Changes in brain biogenic monoamines induced by the nootropic drugs adafenoxate and meclofenoxate and by citicholine (experiments on rats)

Stancheva, S; Tocuschieva, Lidia; Petkov, V.

doi:10.1016/0306-3623(90)90598-g

Cited by 45 publications

(26 citation statements)

References 18 publications

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“…*po0.05 vs the saline plus saline group, # po0.05 vs the saline plus nicotine group. extract inhibited adenylate cyclase activity in rat brain tissues (Petkov, 1978). Taken together, it is likely that GTS may act on DA D 2 receptors as an antagonist.…”

Section: Discussionmentioning

confidence: 83%

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Kim

Shim

Chung

et al. 2005

Neuropsychopharmacol

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Several studies have shown that behavioral hyperactivity induced by psychomotor stimulants is prevented by ginseng saponins. In an attempt to investigate whether the effect of ginseng saponins is through their inhibitory action on the enhanced dopaminergic transmission by psychomotor stimulants, we examined the effects of ginseng total saponin (GTS) presynaptically on nicotine-induced dopamine (DA) release in the striatum of freely moving rats using in vivo microdialysis technique and postsynaptically on the in vitro and in vivo binding of [ 3 H]raclopride to DA D 2 receptors. Also, we examined the effects of GTS on nicotine-induced locomotor hyperactivity and on nicotine-induced Fos protein expression in the nucleus accumbens and striatum. Systemic pretreatment with GTS (100 and 400 mg/kg, intraperitoneally (i.p.)) resulted in a dose-dependent inhibition of locomotor hyperactivity induced by nicotine. GTS decreased nicotine-induced DA release in the striatum in a dose-dependent manner. However, GTS had no effects on resting levels of locomotor activity and extracellular DA in the striatum. GTS inhibited the in vitro binding of [ 3 H]raclopride to rat striatal membranes with an IC 50 of 5.1471.09 mM. High doses of GTS (400 and 800 mg/kg, i.p.) resulted in decreases in the in vivo binding of [ 3 H]raclopride in the striatum. GTS decreased nicotine-induced Fos protein expression in the nucleus accumbens and striatum, reflecting the inhibition by GTS of nicotine-induced enhancement of dopaminergic transmission. The results of the present study suggest that GTS acts not only on dopaminergic neurons directly or indirectly to prevent nicotine-induced DA release but also postsynaptically by binding to DA D 2 receptors. This may explain the blocking effect of GTS on behavioral activation induced by nicotine and conceivably by other psychostimulants. Our data raise the possibility that GTS, by attenuating nicotine-induced enhancement of dopaminergic transmission, may prove to be a useful therapeutic agent for nicotine addiction and warrant further investigation on its effect on nicotine's rewarding property.

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Section: Discussionmentioning

confidence: 83%

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Kim

Shim

Chung

et al. 2005

Neuropsychopharmacol

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“…This effect was analogous to the effects of many substances with known or putative nootropic action (piracetam, aniracetam, citicholine, elymoclavine, Rhodiola rosea extract) (Petkov, 1989;Petkov et al, 1985Petkov et al, , 1990a, and it should be considered of particular importance, bearing in mind the fact that in old animals besides the changes in cholinergic neurotransmission there is a decrease in the 5-HT level in most brain structures (Petkov ef al., 1988;Gozlan et al, 1990).…”

mentioning

confidence: 81%

Effects of standardized extracts GK501, from Ginkgo biloba L., G115 from Panax ginseng C. A. Meyer, and their combination, gincosan® (PHL‐00701), on the brain levels of biogenic monoamines and on the serum content of prolactin, growth hormone and ACTH

