Dopamine Deficiency https://greenmedinfo.com/taxonomy/term/5687/all en "Fucoidan protects against dopaminergic neuron death in vivo and in vitro." https://greenmedinfo.com/article/fucoidan-protects-against-dopaminergic-neuron-death-vivo-and-vitro PMID:  Eur J Pharmacol. 2009 Sep 1 ;617(1-3):33-40. Epub 2009 Jun 21. PMID: 19545563 Abstract Title:  Fucoidan protects against dopaminergic neuron death in vivo and in vitro. Abstract:  Parkinson&#039;s disease is a neurodegenerative disorder of uncertain pathogenesis characterized by a loss of dopaminergic neurons in substantia nigra pars compacta, and can be modeled by the neurotoxin 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP). Oxidative stress may contribute to MPTP- and Parkinson&#039;s disease-related neurodegeneration. Fucoidan is a sulfated polysaccharide extracted from brown seaweeds which possesses a wide variety of biological activities including potent antioxidative effects. Here we investigated the effect of fucoidan treatment on locomoter activities of animals, striatal dopamine and its metabolites and survival of nigral dopaminergic neurons in MPTP-induced animal model of Parkinsonism in C57/BL mice in vivo and on the neuronal damage induced by 1-methyl-4-phenylpyridinium (MPP(+)) in vitro, and to study the possible mechanisms. When administered prior to MPTP, fucoidan reduced behavioral deficits, increased striatal dopamine and its metabolites levels, reduced cell death, and led to a marked increase in tyrosine hydroxylase expression relative to mice treated with MPTP alone. Furthermore, we found that fucoidan inhibited MPTP-induced lipid peroxidation and reduction of antioxidant enzyme activity. In addition, pre-treatment with fucoidan significantly protected against MPP(+)-induced damage in MN9D cells. Taken together, these findings suggest that fucoidan has protective effect in MPTP-induced neurotoxicity in this model of Parkinson&#039;s disease via its antioxidative activity. https://greenmedinfo.com/article/fucoidan-protects-against-dopaminergic-neuron-death-vivo-and-vitro#comments Dopamine Deficiency Fucoidan Parkinson's Disease Antioxidants Apoptotic Neuroprotective Agents Animal Study Tue, 18 Dec 2012 22:57:32 +0000 greenmedinfo 87051 at https://greenmedinfo.com Caffeine has effects on dopaminergic neurotransmission in the human brain, which may be differential in the striatum and the thalamus. https://greenmedinfo.com/article/caffeine-has-effects-dopaminergic-neurotransmission-human-brain-which-may-be-d PMID:  Neuroreport. 2004 Feb 9 ;15(2):281-5. PMID: 15076753 Abstract Title:  Dopaminergic effects of caffeine in the human striatum and thalamus. Abstract:  Epidemiological studies have provided evidence that caffeine, an adenosine receptor antagonist, reduces the risk for Parkinson&#039;s disease. There are indications of specific interactions between striatal adenosine A(2A) and dopamine D(2) receptors, but the in vivo effects of caffeine on human dopamine system have not been investigated. In the present study, the dopaminergic effects of caffeine were examined with [(11)C]raclopride positron emission tomography (PET) in eight healthy habitual coffee drinkers after 24 h caffeine abstinence. Compared to oral placebo, 200 mg oral caffeine induced a 12% decrease in midline thalamic binding potential (p https://greenmedinfo.com/article/caffeine-has-effects-dopaminergic-neurotransmission-human-brain-which-may-be-d#comments Dopamine Deficiency Caffeine Dopaminergic Human Study Mon, 21 Nov 2011 16:28:48 +0000 greenmedinfo 69951 at https://greenmedinfo.com Chronic but not acute treatment with the Ginkgo biloba extract EGb 761(R) increased dopaminergic transmission in the rat prefrontal cortex. https://greenmedinfo.com/article/chronic-not-acute-treatment-ginkgo-biloba-extract-egb-761r-increased-dopaminer PMID:  Br J Pharmacol. 