scholarly journals Erectile response to hypothalamic stimulation in rats: role of peripheral nerves

1997 ◽  
Vol 273 (6) ◽  
pp. R1990-R1997 ◽  
Author(s):  
François Giuliano ◽  
Jacques Bernabé ◽  
Kathleen Brown ◽  
Stéphane Droupy ◽  
Gérard Benoit ◽  
...  
Keyword(s):  
Peripheral Nerves ◽  
Pressure Ratio ◽  
Cauda Equina ◽  
Sympathetic Chain ◽  
Iliac Arteries ◽  
Pelvic Nerves ◽  
Arterial Inflow ◽  
Erectile Response ◽  
6 Hydroxydopamine

The role of peripheral parasympathetic and sympathetic pathways was explored in erectile responses elicited by hypothalamic medial preoptic area (MPOA) stimulation in adult male anesthetized rats. Under control conditions, MPOA stimulation reliably elicited erectile responses evidenced by an increase of the intracavernous pressure-to-blood pressure ratio. The erectile response was abolished by 1) acute bilateral section of cavernous or pelvic nerves or cauda equina and 2) chronic lesions of pelvic nerves or cauda equina. Acute section of the hypogastric nerve did not significantly decrease the erectile response. The erectile response was significantly depressed after acute or chronic sections of the paravertebral sympathetic chain at the L4-L5 level or chemical sympathectomy with 6-hydroxydopamine. The decrease due to acute sympathetic chain lesion was reversed by bilateral ligation of the external iliac arteries. Accordingly MPOA stimulation elicits erectile responses via 1) activation of the parasympathetic outflow conveyed by the pelvic and cavernous nerves and 2) activation of neural fibers conveyed by the sympathetic pathways. We propose that sympathetic fibers running in the paravertebral sympathetic chain are responsible for vasoconstriction of nonpenile areas to divert blood to the penis, allowing the dramatic increase of penile arterial inflow required for erection.

scholarly journals The Protective Role of Brain CYP2J in Parkinson’s Disease Models

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yueran Li ◽  
Jinhua Wu ◽  
Xuming Yu ◽  
Shufang Na ◽  
Ke Li ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Brain Regions ◽  
Protective Role ◽  
Neural Cells ◽  
Endogenous Substrates ◽  
6 Hydroxydopamine ◽  
Myd88 Signaling ◽  
Lps Treatment

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.

scholarly journals Comparing the role of the anterior cingulate cortex and 6-hydroxydopamine nucleus accumbens lesions on operant effort-based decision making

2009 ◽  
Vol 29 (8) ◽  
pp. 1678-1691 ◽  
Author(s):  
Mark E. Walton ◽  
James Groves ◽  
Katie A. Jennings ◽  
Paula L. Croxson ◽  
Trevor Sharp ◽  
...  
Keyword(s):  
Decision Making ◽  
Nucleus Accumbens ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
6 Hydroxydopamine

scholarly journals Laminin γ1 is critical for Schwann cell differentiation, axon myelination, and regeneration in the peripheral nerve

2003 ◽  
Vol 163 (4) ◽  
pp. 889-899 ◽  
Author(s):  
Zu-Lin Chen ◽  
Sidney Strickland
Keyword(s):  
Schwann Cells ◽  
Peripheral Nerves ◽  
Matrix Proteins ◽  
Myelin Proteins ◽  
Sciatic Nerve Crush ◽  
Similar Reduction ◽  
Nerve Crush ◽  
And Function ◽  
Schwann Cell Differentiation

Laminins are heterotrimeric extracellular matrix proteins that regulate cell viability and function. Laminin-2, composed of α2, β1, and γ1 chains, is a major matrix component of the peripheral nervous system (PNS). To investigate the role of laminin in the PNS, we used the Cre–loxP system to disrupt the laminin γ1 gene in Schwann cells. These mice have dramatically reduced expression of laminin γ1 in Schwann cells, which results in a similar reduction in laminin α2 and β1 chains. These mice exhibit motor defects which lead to hind leg paralysis and tremor. During development, Schwann cells that lack laminin γ1 were present in peripheral nerves, and proliferated and underwent apoptosis similar to control mice. However, they were unable to differentiate and synthesize myelin proteins, and therefore unable to sort and myelinate axons. In mutant mice, after sciatic nerve crush, the axons showed impaired regeneration. These experiments demonstrate that laminin is an essential component for axon myelination and regeneration in the PNS.

