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Bashi Rudahindwa, Jonathan. "OHADA and the Making of Transnational Commercial Law in Africa." Law and Development Review 11, no. 2 (June 26, 2018): 371–95. http://dx.doi.org/10.1515/ldr-2018-0024.
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Abstract The Organisation for Harmonisation of Business Law in Africa (OHADA) was established in October 1993 with the ambitious aim of inciting economic development in its Member States. Through the adoption of Uniform Commercial Laws, the organisation is expected to create an enabling environment for business development, thereby providing for a path to economic growth and subsequent development. In light of this professed aim, both the transnational methodological approach and comparative law theories are used in this paper to critically analyse the various processes conducted under the OHADA banner and to engage in discussions on the highly debated role of law as a vehicle for development in sub-Saharan Africa. This exercise, which proves crucial in order to trace its origin within the global governance and law and development theories, allows us to present OHADA as a transnational legal system, while also highlighting both its strengths and limitations.
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Fortin, Anne, and Saidatou Dicko. "The impact of the new OHADA accounting system on the judgments and decisions of Cameroonian bankers." Advances in Accounting 25, no. 1 (June 2009): 89–105. http://dx.doi.org/10.1016/j.adiac.2009.02.006.
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Fontaine, Marcel. "Les objectifs de lharmonisation du droit des contrats Deux projets OHADA et les Principes OHADAC: objectifs contrastés." European Review of Private Law 24, Issue 3/4 (June 1, 2016): 393–408. http://dx.doi.org/10.54648/erpl2016026.
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Abstract: The trend towards harmonization of contract law is increasingly developing, but orientations may be very different, due not only to the respective contexts, but also to the nature of objectives pursued. The present essay describes and compares three recent harmonization projects, two in the African context of the Organisation pour l’harmonisation en Afrique du droit des affaires (OHADA), the third one initiated by the Organisation pour l’harmonisation du droit des affaires dans la Caraïbe (OHADAC). The first African project, as requested by the Council of Ministers of OHADA, took strong inspiration from the UNIDROIT Principles, as the intention was to elaborate a modern instrument apt to attract investors. This project, however, has not been adopted, in particular because of a marked reluctance to depart from the French legal tradition, which is prevailing in most (but not all) member States. An alternative project, based on a private initiative, is in the process of being elaborated, with the view to remain within the dominant legal tradition and to avoid disorienting practitioners. As to the project that has just been prepared in the framework of OHADAC, it takes much inspiration from existing uniform law instruments, including the UNIDROIT Principles. At the same time, it is mainly concerned not to retain rules which could appear to be unacceptable in certain parts of a region where the legal systems are very diverse.
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Santana-Gómez, Cesar Emmanuel, Daniel Pérez-Pérez, Daniel Fonseca-Barriendos, Oscar Arias-Carrión, Walter Besio, and Luisa Rocha. "Transcranial Focal Electrical Stimulation Modifies Biogenic Amines’ Alterations Induced by 6-Hydroxydopamine in Rat Brain." Pharmaceuticals 14, no. 8 (July 21, 2021): 706. http://dx.doi.org/10.3390/ph14080706.
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Transcranial focal stimulation (TFS) is a non-invasive neuromodulation strategy with neuroprotective effects. On the other hand, 6-hidroxidopamine (6-OHDA) induces neurodegeneration of the nigrostriatal system producing modifications in the dopaminergic, serotoninergic, and histaminergic systems. The present study was conducted to test whether repetitive application of TFS avoids the biogenic amines’ changes induced by the intrastriatal injection of 6-OHDA. Experiments were designed to determine the tissue content of dopamine, serotonin, and histamine in the brain of animals injected with 6-OHDA and then receiving daily TFS for 21 days. Tissue content of biogenic amines was evaluated in the cerebral cortex, hippocampus, amygdala, and striatum, ipsi- and contralateral to the side of 6-OHDA injection. Results obtained were compared to animals with 6-OHDA, TFS alone, and a Sham group. The present study revealed that TFS did not avoid the changes in the tissue content of dopamine in striatum. However, TFS was able to avoid several of the changes induced by 6-OHDA in the tissue content of dopamine, serotonin, and histamine in the different brain areas evaluated. Interestingly, TFS alone did not induce significant changes in the different brain areas evaluated. The present study showed that repetitive TFS avoids the biogenic amines’ changes induced by 6-OHDA. TFS can represent a new therapeutic strategy to avoid the neurotoxicity induced by 6-OHDA.
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Firas Basim Ismail, Nizar F.O. Al-Muhsen, and Ain Amira Johari. "Thermal Comfort Analysis for Overhead and Underfloor Air Distribution Systems." CFD Letters 13, no. 12 (December 17, 2021): 113–32. http://dx.doi.org/10.37934/cfdl.13.12.113132.
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Underfloor and overhead air distributions are two types of Heating Ventilating and Air Conditioning (HVAC) system in which both differs in term of channelling the supplied air into a space. Underfloor air distribution (UFAD) system channels the supplied air from the underfloor plenum and goes to the return vent at the ceiling. On the other hand, the overhead air distribution (OHAD) system utilizes the ceiling-to-ceiling air pathway approach. In this study, A developed HVAC model was proposed. Ansys Fluent program was used to numerically investigate the best thermal comfort of the proposed model in terms of occupant satisfaction by referring to ASHRAE Standard. Two scenarios were designed and adopted in the computational investigation which is OHAD and UFAD. Three heat-generating parameters were involved which are a room lamp, personal computer and occupant. The attained computational fluid dynamic (CFD) simulation results were validated. Generally, the attained CFD results showed that the UFAD system could perform better compare to the OHAD system even though the OHAD system could have some benefits. Specifically, the UFAD system provided the best thermal performance whereas the OHAD system was found to be less efficient in providing thermal comfort to the occupant and consumed a greater amount of energy because it was required to cool down the whole room instead of being cooled partly. The CFD results confirmed that the UFAD system was capable of maintaining the room temperature at 26°C at a height below 2.0 m compared to 1.2 m of the OHAD system. In conclusion, the UFAD system could provide better indoor air quality, and it could have superior performance for the tropic weather regions such as Malaysia compared to that of the OHAD system. Besides, using the UFAD system could be represented a preventive action that could be proposed to solve the mould growth inside any occupied room.
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Kaminer, Jaime, Pratibha Thakur, and Craig Evinger. "Effects of subthalamic deep brain stimulation on blink abnormalities of 6-OHDA lesioned rats." Journal of Neurophysiology 113, no. 9 (May 2015): 3038–46. http://dx.doi.org/10.1152/jn.01072.2014.
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Parkinson's disease (PD) patients and the 6-hydroxydopamine (6-OHDA) lesioned rat model share blink abnormalities. In view of the evolutionarily conserved organization of blinking, characterization of blink reflex circuits in rodents may elucidate the neural mechanisms of PD reflex abnormalities. We examine the extent of this shared pattern of blink abnormalities by measuring blink reflex excitability, blink reflex plasticity, and spontaneous blinking in 6-OHDA lesioned rats. We also investigate whether 130-Hz subthalamic nucleus deep brain stimulation (STN DBS) affects blink abnormalities, as it does in PD patients. Like PD patients, 6-OHDA-lesioned rats exhibit reflex blink hyperexcitability, impaired blink plasticity, and a reduced spontaneous blink rate. At 130 Hz, but not 16 Hz, STN DBS eliminates reflex blink hyperexcitability and restores both short- and long-term blink plasticity. Replicating its lack of effect in PD patients, 130-Hz STN DBS does not reinstate a normal temporal pattern or rate to spontaneous blinking in 6-OHDA lesioned rats. These data show that the 6-OHDA lesioned rat is an ideal model system for investigating the neural bases of reflex abnormalities in PD and highlight the complexity of PD's effects on motor control, by showing that dopamine depletion does not affect all blink systems via the same neural mechanisms.
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Yazulla, Stephen, and Keith M. Studholme. "Volume transmission of dopamine may modulate light-adaptive plasticity of horizontal cell dendrites in the recovery phase following dopamine depletion in goldfish retina." Visual Neuroscience 12, no. 5 (September 1995): 827–36. http://dx.doi.org/10.1017/s0952523800009391.
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AbstractWe investigated the recovery of light-adaptive spinule formation following dopamine depletion with intraocular injection of 6-hydroxydopamine (6-OHDA) and subsequent neogeneration of dopamine interplexiform cells (DA-IPC) at the marginal zone. DA-IPCs were gone by 2 weeks postinjection and appeared at the marginal zone by 6 weeks postinjection, at which time DA-IPC neurites grew toward the central retina, reaching within 0.5 mm of the central retina by 1 year. Retinas from day time, light-adapted fish at 2 weeks, 4 weeks, 3 months, and 1 year postinjection with 6-OHDA were processed for pre-embedding tyrosine hydroxylase immunoreactivity (TOH-IR) and compared to sham-injected and control retinas at the electron-microscopical (EM) level. Only 6-OHDA fish that tilted markedly toward the injected eye were used for these experiments. The tilt mimics the dorsal light reaction, indicating a 2–2.5 log unit increase in the photopic sensitivity of the 6-OHDA eye. Spinule formation was reduced by about 60% in the 2- and 4-week 6-OHDA retinas, but returned to control levels throughout the entire retina of 3-month and 1 year 6-OHDA retinas even though the central region of these retinas contained no detectable TOH-IR. Intraocular injection with 10 μM SCH 23390 (a Dl antagonist) reduced light-adaptive spinule formation by 50% both in control eyes as well as those eyes that were 3 months post 6-OHDA injected. The full return of spinule formation with only partial reinnervation of the retina with DA-IPC processes and their subsequent inhibition by SCH 23390 indicates that dopamine diffused large distances within the retina to regulate this synaptic plasticity (i.e. displayed volume transmission). Also, since all 6-OHDA injected fish displayed an increased photopic sensitivity in the injected eye when sacrificed, we suggest that horizontal cell spinules are not required for photopic luminosity coding in the outer retina.