2010 Feb 1 ;159(3):659-68. Epub 2010 Jan 25. PMID: 20105177 Abstract Title:  The Ginkgo biloba extract EGb 761(R) and its main constituent flavonoids and ginkgolides increase extracellular dopamine levels in the rat prefrontal cortex. Abstract:  BACKGROUND AND PURPOSE: Experimental and clinical data suggest that extracts of Ginkgo biloba improve cognitive function. However, the neurochemical correlates of these effects are not yet fully clarified. The purpose of this study was to examine the effects of acute and repeated oral administration of the standardized extract EGb 761((R)) on extracellular levels of dopamine, noradrenaline and serotonin (5-HT), and the dopamine metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the prefrontal cortex (PFC) and striatum of conscious rats. EXPERIMENTAL APPROACH: Monoamines and their metabolites were monitored by the use of microdialysis sampling and HPLC with electrochemical or fluorescence detection. KEY RESULTS: A single oral dose of EGb 761 (100 mg.kg(-1)) had no effect on monoamine levels. However, following chronic (100 mg.kg(-1)/14 days/once daily) treatment, the same dose significantly increased extracellular dopamine and noradrenaline levels, while 5-HT levels were unaffected. Chronic treatment with EGb 761 showed dose-dependent increases in frontocortical dopamine levels and, to a lesser extent, in the striatum. The extracellular levels of HVA and DOPAC were not affected by either acute or repeated doses. Treatment with the main constituents of EGb 761 revealed that the increase in dopamine levels was mostly caused by the flavonol glycosides and ginkgolide fractions, whereas bilobalide treatment was without effect. CONCLUSIONS AND IMPLICATIONS: The present results demonstrate that chronic but not acute treatment with EGb 761 increased dopaminergic transmission in the PFC. This finding may be one of the mechanisms underlying the reported effects of G. biloba in improving cognitive function. https://greenmedinfo.com/article/chronic-not-acute-treatment-ginkgo-biloba-extract-egb-761r-increased-dopaminer#comments Dopamine Deficiency Flavonoids Ginkgo biloba Dopaminergic Plant Extracts Animal Study Sun, 08 Apr 2012 22:01:43 +0000 greenmedinfo 74033 at https://greenmedinfo.com Coffee contains compounds which stimulate dopamine release. https://greenmedinfo.com/article/coffee-contains-compounds-which-stimulate-dopamine-release PMID:  Food Chem Toxicol. 2011 Oct 13. Epub 2011 Oct 13. PMID: 22019894 Abstract Title:  Identification of coffee components that stimulate dopamine release from pheochromocytoma cells (PC-12). Abstract:  Coffee and caffeine are known to affect the limbic system, but data on the influence of coffee and coffee constituents on neurotransmitter release is limited. We investigated dopamine release and Ca(2+)-mobilization in pheochromocytoma cells (PC-12 cells) after stimulation with two lyophilized coffee beverages prepared from either Coffea arabica (AR) or Coffea canephora var. robusta (RB) beans and constituents thereof. Both coffee lyophilizates showed effects in dilutions between 1:100 and 1:10,000. To identify the active coffee compound, coffee constituents were tested in beverage and plasma representative concentrations. Caffeine, trigonelline, N-methylpyridinium, chlorogenic acid, catechol, pyrogallol and 5-hydroxytryptamides increased calcium signaling and dopamine release, although with different efficacies. While N-methylpyridinium stimulated the Ca(2+)-mobilization most potently (EC(200): 0.14±0.29μM), treatment of the cells with pyrogallol (EC(200): 48±14nM) or 5-hydroxytryptamides (EC(200): 10±3nM) lead to the most pronounced effect on dopamine release. In contrast, no effect was seen for the reconstituted biomimetic mixture. We therefore conclude that each of the coffee constituents tested stimulated the dopamine release in PC-12 cells. Since no effect was found for their biomimetic mixture, we hypothesize other coffee constituents being responsible for the dopamine release demonstrated for AR and RB coffee brews. https://greenmedinfo.com/article/coffee-contains-compounds-which-stimulate-dopamine-release#comments 5-hydroxytryptamides Caffeine Catechols Chlorogenic Acid Coffee Dopamine Deficiency N-methylpyridinium Pyrogallol Trigonelline Dopaminergic In Vitro Study Mon, 21 Nov 2011 16:24:59 +0000 greenmedinfo 69949 at https://greenmedinfo.com Expectation of caffeine induces dopaminergic responses in humans. https://greenmedinfo.com/article/expectation-caffeine-induces-dopaminergic-responses-humans PMID:  Eur J Neurosci. 