Degeneration and Regrowth of Adrenergic Nerve Fibers in the Rat Peripheral Tissues after 6-Hydroxydopamine

1971 ◽  
Vol 49 (4) ◽  
pp. 345-355 ◽  
Author(s):  
J. de Champlain
Keyword(s):  
Ganglion Cells ◽  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
High Dose ◽  
Rat Tissues ◽  
Peripheral Tissues ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Noradrenaline Levels

Histofluorescent and biochemical changes in the adrenergic nervous system were followed up in rat tissues after one single intravenous injection of a high dose of 100 mg/kg of 6-hydroxydopamine (6-OH-DA). This treatment results in the rapid disappearance of terminal and preterminal fibers in the iris, atria, and small arteries of rats, whereas endogenous noradrenaline pools of the heart are 95% depleted. The capacity of the adrenergic nerve to take up and accumulate tritiated noradrenaline is reduced proportionally to the reduction in endogenous noradrenaline levels. These changes are compatible with the concept of a complete sympathectomy induced by the specific toxic action of 6-OH-DA on the adrenergic fibers. This sympathectomy is not permanent, however, and numerous bundles of preterminal fibers start to grow in the iris and atria within 4 to 5 days following injection. Progressively, in the following weeks, these fibers distribute over the whole organ and give birth to terminal fibers which form a new adrenergic plexus in these tissues. A completely normal innervation is restored 2 to 3 months after administration of 6-OH-DA. The endogenous noradrenaline levels rise progressively in parallel to the development of the new plexus of fibers. Since a complete regeneration of the adrenergic innervation can be demonstrated in the weeks following injection of 6-OH-DA, it appears that this compound can selectively destroy the adrenergic terminal and preterminal fibers without causing a degeneration of the adrenergic ganglion cells.

Supersensitivity of the Isolated Rat Heart after Chemical Sympathectomy with 6-Hydroxydopamine

1971 ◽  
Vol 49 (1) ◽  
pp. 36-44 ◽  
Author(s):  
R. A. Nadeau ◽  
J. De Champlain ◽  
G. M. Tremblay
Keyword(s):  
Nerve Fibers ◽  
Isolated Rat Heart ◽  
Adrenergic Nerve ◽  
Noradrenaline Content ◽  
Chronotropic Response ◽  
Endogenous Noradrenaline ◽  
6 Hydroxydopamine ◽  
Perfused Hearts ◽  
Supersensitivity To Noradrenaline ◽  
Isolated Rat

Presynaptic supersensitivity was demonstrated in isolated rat atria and perfused hearts 2 h after an intravenous injection of 6-hydroxydopamine (6-OH-DA), 100 mg/kg. This coincided with a maximum depletion of cardiac endogenous noradrenaline, a disappearance of the fluorescence of terminal adrenergic nerve fibers in the atrial myocardium, and an abolished chronotropic response to tyramine. The chronotropic response to dopamine was also significantly diminished. Maximal supersensitivity to the chronotropic effect of noradrenaline was observed 72 h after the injection of 6-OH-DA. Two weeks after the administration of 6-OH-DA, supersensitivity to noradrenaline was less marked, and the response to tyramine was restored. These changes corresponded to an increasing noradrenaline content in the heart and to the reappearance of histofluorescent fibers in the atria.

scholarly journals Galanin is localized in sympathetic neurons of the dog liver

1997 ◽  
Vol 273 (6) ◽  
pp. E1194-E1202 ◽  
Author(s):  
Thomas O. Mundinger ◽  
C. Bruce Verchere ◽  
Denis G. Baskin ◽  
Michael R. Boyle ◽  
Stephan Kowalyk ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Sympathetic Neurons ◽  
Sympathetic Nerves ◽  
Liver Parenchyma ◽  
Nerve Fibers ◽  
Adrenergic Nerve ◽  
Adrenergic Nerve Terminals ◽  
6 Hydroxydopamine ◽  
Hepatic Nerves ◽  
Dog Liver

Stimulation of canine hepatic nerves releases the neuropeptide galanin from the liver; therefore, galanin may be a sympathetic neurotransmitter in the dog liver. To test this hypothesis, we used immunocytochemistry to determine if galanin is localized in hepatic sympathetic nerves and we used hepatic sympathetic denervation to verify such localization. Liver sections from dogs were immunostained for both galanin and the sympathetic enzyme marker tyrosine hydroxylase (TH). Galanin-like immunoreactivity (GALIR) was colocalized with TH in many axons of nerve trunks as well as individual nerve fibers located both in the stroma of hepatic blood vessels and in the liver parenchyma. Neither galanin- nor TH-positive cell bodies were observed. Intraportal 6-hydroxydopamine (6-OHDA) infusion, a treatment that selectively destroys hepatic adrenergic nerve terminals, abolished the GALIR staining in parenchymal neurons but only moderately diminished the GALIR staining in the nerve fibers around blood vessels. To confirm that 6-OHDA pretreatment proportionally depleted galanin and norepinephrine in the liver, we measured both the liver content and the hepatic nerve-stimulated spillover of galanin and norepinephrine from the liver. Pretreatment with 6-OHDA reduced the content and spillover of both galanin and norepinephrine by >90%. Together, these results indicate that galanin in dog liver is primarily colocalized with norepinephrine in sympathetic nerves and may therefore function as a hepatic sympathetic neurotransmitter.

