• Nootropics 9-ME-BC CAS 2527-07-5
  • Nootropics 9-ME-BC CAS 2527-07-5
Nootropics 9-ME-BC CAS 2527-07-5
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9-Me-BC or 9-Methyl-β-carboline is a novel, dopaminergic , cognitive enhancer. It has been shown to improve DA (dopamine, a neurotranmittter vital to mood, focus, vigilance and wakefulness) by inducing growth of hippocampal dopaminergic neurons. The hippocampus, by the way, is the locus of short term memory formation and storage. In addition, 9-Me-BC also has some anti-inflammatory effects. 9-Methyl-9B-Carboline is a dopaminergic enhancer. It operates primarily thorugh up-modulation, differentiation and a protective effect on dendrities and synapses all the while improving dopamine synthesis tasks.

Nootropics 9-ME-BC CAS 2527-07-5

Abstract

β‐Carbolines (BCs) belong to the heterogenous family of carbolines, which have been found exogenously, that is, in various fruits, meats, tobacco smoke, alcohol and coffee, but also endogenously, that is, blood, brain and CSF. These exogenous and endogenous BCs and some of their metabolites can exert neurotoxic effects, however, an unexpected stimulatory effect of 9‐methyl‐β‐carboline (9‐me‐BC) on dopaminergic neurons in primary mesencephalic cultures was recently discovered. The aim of the present study was to extend our knowledge on the stimulatory effects of 9‐me‐BC and to test the hypothesis that 9‐me‐BC may act as a cognitive enhancer. We found that 10 days (but not 5 days) of pharmacological treatment with 9‐me‐BC (i) improves spatial learning in the radial maze, (ii) elevates dopamine levels in the hippocampal formation, and (iii) results after 10 days of treatment in elongated, more complex dendritic trees and higher spine numbers on granule neurons in the dentate gyrus of 9‐me‐BC‐treated rats. Our results demonstrate that beyond its neuroprotective/neurorestorative and anti‐inflammatory effects, 9‐me‐BC acts as a cognitive enhancer in a hippocampus‐dependent task, and that the behavioral effects may be associated with a stimulatory impact on hippocampal dopamine levels and dendritic and synaptic proliferation.


Abbreviations used

Abbreviations used

    • 9‐me‐BC


    • 9‐methyl‐β‐carboline


    • b.w.


    • body weight


    • DA


    • dopamine


    • DOPAC


    • dihydroxyphenylacetic acid


    • HVA


    • homovanillic acid


    • i.p.


    • intraperitoneally


    • P


    • postnatal day


    • RAM


    • eight‐arm radial maze

The management and search for mechanism‐based therapies of neurodegenerative disorders such as Alzheimer′s or Parkinson′s disease (PD) is one of the greatest challenges of modern human societies. As of today PD is an incurable progressive illness, which is usually controlled by various interventions including psychotherapy, surgical treatment options and medication with various dopaminergic and non‐dopaminergic drugs (Obesoet al. 2010Schulz et al. 2011). PD is predominantly characterized by a degeneration of dopaminergic neurons in the substantia nigra caused by presumably multi‐factorial pathomechanisms. For instance, a dysfunction of the mitochondrial respiratory chain, an overshoot in the production of reactive oxygen species, and an involvement of neuroinflammatory processes including the activation of microglia were shown to be involved in the etiology of PD (Obeso et al. 2010; for a recent review see Shulman et al.2011). Thus, the search for new, highly specific and effective drugs, which overcome the limitations and side effects of currently used medications, and which have neurostimulatory, neuroprotective/neurorestorative, and anti‐inflammatory properties, is of major importance (Meissner et al. 2011).

β‐Carbolines (BCs) belong to the heterogenous family of carbolines and have been found in various fruits, fish and beef, in tobacco smoke, alcohol and coffee, and can also be measured in the blood, brain and CSF (for a review see Polanski et al. 2011). Depending on the specific structural characteristics and/or dosage, these exogenous and endogenous BCs and some of their metabolites can exert neurotoxic effects (Neafsey et al. 1995Collins et al.1996Matsubara et al. 1998Hamann et al. 2006). For instance, the endogenously formed 2‐methyl‐β‐carbolinum and 2,9‐dimethyl‐β‐carbolinum ions are suspected to be involved in the pathogenesis of PD (Hamann et al. 2006Lorenc‐Koci et al. 2006). In contrast, an unexpected stimulatory effect of 9‐methyl‐β‐carboline (9‐me‐BC) on dopaminergic neurons was recently discovered in cultures of primary mesencephalic neurons (Hamann et al. 2008Polanski et al. 2010). This finding has now directed the focus of research on the stimulatory and protective action of 9‐me‐BC on the nigro‐striatal dopaminergic system and its potential use as anti‐Parkinson drug (see review by Polanski et al. 2011). In this context, one of the most interesting features of 9‐me‐BC is its uptake via dopamine (DA) transporters into dopaminergic neurons, where in vitro it can act as a neurostimulant by elevating tyrosine‐hydroxylase, the rate‐limiting enzyme of DA synthesis (Polanski et al. 2011). This, together with the inhibitory function of 9‐me‐BC on monoamine oxidases A and B (Ho 1972) may result in enhanced DA release in the target regions of dopaminergic fibers (Polanskiet al. 2011). Furthermore, 9‐me‐BC promotes neurite outgrowth of dopaminergic cells in vitro, and there is evidence that this involves elevations of astrocyte‐derived neurotrophic factors including the brain‐derived neurotrophic factor (Polanski et al. 2011).

Until now, the studies on 9‐me‐BC effects were focused on the nigro‐striatal pathways. The aim of the present study was to extend this to other dopaminergic functional pathways, such as the meso‐cortico‐limbic dopaminergic pathway, and to investigate whether 9‐me‐BC might exert a broader stimulatory effect. In a pharmaco‐behavioural approach, we tested the hypothesis that 9‐me‐BC improves spatial learning in a radial maze (Olton and Samuelson 1976), a hippocampus‐dependent task modulated by the meso‐limbic dopaminergic pathway (McGurk et al. 1992Wilkerson and Levin 1999Tinsley et al. 2001). To unveil the underlying mechanisms of the predicted 9‐me‐BC‐induced cognitive enhancement we assessed the neurochemical and neuromorphological effects of 9‐me‐BC in the hippocampus.



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