AJP - Regulatory, Integrative and Comparative Physiology, Vol 247, Issue 6 995-1002, Copyright © 1984 by American Physiological Society
Responses of primate T1-T5 spinothalamic neurons to gallbladder distension
W. S. Ammons, R. W. Blair and R. D. Foreman
Extracellular unit recordings were obtained from 44 spinothalamic tract
(STT) neurons in the T1-T5 segments of 15 alpha-chloralose anesthesized
monkeys (Macaca fascicularis). Each cell had a somatic receptive field in
the left chest region and was excited by electrical stimulation of
cardiopulmonary sympathetic afferent fibers. Gallbladder distension to
pressures between 20 and 100 mmHg increased activity in 16 of 44 neurons.
Responses usually consisted of bursts of activity associated with increased
gallbladder pressure (phasic responses) followed by maintained activity
during the distension (tonic responses). Magnitude of phasic responses was
linearly related to the distending pressure and was consistently greater
than magnitude of tonic responses. The gallbladder-responsive and
nonresponsive groups included similar proportions of wide dynamic range,
high threshold, and high-threshold inhibitory cells. Nine of 10
gallbladder-responsive cells and 11 of 21 gallbladder-nonresponsive cells
increased their discharge rate after injection of 2 micrograms/kg
bradykinin into left atrium. Activity of cells with gallbladder input
increased from 14 +/- 4 to 33 +/- 4 spikes/s. Cells without gallbladder
input increased their discharge rate to a significantly less degree (10 +/-
3-23 +/- 4 spikes/s). These results indicate that upper thoracic STT
neurons may increase their activity during gallbladder distension.
Convergence of afferent information from the chest and gallbladder may
explain chest pain occurring during gallbladder disease. Furthermore the
tendency of gallbladder-responsive cells to respond to bradykinin
injections with a high rate of discharge could explain how this chest pain
of gallbladder origin may closely mimic pain of angina pectoris.