Insect peripheral nerves: accessibility of neurohaemal regions to lanthanum

1975 ◽  
Vol 18 (1) ◽  
pp. 179-197 ◽  
Author(s):  
N.J. Lane ◽  
R.A. Leslie ◽  
L.S. Swales
Keyword(s):  
Blood Brain Barrier ◽  
Peripheral Nerves ◽  
Rhodnius Prolixus ◽  
Ionic Lanthanum ◽  
Neurosecretory Axon ◽  
Thin Part ◽  
Free Media ◽  
Exogenous Substances

During incubation in vivo, exogenously applied ionic lanthanum comes to surround the numerous neurosecretory terminals which are found lying within or immediately beneath the acellular neural lamella ensheathing the nerves from fifth instar and adult specimens of Rhodnius prolixus. The lanthanum does not penetrate beyond the cellular perineurium, which completely surrounds the non-neurosecretory axons in these nerves and constitutes a form of ‘blood-brain barrier’. In some cases, however, lanthanum is found in the vicinity of a neurosecretory axon lying beneath the perineurium, where it can be assumed to have leaked in from the neurosecretory terminal lying free in the neural lamella. When nerves are incubated in calcium-free media, regions with an attenuated perineurium become ‘leaky’, in that lanthanum is found lying in those extracellular spaces between axons and glia which lie immediately below the thin part of the perineurial layer. Bathing solutions made slightly hyperosmotic to the haemolymph with sucrose have no apparent disruptive effects on the barrier. When the tissues are incubated in more hypertonic solutions, the perineurial barrier becomes ‘leaky’ throughout, and tracer pervades beyond its cells into all the intercellular spaced between glia and axons. The possible role of the zonulae occludentes in both the maintenance of the perineurial barrier and in the formation of interglial occlusions to local penetration of exogenous substances is considered.

scholarly journals A Novel Model of Cancer-Induced Peripheral Neuropathy and the Role of TRPA1 in Pain Transduction

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Ahmad Maqboul ◽  
Bakheet Elsadek
Keyword(s):  
Immune Cells ◽  
Peripheral Nerves ◽  
Morphological Changes ◽  
Nerve Fibres ◽  
Cold Allodynia ◽  
Sciatic Nerves ◽  
Pain Transduction ◽  
Thermal Stimuli ◽  
Novel Model

Background. Models of cancer-induced neuropathy are designed by injecting cancer cells near the peripheral nerves. The interference of tissue-resident immune cells does not allow a direct contact with nerve fibres which affects the tumor microenvironment and the invasion process. Methods. Anaplastic tumor-1 (AT-1) cells were inoculated within the sciatic nerves (SNs) of male Copenhagen rats. Lumbar dorsal root ganglia (DRGs) and the SNs were collected on days 3, 7, 14, and 21. SN tissues were examined for morphological changes and DRG tissues for immunofluorescence, electrophoretic tendency, and mRNA quantification. Hypersensitivities to cold, mechanical, and thermal stimuli were determined. HC-030031, a selective TRPA1 antagonist, was used to treat cold allodynia. Results. Nociception thresholds were identified on day 6. Immunofluorescent micrographs showed overexpression of TRPA1 on days 7 and 14 and of CGRP on day 14 until day 21. Both TRPA1 and CGRP were coexpressed on the same cells. Immunoblots exhibited an increase in TRPA1 expression on day 14. TRPA1 mRNA underwent an increase on day 7 (normalized to 18S). Injection of HC-030031 transiently reversed the cold allodynia. Conclusion. A novel and a promising model of cancer-induced neuropathy was established, and the role of TRPA1 and CGRP in pain transduction was examined.

