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The effect of streptozotocin treatment (65 mg/kg i.v.) on plasma protein extravasation, nociception, and the content of substance P immunoreactivity (SP-IR) and somatostatin immunoreactivity (SOM-IR) was investigated in the rat. Twelve days after treatment, the neurogenic plasma extravasation induced by 5% mustard oil was reduced by 67% in the skin of the hind paw. Extravasation caused by SP, a putative mediator of neurogenic inflammation, was also reduced by 61% in the abdominal skin. While calcitonin gene-related peptide (CGRP) potentiated the SP-induced extravasation in control rats, no potentiation was observed in diabetic rats. Thermonociception or chemonociception was unchanged after streptozotocin treatment. The content of SP-IR and SOM-IR in sensory nerves or spinal ganglia was also not altered. These results indicate that the impairment of neurogenic inflammation in diabetic rats is not the result of depletion of neurogenic mediators like SP. Changes of the microvasculature at the leakage site appear to account for the effects observed.
R Gamse, and
G Jancsó
May 1993,
General pharmacology,
R Gamse, and
G Jancsó
February 1978,
The Journal of pharmacy and pharmacology,
R Gamse, and
G Jancsó
September 1998,
Prostaglandins, leukotrienes, and essential fatty acids,
R Gamse, and
G Jancsó
August 1991,
Neuroscience letters,
R Gamse, and
G Jancsó
November 1985,
Gastroenterology,
R Gamse, and
G Jancsó
January 1973,
Advances in metabolic disorders,
R Gamse, and
G Jancsó
July 2001,
Archives of physiology and biochemistry,
R Gamse, and
G Jancsó
February 2001,
American journal of respiratory cell and molecular biology,
R Gamse, and
G Jancsó
January 1988,
The Japanese journal of physiology,
R Gamse, and
G Jancsó
May 2015,
Cytokine,
