The effect of dopamine depletion on light-evoked and circadian retinomotor movements in the teleost retina

1992 ◽  
Vol 9 (3-4) ◽  
pp. 335-343 ◽  
Author(s):  
R. H. Douglas ◽  
H.-J. Wagner ◽  
M. Zaunreiter ◽  
U. D. Behrens ◽  
M. B. A. Djamgoz
Keyword(s):  
Structural Changes ◽  
Light Adaptation ◽  
Control Mechanism ◽  
Morphological Changes ◽  
Causal Mechanism ◽  
Dopamine Depletion ◽  
Retinal Cells ◽  
Lower Vertebrates ◽  
Teleost Retina ◽  
6 Hydroxydopamine

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.

Depletion of retinal dopamine increases brightness perception in goldfish

1994 ◽  
Vol 11 (4) ◽  
pp. 683-693 ◽  
Author(s):  
Zheng-Shi Lin ◽  
Stephen Yazulla
Keyword(s):  
Light Adaptation ◽  
Marginal Zone ◽  
Sch 23390 ◽  
Partial Recovery ◽  
Dopamine Depletion ◽  
D2 Dopamine Receptor ◽  
Light Reaction ◽  
Brightness Perception ◽  
Dopamine Receptor Antagonists ◽  
6 Hydroxydopamine

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.

Structural changes in uterine tissues after uterine artery embolization in patients with leiomyoma complicated by uterine bleeding

GYNECOLOGY ◽  
2018 ◽  
Vol 20 (1) ◽  
pp. 78-82
Author(s):  
G P Titova ◽  
M M Damirov ◽  
L S Kokov ◽  
O N Oleynikova ◽  
G E Belozerov
Keyword(s):  
Uterine Artery Embolization ◽  
Uterine Artery ◽  
Structural Changes ◽  
Morphological Changes ◽  
Uterine Bleeding ◽  
Small Scale ◽  
Artery Embolization ◽  
Vessel Occlusion ◽  
Uterine Arteries ◽  
Uterine Tumors

Uterine leiomyoma (UL) is often complicated by the development of uterine bleeding. In urgent gynecology for the implementation of endovascular hemostasis, uterine artery embolization (UAE) is used. Performing UAE allows to stop and/or significantly reduce the intensity of bleeding and prepare a patient for surgical intervention. At the same time, the morphological changes that occur in uterine tissues in operated UL patients after performing the UAE are not studied. The aim was to study the peculiarities of pathomorphological changes in uterine tumors and tissues in operated UL patients complicated by uterine bleeding after performing UAE. Material and methods. The results of morphological changes appearing in tumors and tissues of the uterus in 39 operated UL patients, who were used for stopping uterine bleeding, were analyzed. Results. After applying different types of embolizing agents in macroscopic study of the uterus, signs of ischemia of its tissues were revealed, and the most pronounced disorders were detected in the UL nodes. Morphologically it was established that UAE microemboli resulted in vessel occlusion with increasing thrombosis in their distal sections. UAE was not accompanied by occlusal occlusion of the arteries and resulted in small-scale necrosis of the tumor with complete regeneration of the endometrium. Conclusions. The results of the morphological study showed that after the UAE was performed, the myomatous nodes underwent dystrophic, necrobiotic and necrotic changes. Depending on the nature of occlusion of the uterine arteries, various variants of necrosis (scale and completeness of the process) developed in the tumor tissue, which was aseptic in nature.

Thermal characterization of ABS-Graphene blended three dimensional printed functional prototypes for electro chemical energy storage

2018 ◽  
Vol 1 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Kamaljit Singh Boparai ◽  
Rupinder Singh
Keyword(s):  
Energy Storage ◽  
Structural Changes ◽  
Fused Deposition Modeling ◽  
Morphological Changes ◽  
Three Dimensional ◽  
Thermal Characterization ◽  
Chemical Energy ◽  
Flow Index ◽  
Fused Deposition

This study highlights the thermal characterization of ABS-Graphene blended three dimensional (3D) printed functional prototypes by fused deposition modeling (FDM) process. These functional prototypes have some applications as electro-chemical energy storage devices (EESD). Initially, the suitability of ABS-Graphene composite material for FDM applications has been examined by melt flow index (MFI) test. After establishing MFI, the feedstock filament for FDM has been prepared by an extrusion process. The fabricated filament has been used for printing 3D functional prototypes for printing of in-house EESD. The differential scanning calorimeter (DSC) analysis was conducted to understand the effect on glass transition temperature with the inclusion of Graphene (Gr) particles. It has been observed that the reinforced Gr particles act as a thermal reservoir (sink) and enhances its thermal/electrical conductivity. Also, FT-IR spectra realized the structural changes with the inclusion of Gr in ABS matrix. The results are supported by scanning electron microscopy (SEM) based micrographs for understanding the morphological changes.