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Roginsky, Vitaly A., Tatjana K. Barsukova, Gernot Bruchelt, and Hartmut B. Stegmann. "The Oxidation of Catecholamines and 6-Hydroxydopamine by Molecular Oxygen: Effect of Ascorbate." Zeitschrift für Naturforschung C 52, no. 5-6 (June 1, 1997): 380–90. http://dx.doi.org/10.1515/znc-1997-5-617.
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Abstract Comparative kinetic studies on the oxidation of catecholamines (CA) (dopamine (DA), epinephrine (EP). norepinephrine (NEP)) serving as a neuromediator in the sympathetic nervous system, 3,4-dihydroxyphenylalanine (DOPA) and 6-hydroxydopamine (6-OHDA), a wellknown neurotoxic agent, were performed in the presence of ascorbate (AscH- ) in 50 mᴍ phosphate buffer, pH 7.40, at 37 °C by using a Clark electrode, EPR and the absorption spectroscopy. The oxidation of CA and DOPA alone was found to be a self-accelerating process, with quinone products (Q) acting as autocatalysts. The rate of oxygen consumption (Rox) increased with time and reached a steady-state level. A starting value of Rox increased in the order: EP < DOPA ≈ NEP ≪ DA ≪ 6-OHDA, whereas a steady-state value of Rox changed in the order: DOPA < DA < NEP ≪ EP ≪ 6-OHDA. The changes in Rox with time were found to correlate with the resistance of primary Q to the intramolecular cyclization. The effect of AscH- on CA oxidation depended dramatically on whether AscH- was added to non-oxidized or preoxidized CA. Added to non-oxidized CA and DOPA, AscH- inhibited their oxidation (but not that of 6-OHDA). For the case of DA, a pronounced lag period was observed by both a Clark electrode and spectrophotometrically. The addition of AscH- to preoxidized CA, DOPA and 6-OHDA induced an increase in Rox a steadystate concentration of the ascorbyl radical. The kinetic behaviour of the systems was determined by two major factors: 1) AscH- suppressed the formation of Q, a catalyst for CA oxidation, most likely due to the reaction of AscH- with the semiquinone formed from CA; 2) Q derived both from CA and 6-OHDA catalyzed AscH- oxidation. The elevated cytotoxicity of 6-OHDA was found to be in part caused by the condition that 6-OHDA oxidation was not inhibited by AscH- and by the high efficiency of 6-OHDA as a redox cycling agent in combination with A scH−. These observations explain the very pronounced and prolonged cytotoxicity of 6-OHDA even at low concentrations that increases at elevated concentrations of AscH- .
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Oliynyk, Zh, M. Rudyk, V. Svyatetska, T. Dovbynchuk, G. Tolstanova, and L. Skivka. "Systemic inflammation biomarkers in 6-OHDA- and LPS-induced Parkinson’s disease in rats." Ukrainian Biochemical Journal 94, no. 1 (May 10, 2022): 33–43. http://dx.doi.org/10.15407/ubj94.01.033.
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Bonaz, B., L. Martin, E. Beurriand, M. Manier, J. Hostein, and C. Feuerstein. "Modulation of the migrating myoelectric complex by brain noradrenergic systems in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 2 (February 1, 1991): G340—G345. http://dx.doi.org/10.1152/ajpgi.1991.260.2.g340.
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The respective role of central and peripheral noradrenergic systems in the control of migrating myoelectric complex (MMC) was investigated in rats following lesions with 6-hydroxydopamine (6-OHDA). 6-OHDA was injected via intraperitoneal (ip), intracisternal (icis), and intracerebroventricular (icv) routes in rats. Control animals received the vehicle alone. One month later, MMC was recorded in conscious rats chronically fitted with electrodes. The MMC period was significantly lengthened after 6-OHDA ip or icv injection, and slightly shortened after 6-OHDA icis injection. No disruption of central noradrenergic systems was detected after ip lesions. Norepinephrine content was reduced in the digestive tract after ip lesions, in the spinal cord after icis lesions, and in the cortex, the hypothalamus, pons-medulla, and the spinal cord after icv lesions. After icis lesions, noradrenergic perikarya were spared in pons-medulla, whereas only pons noradrenergic perikarya were lesioned after icv lesions. We conclude that lesions of brain noradrenergic systems modify MMC periodicity in rats. The rostral noradrenergic systems may play the major modulatory role.
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Miura, Tomisato, Tsuyoshi Kudo, Akitomo Matsuki, Kenji Sekikawa, Yoh-Ichi Tagawa, Yoichiro Iwakura, and Akio Nakane. "Effect of 6-Hydroxydopamine on Host Resistance against Listeria monocytogenes Infection." Infection and Immunity 69, no. 12 (December 1, 2001): 7234–41. http://dx.doi.org/10.1128/iai.69.12.7234-7241.2001.
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ABSTRACT Recent studies have shown that immunocompetent cells bear receptors of neuropeptides and neurotransmitters and that these ligands play roles in the immune response. In this study, the role of the sympathetic nervous system in host resistance against Listeria monocytogenes infection was investigated in mice pretreated with 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve termini. The norepinephrine contents of the plasma and spleens were significantly lower in 6-OHDA-treated mice than in vehicle-treated mice. The 50% lethal dose of L. monocytogenes was about 20 times higher for 6-OHDA-treated mice than for vehicle-treated mice. Chemical sympathectomy by 6-OHDA upregulated interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-α) production in enriched dendritic cell cultures and gamma interferon (IFN-γ) and TNF-α production in spleen cell cultures, whereas chemical sympathectomy had no apparent effect on phagocytic activities, listericidal activities, and nitric oxide production in peritoneal exudate cells and splenic macrophages. Augmentation of host resistance against L. monocytogenesinfection by 6-OHDA was abrogated in IFN-γ−/− or TNF-α−/− mice, suggesting that upregulation of IFN-γ, IL-12, and TNF-α production may be involved in 6-OHDA-mediated augmentation of antilisterial resistance. Furthermore, adoptive transfer of spleen cells immune to L. monocytogenes from 6-OHDA-treated mice resulted in untreated naive recipients that had a high level of resistance against L. monocytogenesinfection. These results suggest that the sympathetic nervous system may modulate host resistance against L. monocytogenesinfection through regulation of production of IFN-γ, IL-12, and TNF-α, which are critical in antilisterial resistance.
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Joo, Sung-Yeon, Hee-Wang Yoo, Sharad Sarak, Byung-Gee Kim, and Hyungdon Yun. "Enzymatic Synthesis of ω-Hydroxydodecanoic Acid By Employing a Cytochrome P450 from Limnobacter sp. 105 MED." Catalysts 9, no. 1 (January 8, 2019): 54. http://dx.doi.org/10.3390/catal9010054.
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ω-Hydroxylated fatty acids are valuable and versatile building blocks for the production of various adhesives, lubricants, cosmetic intermediates, etc. The biosynthesis of ω-hydroxydodecanoic acid from vegetable oils is one of the important green pathways for their chemical-based synthesis. In the present study, the novel monooxygenase CYP153AL.m from Limnobacter sp. 105 MED was used for the whole-cell biotransformations. We constructed three-component system that was comprised of CYP153AL.m, putidaredoxin and putidaredoxin reductase from Pseudomonas putida. This in vivo study demonstrated that CYP153AL.m is a powerful catalyst for the biosynthesis of ω-hydroxydodecanoic acid. Under optimized conditions, the application of a solid-state powdered substrate rather than a substrate dissolved in DMSO significantly enhanced the overall reaction titer of the process. By employing this efficient system, 2 g/L of 12-hydroxydodecanoic acid (12-OHDDA) was produced from 4 g/L of its corresponding fatty acid, which was namely dodecanoic acid. Furthermore, the system was extended to produce 3.28 g/L of 12-OHDDA using 4 g/L of substrate by introducing native redox partners. These results demonstrate the utility of CYP153AL.m-catalyzed biotransformations in the industrial production of 12-OHDDA and other valuable building blocks.
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Douglas, R. H., H. J. Wagner, M. Zaunreiter, U. D. Behrens, and M. B. A. Djamgoz. "The effect of dopamine depletion on light-evoked and circadian retinomotor movements in the teleost retina." Visual Neuroscience 9, no. 3-4 (October 1992): 335–43. http://dx.doi.org/10.1017/s0952523800010749.
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AbstractThe retinae of lower vertebrates undergo a number of structural changes during light adaptation, including the photomechanical contraction of cone myoids and the dispersion of melanin granules within the epithelial pigment. Since the application of dopamine to dark-adapted retinae is known to produce morphological changes that are characteristic of light adaptation, dopamine is accepted as a causal mechanism for such retinomotor movements. However, we report here that in the teleost fish, Aequidens pulcher, the intraocular injection of 6-hydroxydopamine (6-OHDA), a substance known to destroy dopaminergic retinal cells, has no effect on the triggering of light-adaptive retinomotor movements of the cones and epithelial pigment and only slightly depresses the final level of light adaptation reached. Furthermore, the retina continues to show circadian retinomotor changes even after 48 h in continual darkness that are similar in both control and 6-OHDA injected fish. Biochemical assay and microscopic examination showed that 6-OHDA had destroyed dopaminergic retinal cells. We conclude, therefore, that although a dopaminergic mechanism is probably involved in the control of light-induced retinomotor movements, it cannot be the only control mechanism, nor can it be the cause of circadian retinomotor migrations. Interestingly, 6-OHDA injected eyes never reached full retinomotor dark adaptation, suggesting that dopamine has a role to play in the retina's response to darkness.
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Yoshihara, T., S. Honma, and K. Honma. "Prefeeding release of paraventricular neuropeptide Y is mediated by ascending noradrenergic neurons in rats." American Journal of Physiology-Endocrinology and Metabolism 270, no. 4 (April 1, 1996): E596—E600. http://dx.doi.org/10.1152/ajpendo.1996.270.4.e596.
