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Neuroplasticity and Ruminations

neuroplasticity cbd neurons

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#1 Ruth

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Posted 17 June 2018 - 10:49 PM


http://www.mdpi.com/...-3425/6/1/7/htm

Failing to achieve our goals can be disappointing at best, and devastating at worst. For some individuals, however, failure elicits a particular flurry of negative thoughts and feelings that come to monopolize their attention at the expense of other goal-relevant information. Given that the ability to learn and rebound from failure is a key predictor of life-long success (e.g., [1,2]), it is important to understand how our cognition and emotions interact to influence goal-directed behaviors such as the ability to overcome failure (e.g., [3,4]). In the present study, we use both behavioral and event-related potential (ERP) measures to examine how rumination, a cognitive response to negative mood states, stressful situations, or adverse life events [5],

If ruminations are "stuck plasticity states" does this mean neurogenics are a must to stop them?

#2 Ruth

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Posted 17 June 2018 - 10:52 PM

https://www.ncbi.nlm...les/PMC5447774/


Anxiety is a state of psychological and physiological disturbances manifested by cognitive, emotional, behavioral and somatic elements. All together, these factors provoke an unpleasant sensation coupled with apprehension, fret, disquiet and restlessness. The onset of anxiety is sudden and unexpected without any triggering stimulus and thus is a serious medical state. In order to cope the unusual panic situation, the body is liable to some symptoms, like tension, sweating, palpitations, chest pain, papillary dilatation and shortness of breath (O’Connor et al., 2000; Borkovec and Ruscio, 2001). The current anxiolytic agents like benzodiazepines are associated with numerous side effects, like drug tolerance, abuse and sedation. Consequently, aromatherapy with psychoactive EOs may be a useful alternative therapy to relieve anxiety (Woelk and Schläfke, 2010). Several plants EOs have been reported to possess strong anxiolytic potentials. For instance, L. angustifolia Mill (lavender), Citrus sinensis L. (orange), Santalum album RBr (sandal wood), Rosa damascena Mill (rose), Citrus bergamia Risso. (bergamot), Salvia sclarea L. (clary sage), Anthemis nobilis L (roman chamomile) and Pelargonium species EOs are strong anxiolytic agents (Setzer, 2009; López et al., 2017). The chemical composition and effects of EOs, constituents from Cananga odorata (ylang-ylang) were evaluated by researchers in animal models using behavioral assessment tools (Gaydou et al., 1986; Zhang et al., 2016). Furthermore, the level of neurotransmitters and their metabolites were also assessed subsequent to oil exposure. C. odorata EO exhibited considerable anxiolytic effect in animal models. The constituents of C. odorata including benzyl benzoate, linalool and benzyl alcohol also displayed anxiolytic effect in animal model of anxiety. EOs constituents lowered the dopamine levels in striatum and augmented the level of 5-hydroxytryptamine (5-HT) in hippocampus of experimental animals

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#3 Ruth

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Posted 17 June 2018 - 10:56 PM

Shirodhara an Ayurvedic oil therapy medicated with sesame oil, is commonly known remedy for anxiety and effective in the management of altered state of consciousness (ASC). To evaluate the pharmaco-physio-psychological effects of Shirodhara, lavender EO were added to the formulation. Volunteers were divided into three groups namely, plain Shirodhara group (sesame oil), aroma-Shirodhara (0.3% lavender EO + sesame oil) and control group. The oils were applied via a robotic oil-dripping system. Different parameters including heart rate, anxiety, temperature of hand and feet and ASC were recorded. Strong anxiolytic and ASC effects were observed in aroma group. The significance between anxiolysis-ASC and psychological effects increased foot skin temperature were more obvious in the aroma Shirodhara group as compared to other groups. Authors concluded that the psycho-physiological effects of lavender-Shirodhara were based on relaxing effects of lavender EO via olfactory nerves, better absorption of oils via skin and physiological effects of sesame oil dripping on the forehead mediated by the somatoautonomic reflex through thermosensors or pressure sensors using the trigeminal cranial nerve (Xu et al., 2008).

altered state of consciousness is a right!

