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Alteration of capsaicin and endotoxin‐induced calcitonin gene‐related peptide release from mesenteric arterial bed and spinal cord slice in 18‐month‐old rats
Author(s) -
Sun Wei,
Guo Jingxuan,
Tang Yueming,
Wang Xian
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19980801)53:3<385::aid-jnr13>3.0.co;2-4
Subject(s) - calcitonin gene related peptide , capsaicin , calcitonin , medicine , endocrinology , spinal cord , chemistry , radioimmunoassay , neuropeptide , substance p , basal (medicine) , receptor , psychiatry , insulin
In the present study, we investigated the changes in capsaicin‐ and endotoxin‐induced calcitonin gene‐related peptide (CGRP) release from mesenteric arterial bed (MAB) and spinal cord slices (SCS) in 2‐month‐old and 18‐month‐old Wistar rats. The isolated MAB or SCS was perfused or incubated in vitro. The CGRP‐like immunoreactivity in perfusate or supernatant was measured by radioimmunoassay. The results showed that endotoxin triggered CGRP release from isolated rat MAB and SCS, which represent the peripheral and central terminals of CGRP‐containing sensory nerves, respectively. Either basal or stimulated CGRP release induced by capsaicin and endotoxin was significantly decreased as the rats aged from 2 to 18 months. The basal CGRP release was 14.9 ± 1.8 and 5.8 ± 1.0 pg/ml from MAB and 3.50 ± 0.54 and 1.78 ± 0.16 pg/ml/mg from SCS in 2‐month‐old and 18‐month‐old rats, respectively. The release of CGRP evoked by capsaicin (10 −7 mol/L) and endotoxin (1 ≈ 5 μg/ml) from MAB and SCS was significantly decreased by more than 50% in 18‐month‐old rats. These data suggest that both the basal and capsaicin‐ or endotoxin‐stimulated CGRP release from MAB and SCS display a significant decrement in aged rats that may have some physiological, pathological, and behavioural relevance in age‐related diseases. J. Neurosci. Res. 53:385–392, 1998. © 1998 Wiley‐Liss, Inc.