Noradrenergic Fibers (noradrenergic + fiber)

Distribution by Scientific Domains


Selected Abstracts


Skin sympathetic adrenergic innervation: An immunofluorescence confocal study

ANNALS OF NEUROLOGY, Issue 2 2006
Vincenzo Donadio MD
Objective The aim of this study was to characterize sympathetic adrenergic innervation of the skin in healthy subjects using dopamine , hydroxylase (D,H) as a specific marker for noradrenergic fibers. Methods Sympathetic adrenergic innervation of human skin was studied in 10 healthy subjects by indirect immunofluorescence and confocal microscopy applied to punch skin biopsies. Noradrenergic fibers were identified both in glabrous and hairy skin using D,H antibody. Results D,H immunoreactive fibers were mainly localized in arteriovenous anastomoses, arrector pilorum muscles, and arterioles, whereas few adrenergic fibers were found around sweat glands. Interpretation Our description of sympathetic adrenergic innervation of human skin aims to improve the diagnostic ability of skin biopsy to detect selective autonomic nervous system disorders. Ann Neurol 2006;59;376,381 [source]


Brain-derived neurotrophic factor applied to the motor cortex promotes sprouting of corticospinal fibers but not regeneration into a peripheral nerve transplant

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2002
G.W. Hiebert
Abstract Previous experiments from our laboratory have shown that application of brain-derived neurotrophic factor (BDNF) to the red nucleus or the motor cortex stimulates an increase in the expression of regeneration-associated genes in rubrospinal and corticospinal neurons. Furthermore, we have previously shown that BDNF application stimulates regeneration of rubrospinal axons into a peripheral graft after a thoracic injury. The current study investigates whether application of BDNF to the motor cortex will facilitate regeneration of corticospinal neurons into a peripheral nerve graft placed into the thoracic spinal cord. In adult Sprague Dawley rats, the dorsal columns and the corticospinal tract between T9 and T10 were ablated by suction, and a 5-mm-long segment of predegenerated tibial nerve was autograft implanted into the lesion. With an osmotic pump, BDNF was infused directly into the parenchyma of the motor cortex for 14 days. Growth of the corticospinal tract into the nerve graft was then evaluated by transport of an anterograde tracer. Anterogradely labeled corticospinal fibers were not observed in the peripheral nerve graft in animals treated with saline or BDNF. Serotinergic and noradrenergic fibers, as well as peripheral sensory afferents, were observed to penetrate the graft, indicating the viability of the peripheral nerve graft as a permissive growth substrate for these specific fiber types. Although treatment of the corticospinal fibers with BDNF failed to produce regeneration into the graft, there was a distinct increase in the number of axonal sprouts rostral to the injury site. This indicates that treatment of corticospinal neurons with neurotrophins, e.g., BDNF, can be used to enhance sprouting of corticospinal axons within the spinal cord. Whether such sprouting leads to functional recovery after spinal cord injury is currently under investigation. © 2002 Wiley-Liss, Inc. [source]


Skin sympathetic adrenergic innervation: An immunofluorescence confocal study

ANNALS OF NEUROLOGY, Issue 2 2006
Vincenzo Donadio MD
Objective The aim of this study was to characterize sympathetic adrenergic innervation of the skin in healthy subjects using dopamine , hydroxylase (D,H) as a specific marker for noradrenergic fibers. Methods Sympathetic adrenergic innervation of human skin was studied in 10 healthy subjects by indirect immunofluorescence and confocal microscopy applied to punch skin biopsies. Noradrenergic fibers were identified both in glabrous and hairy skin using D,H antibody. Results D,H immunoreactive fibers were mainly localized in arteriovenous anastomoses, arrector pilorum muscles, and arterioles, whereas few adrenergic fibers were found around sweat glands. Interpretation Our description of sympathetic adrenergic innervation of human skin aims to improve the diagnostic ability of skin biopsy to detect selective autonomic nervous system disorders. Ann Neurol 2006;59;376,381 [source]


Disrupted brain,immune system,joint communication during experimental arthritis

ARTHRITIS & RHEUMATISM, Issue 10 2008
Adriana del Rey
Objective To explore the hypothesis that, in parallel with alterations in the hypothalamus,pituitary,adrenal axis and the sympathetic nervous system, hypothalamic cytokine expression and monoaminergic neurotransmitter concentrations are affected during the course of arthritis development induced by type II collagen. This hypothesis was based on evidence that acute inflammatory processes induce cytokine expression in the brain and affect neuronal activity. We also studied whether depletion of hypothalamic noradrenaline can affect peripheral joint disease. Methods Hypothalamic cytokine gene expression and neurotransmitter concentration, parameters of inflammation, and joint innervation were evaluated during arthritis development in rats induced by injection of type II collagen in Freund's incomplete adjuvant. Noradrenergic neurons in the brain were depleted with 6-hydroxydopamine. Results Transiently increased corticosterone levels, followed by increased adrenaline levels and hypothalamic interleukin-1, (IL-1,) and IL-6 overexpression were observed only during the induction phase of the disease. Hypothalamic noradrenaline content was increased during the symptomatic phase and was paralleled by a gradual loss of noradrenergic fibers in the joints. The positive correlation between hypothalamic IL-1, expression and noradrenaline content in control groups was not observed in rats in which arthritis developed. Depletion of hypothalamic noradrenergic neurons when arthritis was established did not affect the course of the disease. Conclusion The dissociation between hypothalamic cytokine gene expression and noradrenergic neuronal activity, the lack of sustained stimulation of the stress axes, and the loss of sympathetic signals in the joints indicate a disruption in communication between afferent immune messages to the central nervous system and 2 main efferent antiinflammatory pathways under control of the brain during collagen-induced arthritis. [source]