PROTECTS AGAINST ETHANOL-INDUCED NEURODEGENERATION IN ADULT RAT BRAIN

Phachonpai

Wannanon

Thipkaew

et al. 2012

American Journal of Pharmacology and Toxicology

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“…These structures are rich in cholinergic pathways connecting forebrain and brainstem areas, as well as hippocampal and septal regions (Gaykema, Luiten, Nyakas, & Traber, 1990;Rye, Wainer, Mesulam, Mufson, & Saper, 1984). Alcoholism has been demonstrated to exert neurotoxic effects on the cholinergic basal forebrain system, including muscarinic receptors in its target structures (Arendt, 1994;Arendt et al, 1988Arendt et al, , 1989Freund & Ballinger, 1989;Nordberg, Larsson, Perdahl, & Winblad, 1982). In healthy individuals, these cholinergic interactions have been hypothesized to optimize cortical information processing (Baxter & Chiba, 1999).…”

Section: Discussionmentioning

confidence: 99%

Delay discrimination and reversal eyeblink classical conditioning in abstinent chronic alcoholics.

et al. 2008

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Evidence has shown that alcoholism leads to volume reductions in brain regions critical for associative learning using the eyeblink classical conditioning paradigm (EBCC). Evidence indicates that cerebellar shrinkage causes impairment in simple forms of EBCC, whereas changes in forebrain structures result in impairment in more complex tasks. In this study, the ability of abstinent alcoholics and matched control participants to acquire learned responses during delay discrimination and discrimination reversal was examined and related to severity of drinking history and neuropsychological performance. During discrimination learning, one tone (CS+) predicted the occurrence of an airpuff (unconditioned stimulus), and another tone (CS−) served as a neutral stimulus; then the significance of the tones was reversed. Alcoholics who learned the initial discrimination were impaired in acquiring the new CS+ after the tones reversed; this is a function that has previously been linked to forebrain structures. It is suggested that a factor important to alcoholic addiction may be the presence of alcoholic-related associative responses that interfere with the ability to learn new more adaptive associations. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptChronic misuse of alcohol leads to volume reductions in brain regions critical for associative learning using the eyeblink classical conditioning (EBCC) paradigm. First, alcohol is known to cause structural alterations in the cerebellum, a structure that is both necessary and sufficient for all forms of EBCC (R. F. Thompson, 1986). Such alterations have been documented by traditional postmortem inspection (Harper & Kril, 1989) and more recently by in vivo neuroimaging studies, confirming significant volume shrinkage in the cerebellar hemispheres (Sullivan, Rosenbloom, Lim, & Pfefferbaum, 2000).Second, in addition to alcohol-related neuropathological changes in the cerebellum, abundant evidence from different methodologies indicates that the structural alterations due to alcohol extend into prefrontal cortex and frontal circuitry. These are areas of the brain known to be essential for more complex or nonoptimal forms of EBCC. For example, using structural MRI, Sullivan and her colleagues (e.g., Sullivan et al., 2003; have reported that each major node of the frontocerebellar circuit shows volume reductions and each can be independently affected. MRI studies have also revealed greater volume losses in the frontal lobes compared with other structures (Dao-Castellana et al., 1998;Jernigan et al., 1991;Kril, Halliday, Svoboda, & Cartwright, 1997). White matter changes in alcoholics have been documented using diffusion tensor imaging Pfefferbaum et al., 2000). Post-mortem evidence from Harper, Kril, and Daly (1987) showed a 22% reduction in the number of neurons in the superior frontal cortex of alcoholics.Alcoholism also results in degradation of cognitive function. Neuropsychological deficits range from mild to severe (e.g., Korsakoff's syndrome) an...

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“…This treatment has also been shown to reduce the serotonin, dopamine and acetylcholine content in different brain regions (Arendt et al, 1989). In this context, our group demonstrated that a decrease in serotoninergic transmission leads to a decrease in the SRIF receptor density and that dopamine stimulation induces a rise in the number of SRIF receptors (Rodríguez-Sánchez et al, 1997).…”

Section: Discussionmentioning

confidence: 85%

Differential effects of ethanol ingestion on somatostatin content, somatostatin receptors and adenylyl cyclase activity in the frontoparietal cortex of virgin and parturient rats

et al. 2005

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Chronic ethanol ingestion decreases the number of somatostatin (SRIF) receptors in the rat frontoparietal cortex and female sex hormones modulate the effects of ethanol in the brain. Therefore, we investigated the differential effects of ethanol consumption on the SRIFergic system in the frontoparietal cortex of virgin and parturient rats given ethanol in their drinking water before and during gestation. In parturient rats, ethanol consumption decreased the density of SRIF receptors (25%, p b 0.01 vs control parturient group) whereas the SRIF-like immunoreactivity (SRIF-LI) content was increased (140%, p b 0.01). In virgin rats, ethanol ingestion decreased the density of SRIF receptors (42%, p b 0.01) more than in alcoholic parturient rats. SRIF-LI levels were unaffected. The inhibitory effect of SRIF on basal and forskolin-stimulated adenylyl cyclase was significantly lower in alcoholic virgin rats as compared to alcoholic parturient rats. No differences in the levels of the G inhibitory (Gi) a1 and Gia2 proteins were observed among the experimental groups. These results suggest that gestation may confer partial resistance to the ethanol-induced effect on the SRIFergic system. D

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Cholinergic system and memory in the rat: Effects of chronic ethanol, embryonic basal forebrain brain transplants and excitotoxic lesions of cholinergic basal forebrain projection system

Cited by 253 publications

References 83 publications

<i>COSCINIUM FENESTRATUM</i> PROTECTS AGAINST ETHANOL-INDUCED NEURODEGENERATION IN ADULT RAT BRAIN

<i>COSCINIUM FENESTRATUM</i> PROTECTS AGAINST ETHANOL-INDUCED NEURODEGENERATION IN ADULT RAT BRAIN

Delay discrimination and reversal eyeblink classical conditioning in abstinent chronic alcoholics.

Differential effects of ethanol ingestion on somatostatin content, somatostatin receptors and adenylyl cyclase activity in the frontoparietal cortex of virgin and parturient rats

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