Hadjiivanova

Petkov

Milanov

et al. 1993

Phytotherapy Research

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In experiments on old (26 months old) rats, we found that the extracts of Punax ginseng (G115), Ginkgo bilobu (GK501) and their combination Gincosan@ (PHL-00701) administered orally at two doses for 7 days induced changes in the levels of biogenic monoamines in some brain regions (frontal cerebral cortex, hippocampus, striatum, hypothalamus and pons). The most characteristic change was the increase produced by the two extracts and their combination in the serotonin level in all brain structures except for pons compared with controls. In the hippocampus G115, GK501 and their combination decreased the noradrenaline level. The same doses of 6115, GK501 and their combination applied for 7 days to young (3 months old) and old (26 months old) rats caused significant changes in the blood level of prolactin (PRL), growth hormone (GH) and ACTH compared with age-matched controls: both 6115 and GK501 decreased the serum level of PRL compared with age-matched controls; the hormone level being high in old controls, in extract-treated rats it became equal to that in young controls; 6115 and PHL-00701 greatly increased the serum level of ACTH in both age groups compared with age-matched controls. Under conditions of induced immobilization and cold stress in young rats, the 7-day pretreatment with G115, GK501 and their combination led to significant changes in the blood levels of PRL, GH and ACTH compared with control untreated stressed and unstressed rats.

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“…[116] Although the mechanism of action through which citicoline appears to improve cognition and depression is unknown, animal studies reveal that at doses of 100 mg/kg, citicoline increases the essential monoamines (noradrenaline, dopamine and serotonin) involved in MDD in various regions of the brain. [117] Clinically, a recent, small, placebo-controlled study performed in outpatients with bipolar disorder and cocaine dependence suggested that citicoline is safe and well tolerated in humans, and may provide some cognitive benefits. [118] Specifically, the authors of this study reported a significant improvement in verbal learning and memory, measured by the Rey Auditory Verbal Learning Test (RAVLT), which supports prior results in other neurological disorders.…”

Section: Cognitive Impairmentsmentioning

confidence: 98%

Defining and Measuring Functional Recovery from Depression

2010

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Depression is associated with significant functional impairment and reduced quality of life. Disruptions occur both globally as well as in specific functional areas such as work, interpersonal relationships and cognitive function. From both a clinical and research perspective, much focus has been given to the resolution of symptoms associated with depression, while relatively little attention has been given to functional improvements. Definitions of remission in depression are most frequently based on achieving a cut-off score on clinical rating scales of depressive symptoms. Research in this area has sparsely included psychosocial function or health-related quality of life as a primary outcome measure in clinical trials. However, the need to fully understand the impact of depression and its treatments on functioning is great, given the existing evidence of the profound effect that depression has on function. Even mild depressive symptoms and subsyndromal depression result in functional impairment and reduced quality of life, and untreated residual depressive symptomatology can result in an increased likelihood for relapse of the fully symptomatic disorder (i.e. major depressive disorder). Therefore, clinicians and researchers alike need to broaden the focus of treatment to encompass not only the specific symptoms of depression, but the functional consequences as well. Many tools have been developed to assess function and quality of life, both globally as well as within specific domains. In addition, the effect of residual symptoms associated with functional impairment (i.e. insomnia, fatigue, pain [somatic] symptoms and cognition) in depression, even independently of depressive symptoms, warrants evaluation and monitoring. Recommendations for evaluating functional outcomes include: (i) adequately assessing functional impairment; (ii) identifying and/or developing treatment plans that will target symptoms associated with functional impairments; and (iii) monitoring functional impairments and associated symptoms throughout the course of treatment. The development of treatments that specifically target improvements in functional impairments is needed, and may require the use of novel treatment strategies.

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Changes in brain biogenic monoamines induced by the nootropic drugs adafenoxate and meclofenoxate and by citicholine (experiments on rats)

Cited by 45 publications

References 18 publications

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Effects of standardized extracts GK501, from Ginkgo biloba L., G115 from Panax ginseng C. A. Meyer, and their combination, gincosan® (PHL‐00701), on the brain levels of biogenic monoamines and on the serum content of prolactin, growth hormone and ACTH

Defining and Measuring Functional Recovery from Depression

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