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The neuronal system responsible for the release of neuropeptide Y (NPY) in the paraventricular nucleus (PVN) was examined in rats under food deprivation and restricted daily feeding (RF). The ascending noradrenergic bundle (NAB) of neurons from the brain stem were destructed by microinjection of 6-hydroxydopamine (6-OHDA), and the extracellular NPY level in the PVN was measured by push-pull perfusion. 6-OHDA significantly reduced the extracellular norepinephrine level in the PVN to 15% of the control value when injected into the PVN and to 40% when injected into the midbrain ventral NAB. 6-OHDA administration into the NAB affected neither the deprivation-induced increase nor the feeding-induced decrease in the extracellular NPY. The amount of food intake after refeeding was not changed by the 6-OHDA treatment. On the other hand, 6-OHDA injection into the PVN or NAB not only decreased the extracellular NPY level, the amount of food intake was not change by the 6-OHDA treatment. It is concluded that the NAB is involved in the prefeeding NPY release in rats under RF but not in the deprivation-induced NPY release.
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Godinet, Meripa T., Pam Arnsberger, Fenfang Li, and Theresa Kreif. "Disproportionality, Ohana Conferencing, and the Hawai'i Child Welfare System." Journal of Public Child Welfare 4, no. 4 (November 30, 2010): 387–405. http://dx.doi.org/10.1080/15548732.2010.526898.
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Chen, Chao-Hsuan, Pei-Chen Hsu, Shih-Wei Hsu, Kun-Ting Hong, Kai-Yuan Chen, Jie-Long He, Der-Yang Cho, et al. "Protective Effects of Jujubosides on 6-OHDA-Induced Neurotoxicity in SH-SY5Y and SK-N-SH Cells." Molecules 27, no. 13 (June 26, 2022): 4106. http://dx.doi.org/10.3390/molecules27134106.
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6-hydroxydopamine (6-OHDA) is used to induce oxidative damage in neuronal cells, which can serve as an experimental model of Parkinson’s disease (PD). Jujuboside A and B confer free radical scavenging effects but have never been examined for their neuroprotective effects, especially in PD; therefore, in this study, we aimed to investigate the feasibility of jujubosides as protectors of neurons against 6-OHDA and the underlying mechanisms. 6-OHDA-induced neurotoxicity in the human neuronal cell lines SH-SY5Y and SK-N-SH, was used to evaluate the protective effects of jujubosides. These findings indicated that jujuboside A and B were both capable of rescuing the 6-OHDA-induced loss of cell viability, activation of apoptosis, elevation of reactive oxygen species, and downregulation of the expression levels of superoxide dismutase, catalase, and glutathione peroxidase. In addition, jujuboside A and B can reverse a 6-OHDA-elevated Bax/Bcl-2 ratio, downregulate phosphorylated PI3K and AKT, and activate caspase-3, -7, and -9. These findings showed that jujubosides were capable of protecting both SH-SY5Y and SK-N-SH neuronal cells from 6-OHDA-induced toxicity via the rebalancing of the redox system, together with the resetting of the PI3K/AKT apoptotic signaling cascade. In conclusion, jujuboside may be a potential drug for PD prevention.
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Ma, Jing, Ranran Wang, Ting Chen, Shaowei Jiang, and Ajing Xu. "Protective effects of baicalin in a Caenorhabditis elegans model of Parkinson’s disease." Toxicology Research 10, no. 3 (April 26, 2021): 409–17. http://dx.doi.org/10.1093/toxres/tfaa107.
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Abstract Parkinson’s disease (PD) is a common neurodegenerative disorder of the central nervous system. However, the pathogenetic mechanisms of PD are far from understood. The aim of this study was to determine the protective effect of baicalin in a Caenorhabditis elegans model of PD. C. elegans worms were stimulated for 24 h with 6-hydroxydopamine (6-OHDA, 50 mM) and treated with or without baicalin (1, 10, or 100 μM). At all tested concentrations, baicalin improved the reversal and omega turn behavioral phenotypes, as well as the survival, of 6-OHDA-stimulated worms. It also inhibited 6-OHDA-induced oxidative stress by decreasing malondialdehyde levels, increasing superoxide dismutase, glutathione reductase, catalase, and glutathione levels and up-regulating mRNA expression of the antioxidant-related genes sod-1, sod-2, sod-3, daf-2, and daf-16. Additionally, it significantly decreased the expression of the apoptosis-related gene ced-3 and increased that of the anti-apoptosis-related gene ced-9. The expression levels of cleaved caspase-3 and B-cell lymphoma 2 in 6-OHDA-treated worms were reversed by baicalin. Apoptosis was suppressed by 6-OHDA in loss-of-function strains via the p38 mitogen-activated protein kinase (MAPK) signaling pathway. Furthermore, the apoptotic effects of 6-OHDA were blocked in sek-1 and pmk-1 mutants. Finally, the mRNA expression of sek-1 and pmk-1 and the protein expression of p38 MAPK and stress-activated protein kinase/extracellular signal-regulated kinase 1 were up-regulated by 6-OHDA and reversed by baicalin. Baicalin may protect against 6-OHDA injury by inhibiting apoptosis and decreasing oxidative stress through the p38 MAPK signaling pathway.
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Custer, J. R., and C. A. Hales. "Chemical sympathectomy decreases alveolar hypoxic vasoconstriction in lambs but not in sheep." Journal of Applied Physiology 60, no. 1 (January 1, 1986): 32–37. http://dx.doi.org/10.1152/jappl.1986.60.1.32.
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We studied the role of the sympathetic nervous system in the augmented vasoconstrictor response of the newborn lamb, compared with the adult sheep, by producing a chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Seven lambs, age 4–16 days, and five sheep, age 2 yr, were anesthetized and intubated with a double-lumen endotracheal tube, allowing ventilation of one lung with O2 to maintain systemic oxygenation while the contralateral lung was ventilated with N2 as a hypoxic challenge. Distribution of perfusion to each lung was evaluated using positron scintigraphy after inferior vena caval injections of 13N, a positron-emitting isotope. In the lambs, prior to 6-OHDA, distribution of perfusion to the test lung was 43 +/- 3% of total lung perfusion during bilateral O2 ventilation and fell with hypoxia to 24 +/- 2%, a reduction of 44 +/- 3% during N2 ventilation as compared with O2 ventilation. After 6-OHDA, hypoxic challenge reduced perfusion by only 22 +/- 2% (P less than 0.01 compared with pre-6-OHDA). In the adult sheep, hypoxic vasoconstriction reduced perfusion to the test lung by 28 +/- 2% but was unaffected by 6-OHDA. Absence of rise in pulmonary vascular resistance (PVR) or femoral artery pressure (Pfa) in response to Tyramine infusions after 6-OHDA confirmed complete sympathectomy in lambs and sheep. Persistent increases in PVR and Pfa to infusions of prostaglandin F2 alpha before and after 6-OHDA showed that the loss of alveolar hypoxic vasoconstriction in the lamb was specific. Thus sympathetic innervation may contribute to the greater strength of alveolar hypoxic vasoconstriction found in lambs than in sheep.
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TODA, Shinji, Katsuyoshi MIYAKOSHI, Daiei INOUE, Ken'ichiro KUSUNOKI, and Koichi SUZUKI. "Trench Survey for the Ohara Fault of the Yamasaki Fault System at Hurumachi, Ohara Town, Okayama Pref., Japan." Zisin (Journal of the Seismological Society of Japan. 2nd ser.) 48, no. 1 (1995): 57–70. http://dx.doi.org/10.4294/zisin1948.48.1_57.
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Yokote, Hideyoshi, Toru Itakura, Kunio Nakai, Ichiro Kamei, Harumichi Imai, and Norihiko Komai. "A role of the central catecholamine neuron in cerebral circulation." Journal of Neurosurgery 65, no. 3 (September 1986): 370–75. http://dx.doi.org/10.3171/jns.1986.65.3.0370.
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✓ The effect of the central catecholaminergic neurons on the cerebral microcirculation was investigated by means of a unilateral intracerebral injection of 6-hydroxydopamine (6-OHDA) which produced the degeneration of catecholamine (CA) nerve terminals. Subsequent observation with CA histofluorescence revealed an absence of CA fibers in the vicinity of the 6-OHDA injection site. A significant increase in regional cerebral blood flow (rCBF), measured by the hydrogen clearance method, was demonstrated in the CA-depleted cortex under normocapnia as compared with rCBF in the control cortex (CA-depleted cortex 47.0 ± 2.8 ml/100 gm/min; control cortex 38.5 ± 3.5 ml/100 gm/min; p < 0.005). The increased rCBF in the cortex treated with 6-OHDA was suppressed by the iontophoretic replacement of noradrenaline (NA) to the CA-depleted cortex. An iontophoretic replacement of 10−5 M dopamine (DA) mildly suppressed the increased rCBF in the 6-OHDA-treated cortex. The CO2 reactivity in the CA-depleted cortex was significantly lower than that of the control cortex (CA-depleted cortex 2.13% ± 0.67%/mm Hg; control cortex 3.53% ± 0.70%/mm Hg). No change was noticeable in the cerebral glucose metabolism in the CA-depleted cortex in an investigation based on tritiated (3H)-deoxyglucose uptake. It is suggested that the 6-OHDA-induced change in cerebral blood flow (CBF) is not secondary to alterations in cerebral metabolic rate, and that the central NA neuron system innervating intraparenchymal blood vessels regulates CBF through a direct vasoconstrictive effect on the cerebral blood vessels. The central DA neuron system may modulate the cerebral circulation as a mild vasoconstrictor.
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Rodrigues, Ricardo Wilson Pinho, Vânia Canterucci Gomide, and Gerson Chadi. "Striatal injection of 6-hydroxydopamine induces retrograde degeneration and glial activation in the nigrostriatal pathway." Acta Cirurgica Brasileira 18, no. 4 (August 2003): 272–82. http://dx.doi.org/10.1590/s0102-86502003000400004.