scholarly journals Experimental Allergic Neuritis in the Chicken

1967 ◽  
Vol 4 (5) ◽  
pp. 464-476
Author(s):  
M. Petek ◽  
G. L. Quaglio
Keyword(s):  
Peripheral Nerves ◽  
Marek's Disease ◽  
Experimental Allergic Neuritis ◽  
Marek’S Disease ◽  
Autoimmune Processes ◽  
Lymphoid Infiltration ◽  
Experimental Allergic ◽  
Experimental Autoimmune ◽  
Allergic Neuritis

Experimental allergic neuritis was reproduced in chickens, by inoculation of chicken and guinea pig nerves in complete Freund's adjuvant. Paralysis was observed in a percentage of inoculated birds. Histopathologically this experimental autoimmune disease was characterized by severe demyelination of peripheral nerves in all experimental animals. In addition, oedema and/or lymphoid infiltration occurred in some of the animals. The similarity of experimental allergic neuritis to the inflammatory lesions of Marek's disease is stressed and the possible role of autoimmune processes in the pathogenesis of Marek's disease is discussed.

scholarly journals Gli1 regulates the postnatal acquisition of peripheral nerve architecture

2021 ◽  
Author(s):  
Brendan Zotter ◽  
Or Dagan ◽  
Jacob Brady ◽  
Hasna Baloui ◽  
Jayshree Samanta ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Peripheral Nerves ◽  
Hedgehog Signaling ◽  
Target Cells ◽  
Gli1 Expression ◽  
Desert Hedgehog ◽  
Matrix Production ◽  
Endoneurial Cells ◽  
Cellular Compartments

ABSTRACTPeripheral nerves are organized into discrete cellular compartments. Axons, Schwann cells (SCs), and endoneurial fibroblasts (EFs) reside within the endoneurium and are surrounded by the perineurium - a cellular sheath comprised of layers of perineurial glia (PNG). SC secretion of Desert Hedgehog (Dhh) regulates this organization. In Dhh nulls, the perineurium is deficient and the endoneurium is subdivided into small compartments termed minifascicles. Human Dhh mutations cause a peripheral neuropathy with similar defects. Here we examine the role of Gli1, a canonical transcriptional effector of hedgehog signaling, in regulating peripheral nerve organization. We identify PNG, EFs, and pericytes as Gli1-expressing cells by genetic fate mapping. Although expression of Dhh by SCs and Gli1 in target cells is coordinately regulated with myelination, Gli1 expression unexpectedly persists in Dhh null EFs. Thus, Gli1 is expressed in EFs non-canonically i.e., independent of hedgehog signaling. Gli1 and Dhh also have non-redundant activities. In contrast to Dhh nulls, Gli1 nulls have a normal perineurium. Like Dhh nulls, Gli1 nulls form minifascicles, which we show likely arise from EFs. Thus, Dhh and Gli1 are independent signals: Gli1 is dispensable for perineurial development but functions cooperatively with Dhh to drive normal endoneurial development. During development, Gli1 also regulates endoneurial extracellular matrix production, nerve vascular organization, and has modest, non-autonomous effects on SC sorting and myelination of axons. Finally, in adult nerves, induced deletion of Gli1 is sufficient to drive minifascicle formation. Thus, Gli1 regulates the development and is required to maintain the endoneurial architecture of peripheral nerves.SIGNIFICANCE STATEMENTPeripheral nerves are organized into distinct cellular/ECM compartments: the epineurium, perineurium and endoneurium. This organization, with its associated cellular constituents, are critical for the structural and metabolic support of nerves and their response to injury. Here, we show Gli1 - a transcription factor normally expressed downstream of hedgehog signaling - is required for the proper organization of the endoneurium but not the perineurium. Unexpectedly, Gli1 expression by endoneurial cells is independent of, and functions non-redundantly with, Schwann Cell-derived Desert Hedgehog in regulating peripheral nerve architecture. These results further delineate how peripheral nerves acquire their distinctive organization during normal development and highlight mechanisms that may regulate their reorganization in pathologic settings including peripheral neuropathies and nerve injury.

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