2004 Apr ;19(8):2352-6. PMID: 15090062 Abstract Title:  Expectation of caffeine induces dopaminergic responses in humans. Abstract:  Recent neuroimaging studies indicate that placebo treatments can induce clinically relevant neurobiological responses in patients with Parkinson&#039;s disease, depression and pain. The present study aimed to investigate neurotransmitter function in psychostimulant expectation, with the focus on dopaminergic effects of placebo caffeine in healthy human subjects. Eight habitual coffee drinkers were examined twice with [11C]raclopride positron emission tomography after no treatment and after oral placebo tablets in a counter-balanced setting. During the placebo condition the subjects were instructed that they had a 50% chance of receiving caffeine, but all received placebo. As compared with no treatment, placebo induced a significant bilateral dopamine release in the thalamus, as reflected by a 15% reduction in thalamic [11C]raclopride binding (P https://greenmedinfo.com/article/expectation-caffeine-induces-dopaminergic-responses-humans#comments Dopamine Deficiency Dopaminergic Expectation of Caffeine Human Study Mon, 21 Nov 2011 16:35:14 +0000 greenmedinfo 69953 at https://greenmedinfo.com Identifying and Treating the Underlying Causes of Low Libido https://greenmedinfo.com/blog/identifying-and-treating-underlying-causes-low-libido <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2019<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/blank.justin/images/Identifying%20and%20Treating%20the%20Underlying%20Cause%20of%20Low%20Libido.jpg" style="width: 600px; height: 315px;" /></p> <p><span style="font-size:18px;"><em><strong>There are many causes of low libido, but they do not require a pill or drug therapy to be reversed</strong></em></span></p><p><a href="https://greenmedinfo.com/blog/identifying-and-treating-underlying-causes-low-libido" target="_blank">read more</a></p> https://greenmedinfo.com/blog/identifying-and-treating-underlying-causes-low-libido#comments Cortisol: High Dopamine Deficiency Heart Disease Hormone Imbalances Low Libido Low Testosterone Serotonin Disorders Testosterone Antidepressants Hormone Replacement Therapy Hormone Replacement Therapy Sexual Health Stress Low Libido Low Libido cause Low Libido Treatment Sexual dysfunction Sexual Trauma Sexuality Tue, 31 May 2016 17:23:30 +0000 drserenagoldsteinnd 128134 at https://greenmedinfo.com Pot for Parkinson's? The Scientific Evidence Is Compelling https://greenmedinfo.com/blog/pot-parkinsons-scientific-evidence-compelling <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2020<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="Pot for Parkinson's? The Scientific Evidence Is Compelling" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/Sayer Ji/images/24236752_m(1).jpg" style="width: 600px; height: 434px;" /></p> <p><span style="font-size:18px;"><em><strong>Could the very plant that for decades was accused of "frying" users' brains be far superior to pharmaceuticals in treating the "incurable" neurodegenerative condition known as Parkinson's disease?