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PURPOSE: The effect of a highly selective 6-hydroxydopamine (6-OHDA)-induced lesion of the nigrostriatal system on the astroglial and microglial activation was analysed in adult Wistar rats after an unilateral striatal injection of the neurotoxin. METHODS: Male rats received an unilateral stereotaxical injection of the 6-OHDA in the left side of the neostriatum and were sacrificed 22 days later. Control animals received the injection of the solvent. The rotational behaviour was registered by a rotometer just before the sacrifice. Immunohistochemistry was employed for visualization of the tyrosine hydroxylase (TH) positive dopamine cells, glial fibrillary acidic protein (GFAP) immunolabeled astrocytes and OX42 immunoreactive microglia. Stereological method employing the optical disector was used to estimate the degree of the changes. RESULTS: The striatal injection of the 6-OHDA induced a massive disappearance (32% of control) of the TH immunoreactive terminals in a defined area within the striatum surrounding the injection site. A disappearance (54% of control) of dopamine cell bodies was observed in a small region of the ipsilateral pars compacta of the substantia nigra (SNc). The GFAP and OX42immunohistochemistry revealed astroglial and microglial reactions (increases in the number and size of the cells) in the ipsilateral neostriatum and SNc of the 6-OHDA injected rats. CONCLUSIONS: The striatal injection of 6-OHDA leads to retrograde degeneration as well as astroglial and microglial activation in the nigrostriatal dopamine pathway. Modulation of activated glial cells may be related to wound repair and to the trophic paracrine response in the lesioned nigrostriatal dopamine system.
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Tang, Hengfang, Zhiming Zheng, Han Wang, Li Wang, Genhai Zhao, and Peng Wang. "Vitamin K2 Modulates Mitochondrial Dysfunction Induced by 6-Hydroxydopamine in SH-SY5Y Cells via Mitochondrial Quality-Control Loop." Nutrients 14, no. 7 (April 4, 2022): 1504. http://dx.doi.org/10.3390/nu14071504.
Full textAbstract:
Vitamin K2, a natural fat-soluble vitamin, is a potent neuroprotective molecule, owing to its antioxidant effect, but its mechanism has not been fully elucidated. Therefore, we stimulated SH-SY5Y cells with 6-hydroxydopamine (6-OHDA) in a proper dose-dependent manner, followed by a treatment of vitamin K2. In the presence of 6-OHDA, cell viability was reduced, the mitochondrial membrane potential was decreased, and the accumulation of reactive oxygen species (ROS) was increased. Moreover, the treatment of 6-OHDA promoted mitochondria-mediated apoptosis and abnormal mitochondrial fission and fusion. However, vitamin K2 significantly suppressed 6-OHDA-induced changes. Vitamin K2 played a significant part in apoptosis by upregulating and downregulating Bcl-2 and Bax protein expressions, respectively, which inhibited mitochondrial depolarization, and ROS accumulation to maintain mitochondrial structure and functional stabilities. Additionally, vitamin K2 significantly inhibited the 6-OHDA-induced downregulation of the MFN1/2 level and upregulation of the DRP1 level, respectively, and this enabled cells to maintain the dynamic balance of mitochondrial fusion and fission. Furthermore, vitamin K2 treatments downregulated the expression level of p62 and upregulated the expression level of LC3A in 6-OHDA-treated cells via the PINK1/Parkin signaling pathway, thereby promoting mitophagy. Moreover, it induced mitochondrial biogenesis in 6-OHDA damaged cells by promoting the expression of PGC-1α, NRF1, and TFAM. These indicated that vitamin K2 can release mitochondrial damage, and that this effect is related to the participation of vitamin K2 in the regulation of the mitochondrial quality-control loop, through the maintenance of the mitochondrial quality-control system, and repair mitochondrial dysfunction, thereby alleviating neuronal cell death mediated by mitochondrial damage.
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Lee, Gyeong Hee, Won Jin Lee, Jinwoo Hur, Eunsu Kim, Hyuk Gyoon Lee, and Han Geuk Seo. "Ginsenoside Re Mitigates 6-Hydroxydopamine-Induced Oxidative Stress through Upregulation of GPX4." Molecules 25, no. 1 (January 2, 2020): 188. http://dx.doi.org/10.3390/molecules25010188.
Full textAbstract:
Ginsenosides are active components found abundantly in ginseng which has been used as a medicinal herb to modify disease status for thousands of years. However, the pharmacological activity of ginsenoside Re in the neuronal system remains to be elucidated. Neuroprotective activity of ginsenoside Re was investigated in SH-SY5Y cells exposed to 6-hydroxydopamine (6-OHDA) to induce cellular injury. Ginsenoside Re significantly inhibited 6-OHDA-triggered cellular damage as judged by analysis of tetrazolium dye reduction and lactose dehydrogenase release. In addition, ginsenoside Re induced the expression of the antioxidant protein glutathione peroxidase 4 (GPX4) but not catalase, glutathione peroxidase 1, glutathione reductase, or superoxide dismutase-1. Furthermore, upregulation of GPX4 by ginsenoside Re was mediated by phosphoinositide 3-kinase and extracellular signal-regulated kinase but not by p38 mitogen-activated protein kinase or c-Jun N-terminal kinase. Ginsenoside Re also suppressed 6-OHDA-triggered cellular accumulation of reactive oxygen species and peroxidation of membrane lipids. The GPX4 inhibitor (1S,3R)-RSL3 reversed ginsenoside Re-mediated inhibition of cellular damage in SH-SY5Y cells exposed to 6-OHDA, indicating that the neuronal activity of ginsenoside Re is due to upregulation of GPX4. These findings suggest that ginsenoside Re-dependent upregulation of GPX4 reduces oxidative stress and thereby alleviates 6-OHDA-induced neuronal damage.
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Liu, Xiaojie, Hao Yu, Bixuan Chen, Vladislav Friedman, Lianwei Mu, Thomas J. Kelly, Gonzalo Ruiz-Pérez, et al. "CB2 Agonist GW842166x Protected against 6-OHDA-Induced Anxiogenic- and Depressive-Related Behaviors in Mice." Biomedicines 10, no. 8 (July 22, 2022): 1776. http://dx.doi.org/10.3390/biomedicines10081776.
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In addition to motor dysfunction, patients with Parkinson’s disease (PD) are often affected by neuropsychiatric disorders, such as anxiety and depression. In animal models, activation of the endocannabinoid (eCB) system produces anxiolytic and antidepressant-like behavioral effects. CB2 agonists have demonstrated neuroprotective effects against neurotoxin-induced dopamine neuron loss and deficits in motor function. However, it remains unknown whether CB2 agonism ameliorates anxiogenic- and depressive-like behaviors in PD models. Here, we report that the selective CB2 agonist GW842166x exerted neuroprotective effects against 6-hydroxydopamine (6-OHDA)-induced loss of dopaminergic terminals and dopamine release in the striatum, which were blocked by the CB2 antagonist AM630. We found that 6-OHDA-treated mice exhibited anxiogenic- and depressive-like behaviors in the open-field, sucrose preference, novelty-suppressed feeding, marble burying, and forced swim tests but did not show significant changes in the elevated plus-maze and light–dark box test. GW842166x treatments ameliorated 6-OHDA-induced anxiogenic- and depressive-like behaviors, but the effects were blocked by CB2 antagonism, suggesting a CB2-dependent mechanism. These results suggest that the CB2 agonist GW842166x not only reduces 6-OHDA-induced motor function deficits but also anxiogenic- and depressive-like behaviors in 6-OHDA mouse models of PD.
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Ball, Alexander K., William H. Baldridge, and Timothy C. Fernback. "Neuromodulation of pigment movement in the RPE of normal and 6-OHDA-lesioned goldfish retinas." Visual Neuroscience 10, no. 3 (May 1993): 529–40. http://dx.doi.org/10.1017/s0952523800004740.
Full textAbstract:
AbstractThe role of dopamine as the endogenous signal-initiating light-dependent changes in the distribution of pigment granules in goldfish retinal pigment epithelium was investigated. In normal retinas, light adaptation resulted in the dispersion of pigment granules. This effect of light was mimicked by the intraocular injection of dopamine or serotonin, which is thought to increase endogenous dopamine release, into dark-adapted eyes. The effect of light, dopamine, or serotonin on dark-adapted retinas was blocked by the dopamine receptor antagonists haloperidol and sulpiride. However, lesioning the endogenous source of retinal dopamine, by prior intraocular injection of 6-hydroxydopamine (6-OHDA), did not block the dispersion of pigment granules in light-adapted retinas. No significant differences in pigment dispersion were noted between unlesioned and lesioned light- or dark-adapted retinas. However, the effect of light on pigment dispersion was no longer blocked by haloperidol or sulpiride in 6-OHDA lesioned animals. Dopamine and serotonin mimicked the effect of light when injected into lesioned dark-adapted eyes, but their effects were also not blocked by haloperidol or sulpiride. These results suggest that dopamine, acting on D2 receptors, is sufficient to induce pigment migration in unlesioned animals. In 6-OHDA-lesioned animals, however, pigment migration is mediated by a receptor mechanism other than D2.
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Honrath, U., A. T. Veress, C. K. Chong, and H. Sonnenberg. "Effect of sympathetic and angiotensin-aldosterone systems on renal salt conservation in the rat." American Journal of Physiology-Renal Physiology 272, no. 4 (April 1, 1997): F538—F544. http://dx.doi.org/10.1152/ajprenal.1997.272.4.f538.