scholarly journals Neuroprotective Potential of a Small Molecule RET Agonist in Cultured Dopamine Neurons and Hemiparkinsonian Rats

2021 ◽  
pp. 1-24
Author(s):  
Juho-Matti Renko ◽  
Arun Kumar Mahato ◽  
Tanel Visnapuu ◽  
Konsta Valkonen ◽  
Mati Karelson ◽  
...  
Keyword(s):  
Mapk Signaling ◽  
Dopamine Neurons ◽  
Dopamine Depletion ◽  
Wild Type ◽  
Disease Modifying Therapy ◽  
Immortalized Cells ◽  
Midbrain Dopamine ◽  
6 Hydroxydopamine

Background: Parkinson’s disease (PD) is a progressive neurological disorder where loss of dopamine neurons in the substantia nigra and dopamine depletion in the striatum cause characteristic motor symptoms. Currently, no treatment is able to halt the progression of PD. Glial cell line-derived neurotrophic factor (GDNF) rescues degenerating dopamine neurons both in vitro and in animal models of PD. When tested in PD patients, however, the outcomes from intracranial GDNF infusion paradigms have been inconclusive, mainly due to poor pharmacokinetic properties. Objective: We have developed drug-like small molecules, named BT compounds that activate signaling through GDNF’s receptor, the transmembrane receptor tyrosine kinase RET, both in vitro and in vivo and are able to penetrate through the blood-brain barrier. Here we evaluated the properties of BT44, a second generation RET agonist, in immortalized cells, dopamine neurons and rat 6-hydroxydopamine model of PD. Methods: We used biochemical, immunohistochemical and behavioral methods to evaluate the effects of BT44 on dopamine system in vitro and in vivo. Results: BT44 selectively activated RET and intracellular pro-survival AKT and MAPK signaling pathways in immortalized cells. In primary midbrain dopamine neurons cultured in serum-deprived conditions, BT44 promoted the survival of the neurons derived from wild-type, but not from RET knockout mice. BT44 also protected cultured wild-type dopamine neurons from MPP +-induced toxicity. In a rat 6-hydroxydopamine model of PD, BT44 reduced motor imbalance and could have protected dopaminergic fibers in the striatum. Conclusion: BT44 holds potential for further development into a novel, possibly disease-modifying therapy for PD.

scholarly journals In vivo electrophysiology of nigral and thalamic neurons in alpha-synuclein-overexpressing mice highlights differences from toxin-based models of parkinsonism

2013 ◽  
Vol 110 (12) ◽  
pp. 2792-2805 ◽  
Author(s):  
C. J. Lobb ◽  
A. K. Zaheer ◽  
Y. Smith ◽  
D. Jaeger
Keyword(s):  
Primary Motor Cortex ◽  
Alpha Synuclein ◽  
Motor Dysfunction ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Wild Type ◽  
Beta Oscillations ◽  
Nigrostriatal Dopamine ◽  
6 Hydroxydopamine

Numerous studies have suggested that alpha-synuclein plays a prominent role in both familial and idiopathic Parkinson's disease (PD). Mice in which human alpha-synuclein is overexpressed (ASO) display progressive motor deficits and many nonmotor features of PD. However, it is unclear what in vivo pathophysiological mechanisms drive these motor deficits. It is also unknown whether previously proposed pathophysiological features (i.e., increased beta oscillations, bursting, and synchronization) described in toxin-based, nigrostriatal dopamine-depletion models are also present in ASO mice. To address these issues, we first confirmed that 5- to 6-mo-old ASO mice have robust motor dysfunction, despite the absence of significant nigrostriatal dopamine degeneration. In the same animals, we then recorded simultaneous single units and local field potentials (LFPs) in the substantia nigra pars reticulata (SNpr), the main basal ganglia output nucleus, and one of its main thalamic targets, the ventromedial nucleus, as well as LFPs in the primary motor cortex in anesthetized ASO mice and their age-matched, wild-type littermates. Neural activity was examined during slow wave activity and desynchronized cortical states, as previously described in 6-hydroxydopamine-lesioned rats. In contrast to toxin-based models, we found a small decrease, rather than an increase, in beta oscillations in the desynchronized state. Similarly, synchronized burst firing of nigral neurons observed in toxin-based models was not observed in ASO mice. Instead, we found more subtle changes in pauses of SNpr firing compared with wild-type control mice. Our results suggest that the pathophysiology underlying motor dysfunction in ASO mice is distinctly different from striatal dopamine-depletion models of parkinsonism.

