scholarly journals Hyperglycemia Suppresses Age-Related Increases in Corneal Peripheral Sensory Nerves in Wistar Bon Kobori (WBN/Kob) Rats

2019 ◽  
Vol 60 (13) ◽  
pp. 4151
Author(s):  
Kiyokazu Ozaki ◽  
Yui Terayama ◽  
Tetsuro Matsuura
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.


2013 ◽  
Vol 108 (10) ◽  
pp. 1634-1643 ◽  
Author(s):  
Eduardo E Valdez-Morales ◽  
Jeff Overington ◽  
Raquel Guerrero-Alba ◽  
Fernando Ochoa-Cortes ◽  
Charles O Ibeakanma ◽  
...  

1992 ◽  
Vol 263 (1) ◽  
pp. G29-G37
Author(s):  
O. D. Hottenstein ◽  
G. Remak ◽  
E. D. Jacobson

Cessation of perivascular nerve stimulation (NS) elicits a transient increase in intestinal blood flow above the prestimulatory value. This enhancement of blood flow constitutes the phenomenon of post-nerve stimulation hyperemia (PSH). We investigated the involvement of peptidergic sensory nerves in intestinal PSH. In anesthetized rats the velocity of blood flowing through the anterior mesenteric artery (VBF) was measured with a pulsed Doppler velocimeter. PSH was induced by 4 min of postganglionic electrical NS (5 Hz). PSH was abolished by distal periarterial application of tetrodotoxin and intra-arterial lidocaine, which suggests a peripheral sensory nervous mechanism for PSH. The increase in conductance at peak PSH was blocked by pretreatment with the selective, primary afferent neurotoxin capsaicin administered as 1) subcutaneous injection in neonatal life, 2) topical application to periarterial nerves, or 3) injection into the jejunal lumen. In rats pretreated with reserpine, NS evoked a hyperemic response, which was blocked by capsaicin. Treatment with adenosine deaminase inhibited PSH considerably less than capsaicin, suggesting a lesser role for adenosine in PSH. Our findings support the hypothesis that postganglionic NS activates both adrenergic and peptidergic nerves and that the latter release vasodilator peptides in the gut during PSH.


2009 ◽  
Vol 65 ◽  
pp. S212 ◽  
Author(s):  
Seiji Komagata ◽  
Shanlin Chen ◽  
Ryuichi Hishida ◽  
Minoru Shibata ◽  
Katsuei Shibuki

Nature ◽  
1975 ◽  
Vol 254 (5496) ◽  
pp. 146-148 ◽  
Author(s):  
RAINER F. FOELIX

2019 ◽  
Vol 61 (1) ◽  
Author(s):  
R. Van Rensburg ◽  
H. Reuter

Pain is a complex and unique experience. It encompasses several pathways, involving nociceptive signal generation (transduction) and propagation (transmission), as well as perception and modulation of the nociceptive stimuli. Nonsteroidal anti-inflammatory drugs (NSAIDs) primarily exert their analgesic effects through inhibition of cyclooxygenase (COX) enzymes, thereby attenuating prostaglandin synthesis. The COX-2 selective NSAIDs (coxibs) and aspirin have also been shown to reduce colorectal cancers, presumably by prostaglandin-inhibition mechanisms. Paracetamol appears to have both peripheral and central effects. The postulated mechanism for its peripheral effects is indirect COX inhibition, while the central effects are thought to be mediated by modulation of descending pain inhibition pathways. Topical analgesics are available in various formulations. The topical NSAIDs have the same mechanism of action as the systemic formulations, but with less systemic absorption and effects. The local anaesthetics provide a dense sensory block via inhibition of nerve impulse transmission, and are available in percutaneous and transdermal preparations. Capsicum is effective for neuropathic pain, and acts by stimulating and then desensitising peripheral sensory nerves.


1985 ◽  
Vol 79 (1) ◽  
pp. 305-315
Author(s):  
S. Anderson ◽  
D.A. Ede

Pupoid foetus (pf/pf) is a recessive lethal mutation of the mouse causing epidermal hypertrophy and disorganization of peripheral sensory nerves and mesoderm. The comparative behaviour of epidermal cells from normal and pupoid foetus mutant mouse embryos was studied in vitro. Epidermal explants from the snout region of 12.5- to 13-day embryos were grown in culture for periods of up to 2 weeks. Cultures from both phenotypes were filmed using time-lapse cinemicrography for up to 3 days following explantation. Paths of individual cells were traced as they migrated from the explant, and their rate of locomotion and directional persistence were calculated. Differences in these parameters between the two phenotypes were tested statistically. The overall morphology of the cultures, and the tendency of the cells to detach from the periphery of the cell mass were also compared. The results show that, between 25 and 60 h after explantation, epidermal cells from pupoid foetus embryos move consistently more slowly than normal cells, and follow a more erratic path. This situation is reversed, however, between 16 and 25 h. This suggests that the pf mutation causes an alteration in epidermal cells that affects their locomotion, and which is maintained for a minimum of 3 days in the absence of other influencing factors.


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