Full textAbstract:
During dietary salt deprivation, the sympathetic nervous system and the angiotensin-aldosterone system are stimulated. Both systems are thought to be essential for maximal salt conservation by the kidney. To study their relative contributions, we produced negative salt balance in rats by intraperitoneal injection of furosemide, followed by a low-salt diet (<0.008% NaCl). In a 1-wk metabolic study, the animals were unable to replace the drug-induced salt deficit. Six groups of rats were studied. A control group established baseline function, a second group of 6-hydroxydopamine (OHDA) rats were treated with OHDA to destroy sympathetic efferent nerve terminals, and a third group (losartan) were treated with the angiotensin-receptor antagonist losartan. The influence of catecholamines and aldosterone released from the adrenal gland was studied in a further three groups. Rats were sham-adrenalectomized (sham), subjected to bilateral adrenal enucleation (Enuc) to eliminate catecholamine secretion, or were bilaterally adrenalectomized (Adx), eliminating both catecholamine and corticosteroid release. Dexamethasone was used as glucocorticoid replacement in this group. Steady-state urinary salt excretion was not different between control and OHDA rats. The losartan group showed significantly increased sodium but not chloride excretion. Surprisingly, there were no differences in salt excretion among sham, Enuc, and Adx groups. We conclude that, during a state of chronic salt depletion, renal mechanism(s) independent of neuronally released or systemically circulating catecholamines or of adrenally released aldosterone can ensure maximal salt conservation by the kidney. Although our data show that losartan increased sodium excretion under these conditions, we suggest that the losartan effect can be explained by a reduction of bicarbonate reabsorption, obligating simultaneous excretion of the cation.
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Li, Haifeng, Ruona Shi, Fei Ding, Hongyu Wang, Wenjing Han, Fangli Ma, Minghua Hu, Chung Wah Ma, and Zebo Huang. "Astragalus Polysaccharide Suppresses 6-Hydroxydopamine-Induced Neurotoxicity in Caenorhabditis elegans." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4856761.
Full textAbstract:
Astragalus membranaceus is a medicinal plant traditionally used in China for a variety of conditions, including inflammatory and neural diseases. Astragalus polysaccharides are shown to reduce the adverse effect of levodopa which is used to treat Parkinson’s disease (PD). However, the neuroprotective effect of Astragalus polysaccharides per se in PD is lacking. Using Caenorhabditis elegans models, we investigated the protective effect of astragalan, an acidic polysaccharide isolated from A. membranaceus, against the neurotoxicity of 6-hydroxydopamine (6-OHDA), a neurotoxin that can induce parkinsonism. We show that 6-OHDA is able to degenerate dopaminergic neurons and lead to the deficiency of food-sensing behavior and a shorter lifespan in C. elegans. Interestingly, these degenerative symptoms can be attenuated by astragalan treatment. Astragalan is also shown to alleviate oxidative stress through reducing reactive oxygen species level and malondialdehyde content and increasing superoxide dismutase and glutathione peroxidase activities and reduce the expression of proapoptotic gene egl-1 in 6-OHDA-intoxicated nematodes. Further studies reveal that astragalan is capable of elevating the decreased acetylcholinesterase activity induced by 6-OHDA. Together, our results demonstrate that the protective effect of astragalan against 6-OHDA neurotoxicity is likely due to the alleviation of oxidative stress and regulation of apoptosis pathway and cholinergic system and thus provide an important insight into the therapeutic potential of Astragalus polysaccharide in neurodegeneration.
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Lin, Zheng-Shi, and Stephen Yazulla. "Depletion of retinal dopamine does not affect the ERG b-wave increment threshold function in goldfish in vivo." Visual Neuroscience 11, no. 4 (July 1994): 695–702. http://dx.doi.org/10.1017/s095252380000300x.
Full textAbstract:
AbstractIncrement threshold functions of the electroretinogram (ERG) b–wave were obtained from goldfish using an in vivo preparation to study intraretinal mechanisms underlying the increase in perceived brightness induced by depletion of retinal dopamine by 6–hydroxydopamine (6–OHDA). Goldfish received unilateral intraocular injections of 6–OHDA plus pargyline on successive days. Depletion of retinal dopamine was confirmed by the absence of tyrosine-hydroxylase immunoreactivity at 2 to 3 weeks postinjection as compared to sham-injected eyes from the same fish. There was no difference among normal, sham-injected or 6–OHDA-injected eyes with regard to ERG waveform, intensity-response functions or increment threshold functions. Dopamine-depleted eyes showed a Purkinje shift, that is, a transition from rod-to-cone dominated vision with increasing levels of adaptation. We conclude (1) dopamine-depleted eyes are capable of photopic vision; and (2) the ERG b–wave is not diagnostic for luminosity coding at photopic backgrounds. We also predict that (1) dopamine is not required for the transition from scotopic to photopic vision in goldfish; (2) the ERG b–wave in goldfish is influenced by chromatic interactions; (3) horizontal cell spinules, though correlated with photopic mechanisms in the fish retina, are not necessary for the transition from scotopic to photopic vision; and (4) the OFF pathway, not the ON pathway, is involved in the action of dopamine on luminosity coding in the retina.
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Wu, Chi-Rei, Hung-Chi Chang, Yih-Dih Cheng, Wan-Cheng Lan, Shu-Er Yang, and Hui Ching. "Aqueous Extract of Davallia mariesii Attenuates 6-Hydroxydopamine-Induced Oxidative Damage and Apoptosis in B35 Cells Through Inhibition of Caspase Cascade and Activation of PI3K/AKT/GSK-3β Pathway." Nutrients 10, no. 10 (October 6, 2018): 1449. http://dx.doi.org/10.3390/nu10101449.
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The medicinal ferns of Polydiaceae and Davalliaceae species are called “Gusuibu” by Chinese physicians and used as antiaging dietary medicines. Our previous report revealed that Drynaria fortunei (Polydiaceae) protected against 6-hydroxydopamine (6-OHDA)-induced oxidative damage via the PI3K/AKT pathway in B35 neuroblastoma cells. The present study compares the antioxidant phytoconstituent contents and radical scavenging capacities of five Davalliaceae species. The further aim was to clarify the protective mechanism of Davallia mariesii (DM) against 6-OHDA-induced oxidative damage and apoptosis in B35 cells. The results show that Araiostegia perdurans (AP) and DM extracts have better radical scavenging capacities against 1,1-diphenyl-2-picryhydrazyl (DPPH) and reactive oxygen species (ROS) than other Davalliaceae species. However, only DM extract inhibited 6-OHDA autoxidation under cell-free systems and increased cell viability, compared to B35 cells solely exposed to 6-OHDA. DM extract decreased apoptosis and restored mitochondrial expression in 6-OHDA-treated B35 cells. Additional data indicated that DM extract decreased intracellular ROS and nitric oxide levels generated by 6-OHDA exposure. DM extract also restored glutathione (GSH) levels and the activities of glutathione peroxidase and reductase, and then decreased the elevated malondialdehyde (MDA) levels. Finally, DM extract regulated the protein expression of the caspase cascade and PI3K/AKT/GSK-3β pathways. These results suggest that the protective mechanism of DM extract against 6-OHDA-induced oxidative damage and apoptosis might be related to its radical scavenging capacity, maintaining the mitochondrial function to inhibit the Bcl-2/caspase cascade pathway and activating intracellular antioxidant defenses (GSH recycling, HO-1 and NQO-1) by modulating the activation of the PI3K/AKT/GSK-3β pathway.
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Jin, Yufei, Junjun Fan, Fuhang Li, Long Bi, and Guoxian Pei. "Local Sympathetic Denervation of Femoral Artery in a Rabbit Model by Using 6-HydroxydopamineIn Situ." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/874947.
Full textAbstract:
Both artery bundle and sympathetic nerve were involved with the metabolism of bone tissues. Whether the enhancing effects of artery bundle result from its accompanying sympathetic nerve or blood supply is still unknown. There is no ideal sympathetic nerve-inhibited method for thein situdenervation of artery bundle. Therefore, we dipped the femoral artery in the 6-hydroxydopamine (6-OHDA) locally and observed its effect. Compared with control group, thein situtreatment of 6-OHDA did not damage the normal structure of vascular bundle indicated by hematoxylin-eosin (HE) staining. However, the functions of sympathetic nerve was completely inhibited for more than 2 weeks, and only a few function of sympathetic nerve resumed 4 weeks later, evidenced by glyoxylic acid staining and the expression of tyrosine hydroxylase (TH) and nerve peptide Y (NPY). Thus, 6-OHDA is promising as an ideal reagent for the local denervation of sympathetic nerve from artery system.
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Cirmi, Santa, Alessandro Maugeri, Giovanni Enrico Lombardo, Caterina Russo, Laura Musumeci, Sebastiano Gangemi, Gioacchino Calapai, Davide Barreca, and Michele Navarra. "A Flavonoid-Rich Extract of Mandarin Juice Counteracts 6-OHDA-Induced Oxidative Stress in SH-SY5Y Cells and Modulates Parkinson-Related Genes." Antioxidants 10, no. 4 (March 30, 2021): 539. http://dx.doi.org/10.3390/antiox10040539.
Full textAbstract:
Parkinson’s disease (PD) is a degenerative disorder of the nervous system due to unceasing impairment of dopaminergic neurons situated in the substantia nigra. At present, anti-PD drugs acting on dopamine receptors are mainly symptomatic and have only very limited neuroprotective effects, whereas drugs slowing down neurodegeneration of dopaminergic neurons and deterioration of clinical symptoms are not yet available. Given that, the development of more valuable pharmacological strategies is highly demanded. Comprehensive research on innovative neuroprotective drugs has proven that anti-inflammatory and antioxidant molecules from food sources may prevent and/or counteract neurodegenerative diseases, such as PD. The present study was aimed at the evaluation the protective effect of mandarin juice extract (MJe) against 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y human neuroblastoma cell death. Treatment of differentiated SH-SY5Y cells with 6-OHDA brought cell death, and specifically, apoptosis, which was significantly inhibited by the preincubation with MJe through caspase 3 blockage and the modulation of p53, Bax, and Bcl-2 genes. In addition, it showed antioxidant properties in abiotic models as well as in vitro, where it reduced both reactive oxygen and nitrogen species induced by 6-OHDA, along with restored mitochondrial membrane potential, and prevented the oxidative DNA damage evoked by 6-OHDA. Furthermore, MJe restored the impaired balance of SNCA, LRRK2, PINK1, parkin, and DJ-1 gene levels, PD-related factors, caused by 6-OHDA oxidative stress. Overall, these results indicate that MJe exerts neuroprotective effects against 6-OHDA-induced cell death in SH-SY5Y cells by mechanisms involving both the specific interaction with intracellular pathways and its antioxidant capability. Our study suggests a novel possible strategy to prevent and/or ameliorate neurodegenerative diseases, such as PD.
