Responses of thoracic spinoreticular and spinothalamic cells to intracardiac bradykinin

Abstract

The response characteristics of spinoreticular and spinothalamic cells to intracardiac injection of bradykinin were determined in cats anesthetized with chloralose. Extracellular potentials of individual spinoreticular and spinothalamic cells were recorded from the T2-T4 segments of the spinal cord. Only those cells with cardiopulmonary sympathetic afferent input were tested for responses to intracardiac bradykinin (1-6 micrograms/kg). Thirty-seven of the 64 cells studied responded to bradykinin; 36 were excited and one was inhibited. For excited cells, discharge rate increased from 4 +/- 1.0 (SE) spikes/s to a peak of 20 +/- 2.4 spikes/s, a fivefold increase. Latency to onset of cell response was 13 +/- 1.1 s, and latency to peak response was 24 +/- 1.4 s after drug injection. Tachyphylaxis to additional doses of bradykinin was observed in 17 of 32 cells. Occurrence of tachyphylaxis was sometimes altered after bilateral cervical vagotomy. The projection sites in the caudal medulla and thalamus were similar for responsive and nonresponsive cells. Laminar cell locations in the spinal cord had no significant influence on likelihood of cell response to bradykinin. We conclude that spinoreticular and spinothalamic cells have a role in transmitting noxious information from the heart to the brain.

Left vagal stimulation induces dynorphin release and suppresses substance P release from the rat thoracic spinal cord during cardiac ischemia

“…1. Compared with the in vitro control probe (Fig 1F), a probe inserted into the T 4 spinal cord during rest periods shows a less dense image from its tip to ϳ1.5-2.0 mm from its tip (Fig. 1A), indicating inhibition in binding of radiolabeled Dyn along this part of the probe.…”

“…The cell bodies of these afferents are found in the dorsal root ganglia of spinal segments C 8 -T 9 (cervical 8-thoracic 9), with the majority associated with spinal segments T 2 -T 6 (29) and project mainly to laminae I, V, VII, and X (29). Activated cardiac sympathetic afferent fibers excite cells in the spinal thalamic tract (STT) primarily in T 1 -T 6 spinal segments (4,41) and C 1 -C 2 segments (8), as well as other ascending tracts, including the spinoreticular, spinomesencephalic, and spinosolitary tracts (16).…”

Responses of thoracic spinal neurons to activation and desensitization of cardiac TRPV1-containing afferents in rats

“…Physiological and pharmacological studies show that BK activates cardiac nociceptors and sympathoexcitatory responses via kinin B2 receptors located in thinly myelinated A␦ and unmyelinated C-fiber afferent endings in the heart (1,23,39,40). The afferent fibers transmitting the action potentials enter the upper thoracic spinal cord where spinal neurons, spinothalamic tract cells, spinoreticular tract, and other ascending pathway neurons process this information (2)(3)(4)(5)(6)27). However, the signaling mechanisms involved in detection of myocardial ischemia and activation of cardiac sympathetic or spinal afferent nerve endings are not fully known.…”

C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons

“…A number of reports demonstrate the presence of both DYN-ergic fiber endings and cell bodies within the spinal cord (7,31,40) and show opiates, including DYN, reduce transmitter release from nociceptive primary afferents, especially SPcontaining sites (22,29,(37)(38)(39). This correlates with the fact that high cervical SCS decreases thoracic spinothalamic tract neuronal electrical activity, one of the major pathways that conduct the ischemic afferent signal to higher centers (6,13,14,25,28,33). Since both types of electromodulation, vagal and spinal cord stimulation, excite neurons in the upper cervical spinal cord (1,13,14,25,28), we hypothesize that the irDYN released in the thoracic dorsal horn sites is involved with the anti-nociceptive effects of electroneuromodulation.…”