Regeneration of dopaminergic neurons in goldfish retina

Development ◽  
1992 ◽  
Vol 114 (4) ◽  
pp. 913-919 ◽  
Author(s):  
J.E. Braisted ◽  
P.A. Raymond
Keyword(s):  
Dopaminergic Neurons ◽  
Developmental Process ◽  
Ganglion Cells ◽  
Outer Nuclear Layer ◽  
Cell Loss ◽  
Cell Types ◽  
High Dose ◽  
Double Labeling ◽  
6 Hydroxydopamine ◽  
Goldfish Retina

The conditions necessary to trigger regeneration of dopaminergic neurons were investigated in the goldfish retina. Intraocular injection of 6-hydroxydopamine (6-OHDA) was used to destroy dopaminergic neurons, and neuronal regeneration was monitored by injections of the thymidine analog bromodeoxyuridine (BUdR). Regenerated dopaminergic neurons, (identified by double-labeling with anti-tyrosine hydroxylase and anti-BUdR antibodies) were found within 3 weeks after 2 injections of 0.6 mg/ml 6-OHDA (estimated intraocular concentration), but not after injection of lower doses. All retinas with regenerated dopaminergic neurons also contained other types of regenerated neurons, including cones and ganglion cells, consistent with nuclear counts which revealed non-selective cell loss (34–36%) in both the outer and inner nuclear layers after exposure to the high dose, but not lower doses of 6-OHDA. Regenerated neurons were produced by clusters of dividing neuroepithelial cells probably derived from rod precursors in the outer nuclear layer. These results demonstrate that dopaminergic neurons will not regenerate after they are selectively ablated but only as part of a developmental process that involves generation of multiple cell types.

Adrenergic Innervation of Brown Adipose Tissue from the Ground Squirrel (Citellus richardsonii)

1974 ◽  
Vol 52 (1) ◽  
pp. 70-73 ◽  
Author(s):  
M. K. W. Cottle ◽  
W. H. Cottle ◽  
C. W. Nash
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Ground Squirrels ◽  
Brown Fat ◽  
Adrenergic Nerve ◽  
Fat Pad ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose

Determinations of noradrenaline (NA) content and observations of histochemical fluorescence were carried out on the axillary brown fat pad of ground squirrels Citellus richardsonii kept at two temperatures, 20 °C and 5 °C. For comparison, NA content of hearts and intrathoracic brown adipose tissue were also determined. Like interscapular brown adipose tissue from cold-acclimated rats, the axillary brown fat of cold-acclimated ground squirrels contained a high level of NA. The NA content of the fat pad from ground squirrels living at 20 °C, however, though somewhat lower was not statistically different from that of the fat pad from the cold-acclimated animals. Fine adrenergic nerve fibers were observed between the adipocytes and more intense and extensive networks were present around arterioles. The density of adrenergic innervation appeared similar in the axillary brown fat of the two groups. The NA content of the hearts of ground squirrels living at 5 °C was lower than that for hearts from animals at 20 °C. Intrathoracic brown fat tissue from both groups of animals showed large variation.

scholarly journals ADRENERGIC FIBERS IN BROWN FAT OF COLD-ACCLIMATED RATS

1970 ◽  
Vol 18 (2) ◽  
pp. 116-119 ◽  
Author(s):  
MERVA K. W. COTTLE ◽  
W. H. COTTLE
Keyword(s):  
Adrenergic Innervation ◽  
Nerve Fibers ◽  
Brown Fat ◽  
Adrenergic Nerve ◽  
Fat Cells ◽  
Fat Tissue ◽  
Histochemical Technique ◽  
Small Arteries ◽  
Brown Adipose ◽  
Adrenergic Fibers

The adrenergic nerve fibers of brown adipose tissue of warm- and cold-acclimated rats were visualized using the fluorescence histochemical technique. Small arteries and arterioles evidenced by their rich adrenergic innervation appeared more abundant in tissue from cold-acclimated animals. Lengths of fine fibers between the fat cells were demonstrable in the brown fat tissue from cold-acclimated rats because of their abundant, strongly fluorescent varicosities whereas such portions of fine fibers were only occasionally seen in the tissue of warm-acclimated rats.