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Hitchcock, Peter F., and Jeff T. Vanderyt. "Regeneration of the dopamine-cell mosaic in the retina of the goldfish." Visual Neuroscience 11, no. 2 (March 1994): 209–17. http://dx.doi.org/10.1017/s0952523800001577.
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AbstractA fundamental anatomical feature of retinal neurons is that they form planar mosaics. Each mosaic can be described by its density, pattern, and regularity (non-randomness). As part of ongoing studies to quantitatively describe the anatomy of regenerated retina in the goldfish, we determined the planimetric density and regularity of the mosaic of dopaminergic interplexiform cells in patches of regenerated retina and compared this to the mosaic generated de novo. In addition, we selectively ablated dopaminergic neurons with the neurotoxin 6–hydroxydopamine (6–OHDA) before inducing local regeneration and determined whether or not the absence of the extant dopaminergic neurons modulated the planimetric density or number of regenerated ones. The results showed that dopaminergic neurons are regenerated at higher planimetric densities and in less orderly arrays than normal. Furthermore, there was no statistical difference in the density or number of regenerated cells in normal retinas and retinas treated with 6–OHDA.
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Pichla, Monika, Łukasz Pulaski, Katarzyna Dominika Kania, Ireneusz Stefaniuk, Bogumił Cieniek, Natalia Pieńkowska, Grzegorz Bartosz, and Izabela Sadowska-Bartosz. "Nitroxide Radical-Containing Redox Nanoparticles Protect Neuroblastoma SH-SY5Y Cells against 6-Hydroxydopamine Toxicity." Oxidative Medicine and Cellular Longevity 2020 (April 24, 2020): 1–19. http://dx.doi.org/10.1155/2020/9260748.
Full textAbstract:
Parkinson’s disease (PD) patients can benefit from antioxidant supplementation, and new efficient antioxidants are needed. The aim of this study was to evaluate the protective effect of selected nitroxide-containing redox nanoparticles (NRNPs) in a cellular model of PD. Antioxidant properties of NRNPs were studied in cell-free systems by protection of dihydrorhodamine 123 against oxidation by 3-morpholino-sydnonimine and protection of fluorescein against bleaching by 2,2-azobis(2-amidinopropane) hydrochloride and sodium hypochlorite. Model blood-brain barrier penetration was studied using hCMEC/D3 cells. Human neuroblastoma SH-SY5Y cells, exposed to 6-hydroxydopamine (6-OHDA), were used as an in vitro model of PD. Cells were preexposed to NRNPs or free nitroxides (TEMPO or 4-amino-TEMPO) for 2 h and treated with 6-OHDA for 1 h and 24 h. The reactive oxygen species (ROS) level was estimated with dihydroethidine 123 and Fluorimetric Mitochondrial Superoxide Activity Assay Kit. Glutathione level (GSH) was measured with ortho-phtalaldehyde, ATP by luminometry, changes in mitochondrial membrane potential with JC-1, and mitochondrial mass with 10-Nonyl-Acridine Orange. NRNP1, TEMPO, and 4-amino-TEMPO (25-150 μM) protected SH-SY5Y cells from 6-OHDA-induced viability loss; the protection was much higher for NRNP1 than for free nitroxides. NRNP1 were better antioxidants in vitro and permeated better the model BBB than free nitroxides. Exposure to 6-OHDA decreased the GSH level after 1 h and increased it considerably after 24 h (apparently a compensatory overresponse); NRNPs and free nitroxides prevented this increase. NRNP1 and free nitroxides prevented the decrease in ATP level after 1 h and increased it after 24 h. 6-OHDA increased the intracellular ROS level and mitochondrial superoxide level. Studied antioxidants mostly decreased ROS and superoxide levels. 6-OHDA decreased the mitochondrial potential and mitochondrial mass; both effects were prevented by NRNP1 and nitroxides. These results suggest that the mitochondria are the main site of 6-OHDA-induced cellular damage and demonstrate a protective effect of NRNP1 in a cellular model of PD.
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Gaudet, Elisabeth A., Shirley J. Godwin, and Geoffrey A. Head. "Role of central catecholaminergic pathways in the actions of endogenous ANG II on sympathetic reflexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 4 (October 1, 1998): R1174—R1184. http://dx.doi.org/10.1152/ajpregu.1998.275.4.r1174.
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In the present study, we examined the effect of blockade of the brain stem renin-angiotensin system on renal sympathetic baroreflexes and chemoreflexes in conscious rabbits and examined the role of central catecholaminergic pathways in these responses. Eleven rabbits underwent preliminary surgical instrumentation and pretreatment with central 6-hydroxydopamine (6-OHDA, 500 μg/kg) or ascorbic acid 6 wk before the commencement of the experiments. Baroreflex curves were determined under conditions of normoxia and hypoxia (10% O2+ 3% CO2) before and after central administration of either Ringer solution, the ANG II receptor antagonist losartan (10 μg), or the angiotensin-converting enzyme inhibitor enalaprilat (500 ng) on separate days. Losartan increased the upper plateau and the range of the mean arterial pressure (MAP)-renal sympathetic nerve activity (RSNA) curve (79 and 78%, respectively) in intact rabbits, whereas this effect was not observed in 6-OHDA-pretreated rabbits. Hypoxia elicited an increase in resting RSNA (111% in intact rabbits and 74% in 6-OHDA-injected rabbits) and elevated the upper plateau of the RSNA-MAP curve in both groups (89% in intact rabbits and 114% in 6-OHDA-injected rabbits). During hypoxia, losartan and enalaprilat increased the RSNA upper plateau in intact rabbits but had no effect in 6-OHDA-pretreated rabbits. No effects on the MAP-heart rate baroreflex curves were observed. Thus the effect of losartan to increase RSNA, particularly during hypoxia and baroreceptor unloading, being abolished by central noradrenergic depletion suggests that the endogenous ANG II which normally causes an inhibition of renal sympathetic motoneurons is dependent on the integrity of central catecholaminergic pathways.
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Li, Yueran, Jinhua Wu, Xuming Yu, Shufang Na, Ke Li, Zheqiong Yang, Xianfei Xie, Jing Yang, and Jiang Yue. "The Protective Role of Brain CYP2J in Parkinson’s Disease Models." Oxidative Medicine and Cellular Longevity 2018 (June 26, 2018): 1–12. http://dx.doi.org/10.1155/2018/2917981.
Full textAbstract:
CYP2J proteins are present in the neural cells of human and rodent brain regions. The aim of this study was to investigate the role of brain CYP2J in Parkinson’s disease. Rats received right unilateral injection with lipopolysaccharide (LPS) or 6-hydroxydopamine (6-OHDA) in the substantia nigra following transfection with or without the CYP2J3 expression vector. Compared with LPS-treated rats, CYP2J3 transfection significantly decreased apomorphine-induced rotation by 57.3% at day 12 and 47.0% at day 21 after LPS treatment; moreover, CYP2J3 transfection attenuated the accumulation of α-synuclein. Compared with the 6-OHDA group, the number of rotations by rats transfected with CYP2J3 decreased by 59.6% at day 12 and 43.5% at day 21 after 6-OHDA treatment. The loss of dopaminergic neurons and the inhibition of the antioxidative system induced by LPS or 6-OHDA were attenuated following CYP2J3 transfection. The TLR4-MyD88 signaling pathway was involved in the downregulation of brain CYP2J induced by LPS, and CYP2J transfection upregulated the expression of Nrf2 via the inhibition of miR-340 in U251 cells. The data suggest that increased levels of CYP2J in the brain can delay the pathological progression of PD initiated by inflammation or neurotoxins. The alteration of the metabolism of the endogenous substrates (e.g., AA) could affect the risk of neurodegenerative disease.
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Mendes-Pinheiro, Bárbara, Carina Soares-Cunha, Ana Marote, Eduardo Loureiro-Campos, Jonas Campos, Sandra Barata-Antunes, Daniela Monteiro-Fernandes, et al. "Unilateral Intrastriatal 6-Hydroxydopamine Lesion in Mice: A Closer Look into Non-Motor Phenotype and Glial Response." International Journal of Molecular Sciences 22, no. 21 (October 26, 2021): 11530. http://dx.doi.org/10.3390/ijms222111530.
Full textAbstract:
Parkinson’s disease (PD) is a prevalent movement disorder characterized by the progressive loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). The 6-hydroxydopamine (6-OHDA) lesion is still one of the most widely used techniques for modeling Parkinson’s disease (PD) in rodents. Despite commonly used in rats, it can be challenging to reproduce a similar lesion in mice. Moreover, there is a lack of characterization of the extent of behavioral deficits and of the neuronal loss/neurotransmitter system in unilateral lesion mouse models. In this study, we present an extensive behavioral and histological characterization of a unilateral intrastriatal 6-OHDA mouse model. Our results indicate significant alterations in balance and fine motor coordination, voluntary locomotion, and in the asymmetry’s degree of forelimb use in 6-OHDA lesioned animals, accompanied by a decrease in self-care and motivational behavior, common features of depressive-like symptomatology. These results were accompanied by a decrease in tyrosine hydroxylase (TH)-labelling and dopamine levels within the nigrostriatal pathway. Additionally, we also identify a marked astrocytic reaction, as well as proliferative and reactive microglia in lesioned areas. These results confirm the use of unilateral intrastriatal 6-OHDA mice for the generation of a mild model of nigrostriatal degeneration and further evidences the recapitulation of key aspects of PD, thereby being suitable for future studies beholding new therapeutical interventions for this disease.