</strong></em></span></p><p><a href="https://greenmedinfo.com/blog/pot-parkinsons-scientific-evidence-compelling" target="_blank">read more</a></p> https://greenmedinfo.com/blog/pot-parkinsons-scientific-evidence-compelling#comments Aging: Brain Alzheimer's Disease Brain Diseases Cannabidiol Cannabinoid Medicine Dopamine Deficiency Neurodegenerative Diseases Parkinson's Disease Health Guide: Aging Health Guide: Alzheimer's Neuritogenic Neuroprotective Agents Neurorestorative alzheimer's medicinal herbs natural health Sun, 22 Nov 2015 22:39:58 +0000 Sayer Ji 121707 at https://greenmedinfo.com Red sage increases dopamine release in an in vitro study. https://greenmedinfo.com/article/red-sage-increases-dopamine-release-vitro-study PMID:  Phytother Res. 2006 Mar;20(3):191-9. PMID: 16521109 Abstract Title:  Salviae miltiorrhizae radix increases dopamine release of rat and pheochromocytoma PC12 cells. Abstract:  The Radix of Salvia miltiorrhiza Bunge (Labiatae) (SMR), an eminent herb, is often included as an ingredient in various herbal remedies recommended for vascular circulation therapies. The present study investigated the effect of SMR on dopaminergic neurotransmission. Various extracts prepared from the stems of SMR were tested for cytotoxic activity on pheochromocytoma PC12 cells using the XTT assay method. The ethanol extract (IC50 &gt; 100 microg/mL), water extract (IC50 &gt; 100 microg/mL) and chloroform (IC50 = 90 microg/mL) fraction exhibited weak cytotoxic activity. However, the butanol (IC50 = 80 microg/mL) and ethyl acetate (EtOAc; IC50 = 70 microg/mL) fractions exhibited strong cytotoxic activity. Also, the extracts and fractions were investigated for dopamine release effects. The EtOAc fraction showed a stronger stimulatory effect on dopamine release activity than the other fractions. The effect of the crude EtOAc fraction (50 microg/mL) of SMR on K+ (20 mm)-stimulated dopamine (DA) release from rat striatal slices was compared with amphetamine (10(-4) m) using high-performance liquid chromatography with electrochemical detection to measure endogenous DA. The EtOAc fraction significantly increased K+ -stimulated DA release (p &lt; 0.001) from rat striatal slices when compared with K+ -stimulated alone. The EtOAc fraction potentiated the effect of amphetamine on K+ -stimulated DA release (p &lt; 0.001) when compared with amphetamine alone. To examine whether in vitro the EtOAc fraction treatment induces DA release in PC12 cells, the role of protein kinases was investigated in the induction of the EtOAc fraction-mediated events by using inhibitors of protein kinase C (PKC), mitogen activated protein kinase (MAP kinase) or protein kinase A (PKA). The PKC inhibitors chelerythrine (50 nm and 100 nm) and Ro31-8220 (100 nm) and the MAP kinase kinase inhibitor, PD98059 (20 microm), inhibited the ability of the EtOAc fraction of SMR to elicit the EtOAc fraction-stimulated DA release. The PKC activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA, 100 nm) mimicked the ability of the EtOAc fraction of SMR to elicit DA release. In contrast, a selective PKA inhibitor, 50 microm Rp-8-Br-cAMP, blocked the development of EtOAc fraction-stimulated DA release. It was demonstrated that the EtOAc fraction of SMR stimulated DA release. Therefore the mechanism by which the EtOAc fraction of SMR induced the enhancement in EtOAc fraction-stimulated DA release is apparent. Copyright 2006 John Wiley &amp; Sons, Ltd. https://greenmedinfo.com/article/red-sage-increases-dopamine-release-vitro-study#comments Dopamine Deficiency Parkinson's Disease Red Sage Dopaminergic In Vitro Study Sat, 16 May 2009 13:18:10 +0000 greenmedinfo 44280 at https://greenmedinfo.com Resveratrol attenuates 6-hydroxydopamine-induced oxidative damage and dopamine depletion in rat model of Parkinson's disease. https://greenmedinfo.com/article/resveratrol-attenuates-6-hydroxydopamine-induced-oxidative-damage-and-dopamine PMID:  Brain Res. 2010 Apr 30;1328:139-51. Epub 2010 Feb 16. PMID: 20167206 Abstract Title:  Resveratrol attenuates 6-hydroxydopamine-induced oxidative damage and dopamine depletion in rat model of Parkinson&#039;s disease. Abstract:  The present study was undertaken to investigate the neuroprotective effects of resveratrol (RES) on 