Melatonin As a Modulator of Degenerative and Regenerative Signaling Pathways in Injured Retinal Ganglion Cells

2019 ◽  
Vol 25 (28) ◽  
pp. 3057-3073 ◽  
Author(s):  
Kobra B. Juybari ◽  
Azam Hosseinzadeh ◽  
Habib Ghaznavi ◽  
Mahboobeh Kamali ◽  
Ahad Sedaghat ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Retinal Ganglion Cells ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Ganglion Cells ◽  
Axon Growth ◽  
Nerve Fibers ◽  
Retinal Ganglion

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.

Adrenergic Nerve Fibers in the Human Fetal Sciatic Nerve

1991 ◽  
Vol 140 (4) ◽  
pp. 369-372 ◽  
Author(s):  
J. Koistinaho
Keyword(s):  
Sciatic Nerve ◽  
Nerve Fibers ◽  
Adrenergic Nerve

Electron Microscopic Findings in Presbycusic Degeneration of the Basal Turn of the Human Cochlea

1979 ◽  
Vol 87 (6) ◽  
pp. 818-836 ◽  
Author(s):  
Joseph B. Nadol
Keyword(s):  
Light Microscopy ◽  
Hair Cells ◽  
Basilar Membrane ◽  
Ganglion Cells ◽  
Nerve Fibers ◽  
Degenerative Changes ◽  
Supporting Cells ◽  
Neural Degeneration ◽  
Basal Turn ◽  
Temporal Bones

Three human temporal bones with presbycusis affecting the basal turn of the cochlea were studied by light and electron microscopy. Conditions in two ears examined by light microscopy were typical of primary neural degeneration, with a descending audiometric pattern, loss of cochlear neurons in the basal turn, and preservation of the organ of Corti. Ultrastructural analysis revealed normal hair cells and marked degenerative changes of the remaining neural fibers, especially in the basal turn. These changes included a decrease in the number of synapses at the base of hair cells, accumulation of cellular debris in the spiral bundles, abnormalities of the dendritic fibers and their sheaths in the osseous spiral lamina, and degenerative changes in the spiral ganglion cells and axons. These changes were interpreted as an intermediate stage of degeneration prior to total loss of nerve fibers and ganglion cells as visualized by light microscopy. In the third ear the changes observed were typical of primary degeneration of hair and supporting cells in the basal turn with secondary neural degeneration. Additional observations at an ultrastructural level included maintenance of the tight junctions of the scala media despite loss of both hair and supporting cells, suggesting a capacity for cellular “healing” in the inner ear. Degenerative changes were found in the remaining neural fibers in the osseous spiral lamina. In addition, there was marked thickening of the basilar membrane in the basal turn, which consisted of an increased number of fibrils and an accumulation of amorphous osmiophilic material in the basilar membrane. This finding supports the concept that mechanical alterations may occur in presbycusis of the basal turn.

scholarly journals Neuronal release of endogenous dopamine from corpus of guinea pig stomach

1997 ◽  
Vol 273 (5) ◽  
pp. G1044-G1050
Author(s):  
Kazuko Shichijo ◽  
Yasuko Sakurai-Yamashita ◽  
Ichiro Sekine ◽  
Kohtaro Taniyama
Keyword(s):  
Guinea Pig ◽  
Ganglion Cells ◽  
Splanchnic Nerve ◽  
Muscle Layer ◽  
Nerve Fibers ◽  
Endogenous Dopamine ◽  
Dopamine Content ◽  
Release Of Acetylcholine ◽  
Gastric Corpus ◽  
Guinea Pig Stomach

Neuronal release of endogenous dopamine was identified in mucosa-free preparations (muscle layer including intramural plexus) from guinea pig stomach corpus by measuring tissue dopamine content and dopamine release and by immunohistochemical methods using a dopamine antiserum. Dopamine content in mucosa-free preparations of guinea pig gastric corpus was one-tenth of norepinephrine content. Electrical transmural stimulation of mucosa-free preparations of gastric corpus increased the release of endogenous dopamine in a frequency-dependent (3–20 Hz) manner. The stimulated release of dopamine was prevented by either removal of external Ca2+ or treatment with tetrodotoxin. Dopamine-immunopositive nerve fibers surrounding choline acetyltransferase-immunopositive ganglion cells were seen in the myenteric plexus of whole mount preparations of gastric corpus even after bilateral transection of the splanchnic nerve proximal to the junction with the vagal nerve (section of nerves between the celiac ganglion and stomach). Domperidone and sulpiride potentiated the stimulated release of acetylcholine and reversed the dopamine-induced inhibition of acetylcholine release from mucosa-free preparations. These results indicate that dopamine is physiologically released from neurons and from possible dopaminergic nerve terminals and regulates cholinergic neuronal activity in the corpus of guinea pig stomach.

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