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Kim, Ka Young, and Keun-A. Chang. "Therapeutic Potential of Magnetic Nanoparticle-Based Human Adipose-Derived Stem Cells in a Mouse Model of Parkinson’s Disease." International Journal of Molecular Sciences 22, no. 2 (January 11, 2021): 654. http://dx.doi.org/10.3390/ijms22020654.
Full textAbstract:
Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Several treatments for PD have focused on the management of physical symptoms using dopaminergic agents. However, these treatments induce various adverse effects, including hallucinations and cognitive impairment, owing to non-targeted brain delivery, while alleviating motor symptoms. Furthermore, these therapies are not considered ultimate cures owing to limited brain self-repair and regeneration abilities. In the present study, we aimed to investigate the therapeutic potential of human adipose-derived stem cells (hASCs) using magnetic nanoparticles in a 6-hydroxydopamine (6-OHDA)-induced PD mouse model. We used the Maestro imaging system and magnetic resonance imaging (MRI) for in vivo tracking after transplantation of magnetic nanoparticle-loaded hASCs to the PD mouse model. The Maestro imaging system revealed strong hASCs signals in the brains of PD model mice. In particular, MRI revealed hASCs distribution in the substantia nigra of hASCs-injected PD mice. Behavioral evaluations, including apomorphine-induced rotation and rotarod performance, were significantly recovered in hASCs-injected 6-OHDA induced PD mice when compared with saline-treated counterparts. Herein, we investigated whether hASCs transplantation using magnetic nanoparticles recovered motor functions through targeted brain distribution in a 6-OHDA induced PD mice. These results indicate that magnetic nanoparticle-based hASCs transplantation could be a potential therapeutic strategy in PD.
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Kim, Ka Young, and Keun-A. Chang. "Therapeutic Potential of Magnetic Nanoparticle-Based Human Adipose-Derived Stem Cells in a Mouse Model of Parkinson’s Disease." International Journal of Molecular Sciences 22, no. 2 (January 11, 2021): 654. http://dx.doi.org/10.3390/ijms22020654.
Full textAbstract:
Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Several treatments for PD have focused on the management of physical symptoms using dopaminergic agents. However, these treatments induce various adverse effects, including hallucinations and cognitive impairment, owing to non-targeted brain delivery, while alleviating motor symptoms. Furthermore, these therapies are not considered ultimate cures owing to limited brain self-repair and regeneration abilities. In the present study, we aimed to investigate the therapeutic potential of human adipose-derived stem cells (hASCs) using magnetic nanoparticles in a 6-hydroxydopamine (6-OHDA)-induced PD mouse model. We used the Maestro imaging system and magnetic resonance imaging (MRI) for in vivo tracking after transplantation of magnetic nanoparticle-loaded hASCs to the PD mouse model. The Maestro imaging system revealed strong hASCs signals in the brains of PD model mice. In particular, MRI revealed hASCs distribution in the substantia nigra of hASCs-injected PD mice. Behavioral evaluations, including apomorphine-induced rotation and rotarod performance, were significantly recovered in hASCs-injected 6-OHDA induced PD mice when compared with saline-treated counterparts. Herein, we investigated whether hASCs transplantation using magnetic nanoparticles recovered motor functions through targeted brain distribution in a 6-OHDA induced PD mice. These results indicate that magnetic nanoparticle-based hASCs transplantation could be a potential therapeutic strategy in PD.
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Lin, Zheng-Shi, and Stephen Yazulla. "Depletion of retinal dopamine increases brightness perception in goldfish." Visual Neuroscience 11, no. 4 (July 1994): 683–93. http://dx.doi.org/10.1017/s0952523800002996.
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AbstractThe effect of unilateral depletion of retinal dopamine on goldfish visual behavior was studied using a behavioral reflex, the dorsal light reaction (DLR). Retinal dopamine was depleted by intraocular injections of 6–hydroxydopamine (6–OHDA) on two successive days. By 2 weeks postinjection, dopamine interplexiform cells (DA-IPC) were not detected using tyrosine-hydroxylase immunoreactivity (TH-IR). By 6 weeks postinjection, generation of DA-IPC was observed at the marginal zone and by 9 months postinjection, 2–3 rows of DA-IPC were present at the marginal zone. Neurites extended several hundred micrometers toward the central retina. By 2 weeks postinjection, all 6–OHDA lesioned fish tilted 7–15 deg toward the injected eye under uniform overhead illumination. The tilting did not occur under scotopic illumination and reappeared within 1 min of light adaptation. Quantitation of the DLR showed that 6–OHDA lesioned fish behaved as if light were 2.4 log units more intense to the injected eye. Partial recovery was observed by 9 months postinjection, paralleling the reappearance of DA-IPC at the marginal zone. Tilting also was induced by unilateral intraocular injection with Dl and D2 dopamine receptor antagonists, SCH 23390 and S(—)-sulpiride, respectively. Fish did not tilt if they were light adapted at the time of injection. Tilting was observed if the animals were dark-adapted for 3 h and left in the dark for 1 h postinjection. Fish tilted toward the drug-injected eye within 2 min of light adaptation and gradually returned to vertical within 2 h. The tilting response to S(—)-sulpiride was stronger (˜20 deg vs. ˜5 deg) and occurred at lower concentration (1 μM vs. 10 μM) compared to SCH 23390. We conclude that dopamine depletion mimics the dorsal light reaction by increasing the luminosity output of the eye and that dopamine is directly involved in photopic luminosity function.
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Ajah, Paul O. "The Limnology of Ohana Lake, a Potential Manmade Aquaculture System in Nigeria." Open Journal of Applied Sciences 03, no. 02 (2013): 232–46. http://dx.doi.org/10.4236/ojapps.2013.32031.
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Bhebhe, Sindiso, and Mpho Ngoepe. "A forgotten past is the past that is yet to be." ESARBICA Journal: Journal of the Eastern and Southern Africa Regional Branch of the International Council on Archives 40 (November 6, 2021): 60–78. http://dx.doi.org/10.4314/esarjo.v40i1.5.
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South Africa is one of the few countries in Africa that has a running oral history association. In some countries, especially in southern Africa, these oral history associations have arisen and then died a natural death. For example, Oral Traditions Association of Zimbabwe (OTAZI) did not last long. Therefore, it is a positive development for South Africa to have a functioning oral history association. The Oral History Association of South Africa (OHASA) is the brainchild of the government and is mainly funded by the government. It is involved in the coordination and documentation of stories that were silent during the apartheid era. Therefore, with this highly perceived task it is necessary to critically evaluate its successes and failures in meeting the objectives of the National Oral History Programme (NOHP). This paper, through document analysis and purposively selected interviews, critically evaluates the achievements and shortcomings of the OHASA from its inception to present with the aim of proposing a ‘working’ model which involves the setting up of a monitoring and evaluating system. The paper concludes that although OHASA unveiled the muted marginalised voices, it soral history programme demonstrate elitism in critical emancipatory as mostly the stories of the elites are covered. Furthermore, such recorded stories are not accessible as the recordings are stashed in the boxes in archives repositories.
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Bhebhe, Sindiso, and Mpho Ngoepe. "A forgotten past is the past that is yet to be." ESARBICA Journal: Journal of the Eastern and Southern Africa Regional Branch of the International Council on Archives 40 (November 6, 2021): 60–78. http://dx.doi.org/10.4314/esarjo.v40i.5.
Full textAbstract:
South Africa is one of the few countries in Africa that has a running oral history association. In some countries, especially in southern Africa, these oral history associations have arisen and then died a natural death. For example, Oral Traditions Association of Zimbabwe (OTAZI) did not last long. Therefore, it is a positive development for South Africa to have a functioning oral history association. The Oral History Association of South Africa (OHASA) is the brainchild of the government and is mainly funded by the government. It is involved in the coordination and documentation of stories that were silent during the apartheid era. Therefore, with this highly perceived task it is necessary to critically evaluate its successes and failures in meeting the objectives of the National Oral History Programme (NOHP). This paper, through document analysis and purposively selected interviews, critically evaluates the achievements and shortcomings of the OHASA from its inception to present with the aim of proposing a ‘working’ model which involves the setting up of a monitoring and evaluating system. The paper concludes that although OHASA unveiled the muted marginalised voices, it soral history programme demonstrate elitism in critical emancipatory as mostly the stories of the elites are covered. Furthermore, such recorded stories are not accessible as the recordings are stashed in the boxes in archives repositories.
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Szafarczyk, A., V. Guillaume, B. Conte-Devolx, G. Alonso, F. Malaval, N. Pares-Herbute, C. Oliver, and I. Assenmacher. "Central catecholaminergic system stimulates secretion of CRH at different sites." American Journal of Physiology-Endocrinology and Metabolism 255, no. 4 (October 1, 1988): E463—E468. http://dx.doi.org/10.1152/ajpendo.1988.255.4.e463.