6-hydroxydopamine (6-OHDA)-induced Parkinson&#039;s disease (PD) in rats. PD is an age-related neurodegenerative disorder in which the role of reactive oxygen species (ROS) is strongly implicated. RES, a polyphenolic antioxidant compound enriched in grapes, has been shown to have antioxidant and anti-inflammatory actions and thus was tested for its beneficial effects using 6-OHDA-induced PD rat model. Male Wistar rats were pretreated with RES (20mg/kg body weight i.p.) once daily for 15 days and subjected to unilateral intrastriatal injection of 6-OHDA (10 microg in 0.1% ascorbic acid in normal saline). Three weeks after 6-OHDA infusion, rats were tested for neurobehavioral activity and were killed after 4 weeks of 6-OHDA infusion for the estimation of lipid peroxidation, glutathione content, and activity of antioxidant enzymes (glutathione peroxidase [GPx], glutathione reductase [GR], catalase [CAT], and superoxide dismutase [SOD]. RES was found to be successful in upregulating the antioxidant status and lowering the dopamine loss. Conversely, the elevated level of thiobarbituric acid reactive substances (TBARS), protein carbonyl (PC), and activity of phospholipase A2 in 6-OHDA group was attenuated significantly in RES-pretreated group when compared with 6-OHDA-lesioned group. These results were supported by the immunohistochemical findings in the substantia nigra that has shown the protection of neurons by RES from deleterious effects of 6-OHDA. Thus, RES may be used to reduce the deterioration caused by free radicals thereby preventing subsequent behavioral, biochemical, and histopathological changes that occur during PD. https://greenmedinfo.com/article/resveratrol-attenuates-6-hydroxydopamine-induced-oxidative-damage-and-dopamine#comments Dopamine Deficiency Lipid Peroxidation Oxidative Stress Parkinson's Disease Resveratrol Stilbenes Antioxidants Dopaminergic Animal Study Thu, 19 May 2011 19:03:50 +0000 greenmedinfo 64050 at https://greenmedinfo.com Resveratrol protects against dopaminergic cell death https://greenmedinfo.com/article/resveratrol-protects-against-dopaminergic-cell-death PMID:  Br J Nutr. 2009 Dec;102(11):1620-8. Epub 2009 Jul 22. PMID: 19145491 Abstract Title:  Endoplasmic reticulum stress-induced cell death in dopaminergic cells: effect of resveratrol. Abstract:  Resveratrol, a naturally occurring polyphenol, exhibits antioxidant, antiaging, and anticancer activity. Resveratrol has also been shown to inhibit tumor initiation, promotion, and progression in a variety of cell culture systems. Earlier, we showed that paraquat, a bipyridyl herbicide, triggers endoplasmic reticulum stress, cell dysfunction, and dopaminergic cell death. Due to its antioxidant activity, we assessed the ability of resveratrol to rescue cells from the toxic effects of paraquat. While resveratrol did not have any protective effect at low concentrations, it triggered endoplasmic reticulum (ER) stress-induced cell death at higher concentrations (50-250 microM). The present study was carried out to determine the mechanism by which resveratrol triggers ER stress and cell death in dopaminergic N27 cells. Our studies demonstrate that resveratrol triggers ER stress and cell dysfunction, caspase activation, p23 cleavage and inhibition of proteasomal activity in dopaminergic N27 cells. While over expression of uncleavable p23 was associated with decreased cell death, downregulation of p23 protein expression by siRNA resulted in enhancement of ER stress-induced cell death triggered by resveratrol indicating a protective role for the small co-chaperone p23 in dopaminergic cell death. https://greenmedinfo.com/article/resveratrol-protects-against-dopaminergic-cell-death#comments Dopamine Deficiency Resveratrol Anti-Apoptotic Antioxidants Stilbenes In Vitro Study Sun, 14 Feb 2010 17:42:50 +0000 greenmedinfo 51383 at https://greenmedinfo.com Sulforaphane has a protective effect against dopaminergic cell