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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 110 (1996), S. 151-162 
    ISSN: 1432-1106
    Keywords: Nociception ; Autonomic ; Locus coeruleus ; Norepinephrine ; Catecholamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In addition to giving primary projections to the parabrachial and periaqueductal gray regions, ascending lamina I projections course through and terminate in brainstem regions known to contain catecholaminergic cells. For this reason, double-labeling experiments were designed for analysis with light and electron microscopy. The lamina I projections in the Cynomolgus monkey were anterogradely labeled with Phaseolus vulgaris leucoagglutinin (PHA-L) and catecholamine-containing neurons were labeled immunocytochemically for tyrosine hydroxylase (TH). Light level double-labeling experiments revealed that the terminations of the lamina I ascending projections through the medulla and pons strongly overlap with the localization of catecholamine cells in: the entire rostrocaudal extent of the ventrolateral medulla (A1 caudally, C1 rostrally); the solitary nucleus and the dorsomedial medullary reticular formation (A2 caudally, C2 rostrally); the ventrolateral pons (A5); the locus coeruleus (A6); and the subcoerulear region, the Kölliker-Fuse nucleus, and the medial and lateral parabrachial nuclei (A7). At the light microscopic level, close appositions between PHA-L-labeled lamina I terminal varicosities and TH-positive dendrites and somata were observed, particularly in the A1, A5 and the A7 cell groups on the contralateral side. At the electron microscopic level, examples of lamina I terminals were found synapsing on cells of the ventrolateral catecholamine cell groups in preliminary studies. The afferent input relayed by these lamina I projections could provide information about pain, temperature, and metabolic state as described previously. Lamina I input could impact interactions of the catecholamine system with higher brain centers modulating complex autonomic, endocrine, sensory, motor, limbic and cortical functions such as memory and learning. Nociceptive lamina I input to catecholamine cell regions with projections back to the spinal cord could form a feedback loop for control of spinal sensory, autonomic and motor activity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Key words Nitric oxide ; Adjuvant arthritis ; Chronic inflammation ; Central canal ; Ependymal cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Nitric oxide (NO) possibly plays an important role in the events resulting in hyperalgesia. Nitric oxide synthase (NOS) is a key enzyme in the production of NO. In this study, the relationship between NOS and hyperalgesia in a rat chronic arthritis model was tested. Chronic arthritis was induced by injection of incomplete Freund’s adjuvant into the knee joint cavity unilaterally. The paw withdrawal latency (PWL) to radiant heat was used to detect secondary thermal hyperalgesia induced by the arthritis. After 1 day the PWL of the arthritic hindpaw decreased and it reached its nadir at 3 days after induction of arthritis. The lumbar and cervical enlargement of the spinal cord were removed in different groups of animals 3, 7, 14, or 21 days after induction of arthritis, and frozen tissue sections were cut. Two series of sections were incubated with polyclonal antibodies to neuronal NOS (nNOS) or to inducible NOS (iNOS). nNOS was found to increase gradually in laminae I–III in the lumber but not in the cervical enlargement. The change became most obvious 14 days after induction of arthritis as compared to the control animals. Ependymal cells around the central canal of the lumbar enlargement were more densely stained by anti-iNOS after arthritis. A corresponding change was also found in the cervical enlargement. Computer-assisted image analysis revealed that the mean density of the affected areas in the treated group increased significantly compared with the control animals. This study suggests that the expression of both nNOS and iNOS increase following induction of chronic arthritis, which in turn would presumably lead to an increase in the production of NO. This process could be involved in mediation of the secondary thermal hyperalgesia induced by chronic arthritis.
    Type of Medium: Electronic Resource
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  • 3
    Publication Date: 2013-05-02
    Description: The present study investigated transient receptor potential vanilloid type 4 (TRPV4) ion channels in pancreatic stellate cells (PSCs) isolated from rats with high-fat and alcohol diet (HFA)-induced chronic pancreatitis. TRPV4 is a calcium-permeable nonselective ion channel responsive to osmotic changes, alcohol metabolites arachidonic acid, anandamide, their derivatives, and injury-related lipid mediators. Male Lewis rats were fed HFA for 6–8 wk before isolation and primary culture of PSCs. Control PSCs were harvested from rats fed standard chow. Immunoreactivity for cytoskeletal protein activation product α-smooth muscle actin (α-SMA) and platelet-derived growth factor receptor-β subunit (PDGFR-β) characterized the cells as PSCs. TRPV4 expression increased in PSCs of HFA-fed rats and control cultures after alcohol treatment (50 mM). Cell responses to activation of inducible TRPV4 were assessed with live cell calcium imaging. Threefold increased and sustained intracellular calcium mobilization responses occurred in 70% of pancreatic stellate cells from HFA-fed rats in response to TRPV4 activators arachidonic acid, lipid second messenger, phorbol ester 4 α-phorbol 12,13-didecanoate (4αPDD), and 50% hypoosmotic media compared with relatively unresponsive PSCs from control rats. Activation responses were attenuated by nonselective TRPV channel blocker ruthenium red. Tumor necrosis factor-α (TNF-α, 1 ng/ml, 16 h) increased responses to 4αPDD in control PSCs. These findings implicate TRPV4-mediated calcium responses inducible after HFA exposure and inflammation in reactive responses of activated PSCs that impair pancreatic function, such as responsiveness to cytokines and the deposition of collagen fibrosis that precipitates ductal blockage and pain.
    Print ISSN: 0363-6119
    Electronic ISSN: 1522-1490
    Topics: Medicine
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  • 4
    Publication Date: 2017-09-29
    Description: Every institution that is involved in research with animals is expected to have in place policies and procedures for the management of allegations of noncompliance with the Animal Welfare Act and the U.S. Public Health Service Policy on the Humane Care and Use of Laboratory Animals. We present here a model set of recommendations for institutional animal care and use committees and institutional officials to ensure appropriate consideration of allegations of noncompliance with federal Animal Welfare Act regulations that carry a significant risk or specific threat to animal welfare. This guidance has 3 overarching aims: 1 ) protecting the welfare of research animals; 2 ) according fair treatment and due process to an individual accused of noncompliance; and 3 ) ensuring compliance with federal regulations. Through this guidance, the present work seeks to advance the cause of scientific integrity, animal welfare, and the public trust while recognizing and supporting the critical importance of animal research for the betterment of the health of both humans and animals.—Hansen, B. C., Gografe, S., Pritt, S., Jen, K.-L. C., McWhirter, C. A., Barman, S. M., Comuzzie, A., Greene, M., McNulty, J. A., Michele, D. E., Moaddab, N., Nelson, R. J., Norris, K., Uray, K. D., Banks, R., Westlund, K. N., Yates, B. J., Silverman, J., Hansen, K. D., Redman, B. Ensuring due process in the IACUC and animal welfare setting: considerations in developing noncompliance policies and procedures for institutional animal care and use committees and institutional officials.
    Print ISSN: 0892-6638
    Electronic ISSN: 1530-6860
    Topics: Biology
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