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To explore a possible differential role of distinct catecholamine (CA) innervation sites in corticotropin-releasing hormone (CRH) secretion, especially under stress conditions, we compared the effects in adult female rats of selective CA denervation of either the whole hypothalamus, by a discrete pharmacological lesion of the ventral noradrenergic ascending bundle [VNAB; 3 micrograms of 6-hydroxydopamine (6-OHDA) in 0.2 microliter of vehicle, bilaterally] or of the paraventricular nuclei (PVN) alone (1 microgram of 6-OHDA in 0.2 microliter of vehicle, bilaterally). Although both procedures induced a similar dramatic fall in norepinephrine and epinephrine concentrations (-55 to -65%) measured by high-performance liquid chromatography in PVN punches, the VNAB lesion, unlike PVN denervation, depleted the median eminence (ME) of both amines (-80%). Concomitantly, the VNAB lesion led to a 97% reduction of the immunoreactive (ir) CRH-41 concentration in the hypophysial portal vessels, associated with a 64% fall in plasma adrenocorticotropic hormone (ACTH), and, in another group, with an 80% inhibition of ether stress-induced ACTH surge. The deletion of CA innervation of the PVN alone reduced irCRH-41 levels in the portal vessels by only 57% and plasma ACTH by 35%. This lesion did not significantly impair stress-induced ACTH release. These results suggest that the CA innervation of the hypothalamus exerts a stimulatory control on CRH-41-secreting neurons not only directly at the perikaryal level but also at other hypothalamic sites of VNAB innervation including peripheral contacts between the terminals of CA and CRH nerves in the external ME.
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Todurga, Zeynep Gizem, Ozgur Gunduz, Cetin Hakan Karadag, and Ahmet Ulugol. "Descending serotonergic and noradrenergic systems do not regulate the antipruritic effects of cannabinoids." Acta Neuropsychiatrica 28, no. 6 (April 8, 2016): 321–26. http://dx.doi.org/10.1017/neu.2016.16.
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BackgroundFor centuries, cannabinoids have been known to be effective in pain states. Itch and pain are two sensations sharing a lot in common.ObjectiveThe goal of this research was to observe whether the cannabinoid agonist WIN 55,212-2 reduces serotonin-induced scratching behaviour and whether neurotoxic destruction of descending serotonergic and noradrenergic pathways mediate the antipruritic effect of WIN 55,212-2.Material and methodsScratching behaviour was induced by intradermal injection of serotonin (50 µg/50 µl/mouse) to Balb/c mice. The neurotoxins 5,7-dihydroxytryptamine (5,7-DHT, 50 μg/mouse) and 6-hydroxydopamine (6-OHDA, 20 μg/mouse) are applied intrathecally to deplete serotonin and noradrenaline in the spinal cord. WIN 55,212-2 (1, 3, 10 mg/kg, i.p.) dose-dependently attenuated serotonin-induced scratches. Neurotoxic destruction of neither the serotonergic nor the noradrenergic systems by 5,7-DHT and 6-OHDA, respectively, had any effect on the antipruritic action of WIN 55,212-2.ConclusionOur findings indicate that cannabinoids dose-dependently reduce serotonin-induced scratching behaviour and neurotoxic destruction of descending inhibitory pathways does not mediate this antipruritic effect.
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Kim, Yong S., Wan S. Joo, Byung K. Jin, Yong H. Cho, Hyung H. Baik, and Chan W. Park. "Melatonin protects 6-OHDA-induced neuronal death of nigrostriatal dopaminergic system." NeuroReport 9, no. 10 (July 1998): 2387–90. http://dx.doi.org/10.1097/00001756-199807130-00043.
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Wagner, H. J., U. D. Behrens, M. Zaunreiter, and R. H. Douglas. "The circadian component of spinule dynamics in teleost retinal horizontal cells is dependent on the dopaminergic system." Visual Neuroscience 9, no. 3-4 (October 1992): 345–51. http://dx.doi.org/10.1017/s0952523800010750.
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AbstractDuring the light phase of a light/dark cycle, dendrites of teleost cone horizontal cells display numerous finger-like projections, called spinules, which are formed at dawn and degraded at dusk, and are thought to be involved in chromatic feedback processes. We have studied the oscillations of these spinules during a normal light/dark cycle and during 48 h of constant darkness in two groups of strongly rhythmic, diurnal fish, Aequidens pulcher. In one group the retinal dopaminergic system had been destroyed by the application of 6-OHDA, while in the other (control) group, the dopaminergic system was intact. In control fish, oscillations of spinule numbers were observed under both normal and constant dark conditions, indicating the presence of a robust circadian rhythm. However, spinule dynamics were severely affected by the absence of retinal dopamine. During the normal light phase, the number of spinules in 6-OHDA injected retinae was strongly reduced, and throughout continual darkness, spinule formation was almost completely suppressed. These results indicate that dopamine is essential for both light-evoked and circadian spinule formation; furthermore, we conclude that there is no circadian oscillator within horizontal cells controlling the formation of spinules.
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de Araújo, Dayane Pessoa, Caren Nádia Soares De Sousa, Paulo Victor Pontes Araújo, Carlos Eduardo de Souza Menezes, Francisca Taciana Sousa Rodrigues, Sarah Souza Escudeiro, Nicole Brito Cortez Lima, et al. "Behavioral and Neurochemical Effects of Alpha-Lipoic Acid in the Model of Parkinson’s Disease Induced by Unilateral Stereotaxic Injection of 6-Ohda in Rat." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–13. http://dx.doi.org/10.1155/2013/571378.
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This study aimed to investigate behavioral and neurochemical effects ofα-lipoic acid (100 mg/kg or 200 mg/kg) alone or associated with L-DOPA using an animal model of Parkinson’s disease induced by stereotaxic injection of 6-hydroxydopamine (6-OHDA) in rat striatum. Motor behavior was assessed by monitoring body rotations induced by apomorphine, open field test and cylinder test. Oxidative stress was accessed by determination of lipid peroxidation using the TBARS method, concentration of nitrite and evaluation of catalase activity.α-Lipoic acid decreased body rotations induced by apomorphine, as well as caused an improvement in motor performance by increasing locomotor activity in the open field test and use of contralateral paw (in the opposite side of the lesion produced by 6-OHDA) at cylinder test.α-lipoic acid showed antioxidant effects, decreasing lipid peroxidation and nitrite levels and interacting with antioxidant system by decreasing of endogenous catalase activity. Therefore,α-lipoic acid prevented the damage induced by 6-OHDA or by chronic use of L-DOPA in dopaminergic neurons, suggesting thatα-lipoic could be a new therapeutic target for Parkinson's disease prevention and treatment.
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Masini, Débora, Carina Plewnia, Maëlle Bertho, Nicolas Scalbert, Vittorio Caggiano, and Gilberto Fisone. "A Guide to the Generation of a 6-Hydroxydopamine Mouse Model of Parkinson’s Disease for the Study of Non-Motor Symptoms." Biomedicines 9, no. 6 (May 25, 2021): 598. http://dx.doi.org/10.3390/biomedicines9060598.
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In Parkinson’s disease (PD), a large number of symptoms affecting the peripheral and central nervous system precede, develop in parallel to, the cardinal motor symptoms of the disease. The study of these conditions, which are often refractory to and may even be exacerbated by standard dopamine replacement therapies, relies on the availability of appropriate animal models. Previous work in rodents showed that injection of the neurotoxin 6-hydroxydopamine (6-OHDA) in discrete brain regions reproduces several non-motor comorbidities commonly associated with PD, including cognitive deficits, depression, anxiety, as well as disruption of olfactory discrimination and circadian rhythm. However, the use of 6-OHDA is frequently associated with significant post-surgical mortality. Here, we describe the generation of a mouse model of PD based on bilateral injection of 6-OHDA in the dorsal striatum. We show that the survival rates of males and females subjected to this lesion differ significantly, with a much higher mortality among males, and provide a protocol of enhanced pre- and post-operative care, which nearly eliminates animal loss. We also briefly discuss the utility of this model for the study of non-motor comorbidities of PD.
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MORA-FERRER, CARLOS, and VOLKER GANGLUFF. "D2-dopamine receptor blockade modulates temporal resolution in goldfish." Visual Neuroscience 19, no. 6 (November 2002): 807–15. http://dx.doi.org/10.1017/s0952523802196106.
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A possible effect of dopamine on the temporal resolution of goldfish was investigated in a behavioral, two-alternative, forced-choice procedure. Flicker fusion frequency (FFF) was measured before and after bilateral intravitreal injections of D1- or D2-dopamine receptor (D1-/D2-R) antagonists, or after depletion of retinal dopamine by bilateral intravitreal injections of the dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA). Prior to drug injections, fish achieved FFFs of 33–39 Hz. A D1-R antagonist, SCH 23390, reduced FFF by about 12% (P > 0.1), whereas a D2 antagonist, sulpiride, reduced the relative FFF by 25% (P < 0.03). Depletion of retinal dopamine with 6-OHDA induced a gradual reduction in the FFF to a maximal reduction of 50% (P < 0.001) at 2 weeks postinjection. There was recovery to control levels after 3–4 weeks postinjection. The recovery of FFF, at least in one animal, was due to the return of retinal dopamine because FFF could be reduced by intravitreal injections of sulpiride during the recovery phase. These experiments demonstrate that retinal dopamine, particularly acting on D2-R, is important for photopic temporal resolution.
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Bonaz, B., L. Martin, E. Beurriand, M. Manier, J. Hostein, and C. Feuerstein. "Locus ceruleus modulates migrating myoelectric complex in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 6 (June 1, 1992): G1121—G1126. http://dx.doi.org/10.1152/ajpgi.1992.262.6.g1121.
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The role of the locus ceruleus (LC) in the control of migrating myoelectric complex (MMC) was investigated in rats with lesions induced by injections of 6-hydroxydopamine (6-OHDA). Control animals received the vehicle alone. MMC was recorded in conscious rats chronically fitted with electrodes. After 6-OHDA was injected into the LC, lesions of the LC were total, partial (mostly rostral), or ineffective. The MMC period was significantly longer in animals with a total or partial lesion but was unchanged in animals with an ineffective lesion. No lesion of other brain noradrenergic nuclei was observed. The longer MMC period is comparable to that obtained after intracerebroventricular injection of 6-OHDA, which is responsible for a more diffuse destruction of brain noradrenergic systems, including LC itself. Bilateral lesions of the central tegmental tract, which carries ascending noradrenergic axons from the medullary and pontine cell groups outside the LC, do not alter the MMC cycle. Consequently, the LC is most likely the major brain noradrenergic candidate for modulating the MMC pattern in rats.