ASCs can't not be grounded in legalism.

We are Human.

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#4 Ruth

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Posted 17 June 2018 - 11:11 PM

https://www.ncbi.nlm...pubmed/18845194 Synergistic effect of galantamine on nicotine-induced neuroprotection in hemiparkinsonian rat model.

Recent studies have reported that smokers tend to be less susceptible to Parkinson's disease (PD) and the stimulation of nicotinic acetylcholine receptor (nAChR) is considered to confer a neuroprotective effect. Galantamine is an acetylcholinesterase inhibitor and an allosteric potentiating ligand for nAChRs. However, the effects of galantamine and nicotine on dopaminergic neurons remain unclear. This study evaluated the neuroprotective effects of galantamine and nicotine in a rat 6-hydroxydopamine (6-OHDA)-induced hemiparkinsonian model. 6-OHDA with or without galantamine and/or nicotine were injected into unilateral substantia nigra of rats. Although methamphetamine-stimulated rotational behavior and dopaminergic neuronal loss induced by 6-OHDA were not inhibited by galantamine alone, those were moderately inhibited by nicotine alone. In addition, 6-OHDA-induced neuronal loss and rotational behavior were synergistically inhibited by co-injection of galantamine and nicotine. These protective effects were abolished by mecamylamine, an nAChR antagonist. We further found that alpha7 nAChR was expressed on both tyrosine hydroxylase (TH)-immunopositive and TH-immunonegative neurons in the SNpc. A combination of galantamine and nicotine greatly suppressed 6-OHDA-induced reduction of TH-immunopositive/alpha7 nAChR-immunopositive neurons. These results suggest that galantamine synergistically enhances the neuroprotective effect of nicotine against 6-OHDA-induced dopaminergic neuronal loss through an allosteric modulation of alpha7 nAChR activation.
Galantamine Enhances Dopaminergic Neurotransmission In Vivo Via Allosteric Potentiation of Nicotinic Acetylcholine Receptors
Bjo ¨rn Schilstro ¨m*,1, Vladimir B Ivanov1, Charlotte Wiker1 and Torgny H Svensson1 1Section of Neuropsychopharmacology, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
Clinical studies suggest that adjunct galantamine may improve negative and cognitive symptoms in schizophrenia. These symptoms may be related to impaired dopaminergic function in the prefrontal cortex. Indeed, galantamine has been shown to increase dopamine release in vitro. Galantamine is an allosteric modulator of nicotinic acetylcholine receptors (nAChRs) and, at higher doses, an acetylcholine esterase (AChE) inhibitor. We have previously shown that nicotine, through stimulation of nAChRs in the ventral tegmental area (VTA), activates midbrain dopamine neurons and, hence, potentiation of these receptors could be an additional mechanism by which galantamine can activate dopaminergic pathways. Therefore, the effects of galantamine (0.01–1.0mg/kg s.c.) on dopamine cell firing were tested in anaesthetized rats. Already at a low dose, unlikely to result in significant AchE inhibition, galantamine increased firing activity of dopaminergic cells in the VTA. The effect of galantamine was prevented by the nAChR antagonist mecamylamine (1.0mg/kg s.c.), but not the muscarinic receptor antagonist scopolamine (0.1mg/kg s.c.), and it was not mimicked by the selective AChE inhibitor donepezil (1.0mg/kg s.c.). Our data thus indicate that galantamine increases dopaminergic activity through allosteric potentiation of nAChRs. Galantamine’s effect was also prevented by the a7 nAChR antagonist methyllycaconitine (6.0mg/kg i.p.) as well as the N-methyl-Daspartate antagonist CGP39551 (2.5mg/kg s.c.), indicating a mechanism involving presynaptic facilitation of glutamate release. In parallel microdialysis experiments, galantamine was found to increase extracellular levels of dopamine in the medial prefrontal cortex. These results may have bearing on the enhancement of negative and cognitive symptoms in schizophrenia.





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