Resveratrol attenuates 6-hydroxydopamine-induced oxidative damage and dopamine depletion in rat model of Parkinson's disease

2010 ◽  
Vol 1328 ◽  
pp. 139-151 ◽  
Author(s):  
Mohd.Moshahid Khan ◽  
Ajmal Ahmad ◽  
Tauheed Ishrat ◽  
M. Badruzzaman Khan ◽  
Md. Nasrul Hoda ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oxidative Damage ◽  
Rat Model ◽  
Dopamine Depletion ◽  
6 Hydroxydopamine

Staphylococcal infection and pathomurfological characteristic of the pituitary-adrenal-thyroid system

2020 ◽  
Vol 03 (04) ◽  
pp. 69-73
Author(s):  
Samira Mammadhasan Yagubova ◽  
◽  
Elchin Chingiz Akbarov ◽  
Tarana Nadir Mirzayeva ◽  
◽  
...  
Keyword(s):  
Structural Changes ◽  
Adrenal Glands ◽  
Early Stage ◽  
Morphological Changes ◽  
Endocrine System ◽  
Staphylococcal Infection ◽  
The Body ◽  
Glandular Cells ◽  
Exogenous Factors ◽  
Specific Symptoms

During the staphylococcal infection, changes in the interaction of glandular cells, dystrophic and disorganizing pathologies in tissues, especially acute structural and hemodynamic changes in the stroma of the glands in the pituitary-adrenal-thyroid system, develop from the first day of the experiment. At the end of the experiment, on the background of a decrease in exudative processes, fibroplastic reactions are significantly activated, resulting in signs of incomplete regeneration – mainly sclerotic processes and cystic-atrophic changes in the parenchyma. Structural changes in tissues in the early stages of staphylococcal infection and the dynamics of development are characterized by specific symptoms in each of the glands. Since the pituitary gland is exposed to endogenous and exogenous factors earlier and more often than the adrenal glands, and the adrenal glands are earlier than the thyroid gland, dystrophic and destructive changes in the pituitary and adrenal glands are more pronounced at the early stage of the experiment. These morphological changes can change the hormonal status of the body and lead to dysfunction of the endocrine system as a whole – a decrease in the functional activity of the glands to some extent, and even inhibition of adenohypophyseal cells. Key words: staphylococcal infection, peritonitis, pituitary, adrenal and thyroid glands

High levels of androgens cause chondrocyte accumulation and loss of smooth muscle in the mouse penile body†

2020 ◽  
Vol 102 (6) ◽  
pp. 1225-1233
Author(s):  
Deepak S Hiremath ◽  
Elizabeth C Geerling ◽  
Lan Hai ◽  
Prema Narayan
Keyword(s):  
Smooth Muscle ◽  
Structural Changes ◽  
Morphological Changes ◽  
Serum Testosterone ◽  
Fold Increase ◽  
Luteinizing Hormone Receptor ◽  
Corpora Cavernosa ◽  
Structural Abnormalities ◽  
Very High ◽  
Androgen Levels

Abstract Androgens are essential for penile development and for maintaining penile structural and functional integrity. Loss of androgen levels or function results in a decrease in smooth muscle content, accumulation of adipocytes in the corpora cavernosa, and inhibition of erectile function. Our previous studies with a mouse model (KiLHRD582G) of constitutive luteinizing hormone receptor activity also showed structural abnormalities in the penis caused by a decrease in smooth muscle content, accumulation of chondrocytes, and sexual dysfunction. As KiLHRD582G mice exhibit very high levels of testosterone at all postnatal ages, the goal of this study was to determine if the elevated androgen levels were responsible for the morphological changes in the penis. Implantation of testosterone capsules in wild-type mice at neonatal (2 weeks) and postpubertal (5 weeks) ages resulted in the accumulation of chondrocytes in the corpora cavernosa of the adult animals. Mice implanted with testosterone capsules at 2 weeks of age exhibited a 4-fold increase in serum testosterone with a 1.5-fold loss of smooth muscle at 24 weeks of age. Collagen content was unchanged. Only 57% of testosterone implanted mice were fertile at 24 weeks of age. Mice implanted with testosterone capsules at 5 weeks of age showed no decrease in smooth muscle content at 24 weeks, although serum testosterone levels were elevated 5-fold. Implantation with dihydrotestosterone also resulted in chondrocyte accumulation and a 2-fold loss in smooth muscle content. Together, these studies demonstrate that supraphysiological levels of androgens cause structural changes in the penile corpora cavernosa and impair fertility.

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