Calcutt N A, Chen P, Hua X Y
Department of Pathology, University of California San Diego, La Jolla 92093-0612, USA.
Neurosci Lett. 1998 Oct 2;254(3):129-32. doi: 10.1016/s0304-3940(98)00692-2.
We measured the evoked release of calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) from sensory nerve terminals in tracheas from control and diabetic rats using an in vitro perfusion system and also the CGRP-LI content of the vagus nerve and trachea. Diabetes caused a 29% (P < 0.05) reduction in CGRP-LI content of the vagus nerve and a decrease in CGRP-LI release from nerve endings in the trachea evoked by either capsaicin (30% decrease, P < 0.05) or electrical field stimulation (50% decrease: P < 0.05). In contrast, there was a 50% increase in the CGRP-LI content of the unstimulated trachea. Thus, diabetes induces an impairment in neuropeptide release from peripheral terminals of sensory nerves that corresponds to decreased levels in the supplying nerve but is not reflected in tissue measurements that incorporate nerve terminals. Impaired neuropeptide release may contribute to peripheral and central sensory dysfunction in diabetic rats.