death. https://greenmedinfo.com/article/sulforaphane-has-protective-effect-against-dopaminergic-cell-death PMID:  J Pharmacol Exp Ther. 2007 Apr;321(1):249-56. Epub 2007 Jan 26. PMID: 17259450 Abstract Title:  Protective effect of sulforaphane against dopaminergic cell death. Abstract:  Parkinson&#039;s disease (PD) is a progressive neurodegenerative disorder with a selective loss of dopaminergic neurons in the substantia nigra. Evidence suggests oxidation of dopamine (DA) to DA quinone and consequent oxidative stress as a major factor contributing to this vulnerability. We have previously observed that exposure to or induction of NAD(P)H:quinone reductase (QR1), the enzyme that catalyzes the reduction of quinone, effectively protects DA cells. Sulforaphane (SF) is a drug identified as a potent inducer of QR1 in various non-neuronal cells. In the present study, we show that SF protects against compounds known to induce DA quinone production (6-hydroxydopamine and tetrahydrobiopterin) in DAergic cell lines CATH.a and SK-N-BE(2)C as well as in mesencephalic DAergic neurons. SF leads to attenuation of the increase in protein-bound quinone in tetrahydrobiopterin-treated cells, but this does not occur in cells that have been depleted of DA, suggesting involvement of DA quinone. SF pretreatment prevents membrane damage, DNA fragmentation, and accumulation of reactive oxygen species. SF causes increases in mRNA levels and enzymatic activity of QR1 in a dose-dependent manner. Taken together, these results indicate that SF causes induction of QR1 gene expression, removal of intracellular DA quinone, and protection against toxicity in DAergic cells. Thus, this major isothiocyanate found in cruciferous vegetables may serve as a potential candidate for development of treatment and/or prevention of PD. https://greenmedinfo.com/article/sulforaphane-has-protective-effect-against-dopaminergic-cell-death#comments Dopamine Deficiency Parkinson's Disease Sulforaphane Anti-Apoptotic Neuroprotective Agents In Vitro Study Wed, 27 Oct 2010 02:14:05 +0000 greenmedinfo 58096 at https://greenmedinfo.com Sunlight exposure may increase striatal dopamine receptor availability. https://greenmedinfo.com/article/sunlight-exposure-may-increase-striatal-dopamine-receptor-availability PMID:  Prog Neuropsychopharmacol Biol Psychiatry. 2010 Sep 25. Epub 2010 Sep 25. PMID: 20875835 Abstract Title:  Sunshine-exposure variation of human striatal dopamine D(2)/D(3) receptor availability in healthy volunteers. Abstract:  BACKGROUND: In addition to the serotonergic system, the central dopaminergic system has been reported to be correlated with seasonality. The aim of this study was to explore the difference in striatal dopamine D(2)/D(3) receptor availability between healthy volunteers who had a high sunshine exposure and those who had a low exposure. METHODS: Sixty-eight participants were enrolled, and those in the upper and lower quartiles in terms of sunshine exposure were categorized into high- (n=17) and low- sunshine-exposure (n = 18) subgroups. Single photon emission computed tomography with [(123)I] iodo-benzamide was used to measure striatal dopamine D(2)/D(3) receptor availability. RESULTS: Striatal dopamine D(2)/D(3) receptor availability was significantly greater in the subjects with high sunshine exposure than in those with low sunshine exposure (F=7.97, p=0.01) after controlling for age, sex, and smoking status. LIMITATIONS: Different subjects were examined at different time points in our study. In addition, the sex and tobacco use distributions differed between groups. CONCLUSION: The central dopaminergic system may play a role in the neurobiological characteristics of sunshine exposure variation. https://greenmedinfo.com/article/sunlight-exposure-may-increase-striatal-dopamine-receptor-availability#comments Dopamine Deficiency Sunlight exposure Human Study Thu, 07 Oct 2010 01:01:41 +0000 greenmedinfo 57550 at https://greenmedinfo.com