Showing papers by "Peter W. Reeh published in 1997"
TL;DR: It is suggested that inflammatory mediators may act to modulate ionic channels, that are operated by protons, possibly via intracellular second messenger action.
61 citations
TL;DR: Responsiveness of neurons in the caudal nucleus of the trigeminal brain stem to inflammatory mediators may play a role in the generation and maintenance of headache, e.g., migraine.
Abstract: Ebersberger, A., M. Ringkamp, P. W. Reeh, and H. O. Handwerker. Recordings from brain stem neurons responding to chemical stimulation of the subarachnoid space. J. Neurophysiol. 77: 3122–3133, 1997...
54 citations
TL;DR: The decreased RSNA in the absence of cardiac and abdominal vagal afferents and the strong response of 20% of pulmonary single fibers to intravenous PBG suggest that pulmonary fibers play a role in a 5-HT3 serotenergic reflex, suggesting pulmonary serotonin could influence the neural control of renal function.
Abstract: Cardiopulmonary reflexes with vagal afferents may control volume homeostasis by influencing renal nerve activity. Such reflexes can be stimulated mechanically and chemically, e.g., by serotonin 5-HT). We have demonstrated that stimulation of epicardial 5-HT3 receptors inhibits renal sympathetic nerve activity (RSNA) by a cardiorenal reflex. We now tested the hypothesis that pulmonary 5-HT3-sensitive vagal afferent fibers participate in the control of renal nerve activity. Two sets of experiments were performed. First, the responses of multifiber RSNA, heart rate (HR), and blood pressure (BP) to the 5-HT3-receptor agonist phenylbiguanide (PBG; 10 microg iv) were recorded in the presence of intact pulmonary afferents. Abdominal afferents were removed by subdiaphragmatic vagotomy. Cardiac afferents were blocked by intrapericardial injection of 10% procaine. Second, the responses of 25 single vagal pulmonary afferent C fibers to PBG were assessed. PBG decreased BP, HR, and RSNA (-90 +/- 8%). When cardiac afferents were blocked by procaine, BP and HR failed to decrease in response to PBG; however, the RSNA decrease was still -48 +/- 8%. Single fibers generally responded to PBG by a slight increase in firing rate. A distinct subset of fibers (5 of 25) showed an activity increase of >15 Hz that preceded changes in BP and HR. The decreased RSNA in the absence of cardiac and abdominal vagal afferents and the strong response of 20% of pulmonary single fibers to intravenous PBG suggest that pulmonary fibers play a role in a 5-HT3 serotenergic reflex. Thus pulmonary serotonin could influence the neural control of renal function.
27 citations
TL;DR: Neither indurations nor hyperalgesia could be detected at the injection sites of serum or vehicle, and the pathophysiological significance of this new inflammatory model for the research of posttraumatic hyperalGESia is discussed.
25 citations
TL;DR: It is suggested that methylene blue studies with excitable cells or tissues need to be interpreted with caution, as the impeded sodium inactivation together with the blockade of potassium currents may contribute to the depolarization and discharge activity observed in primary afferents in vitro as well as in dissociated sensory neurons in culture.
Abstract: The dye methylene blue is known as a blocker of guanylyl cyclase and it has been widely used to deplete cells of internal cyclic GMP. The data presented demonstrate an activation of adult rat sensory neurons by methylene blue via a photosensitive mechanism. In single fiber recordings from primary afferents of the rat skin in vitro, methylene blue, applied to the receptive field, induced discharge activity: 2/2 Aβ-, 2/4 Aδ- and 5/7 C-fibers showed significantly enhanced firing upon 10 μM methylene blue in the presence of light, whereas the dye was ineffective when illumination was prevented. In whole cell current clamp experiments with dissociated dorsal root ganglion neurons, 100 μM methylene blue was ineffective in the dark but evoked a membrane depolarization of 15.3 ± 3.5 mV (n = 5) accompanied by discharge activity upon illumination. In whole cell voltage clamp experiments, methylene blue (100 μM) caused a significant slowing of the inactivation of voltage-dependent sodium currents. In addition, an inhibition of fast and slow outward currents was observed with prolonged exposure. The impeded sodium inactivation together with the blockade of potassium currents may contribute to the depolarization and discharge activity observed in primary afferents in vitro as well as in dissociated sensory neurons in culture. We therefore suggest that methylene blue studies with excitable cells or tissues need to be interpreted with caution.
17 citations
TL;DR: The results may help to explain aspirin's antinociceptive action and the role of prostaglandin synthesis inhibition is discussed.
Abstract: The effects of acetylsalicylic acid (ASA) and of salicylic acid (SA) on pH-induced nociceptor excitation were investigated in a rat skin-saphenous nerve preparation in vitro, where isolated receptive fields of identified single nerve fibers were superfused at the corium side with controlled solutions to test their chemosensitivity. A total of 133 unmyelinated mechano-heat-sensitive ('polymodal') C-fibers were superfused with an acidic solution (CO2-saturated synthetic interstitial fluid; pH 6.1) for at least 10 min. If fibers responded to the acid pH (n=89; 67%), ASA or SA was added after 10 min for a 10 min period in various concentrations (ASA: 10-5 up to 10-3 M; SA: 10-7 up to 10-3 M), and the pH stimulation was continued for at least another 15 min. In most cases, only one substance was applied at one concentration per fiber. A bell-shaped dose-response curve of reversible, weak effects on pH-induced discharge resulted from SA, with a maximum effect at 10-5 M (14% suppression, n=16, P<0.01); at 10-3 M an excitatory action of SA in acidic solution became apparent (17% increase in discharge, n=9, P= NS). The application of freshly dissolved ASA led to a linear dose-response curve, with a significant reduction in discharge rate (10-4 M: 12.4%, n=11, P<0.02; 10-3 M: 42%, n=10, P<0.03). The major reduction was irreversible within at least 26 min of wash-out. Before and after each experiment, the threshold to punctuate mechanical stimulation (von Frey) was determined and found not to be significantly altered with both ASA and SA. Plasma concentrations in the 10-4 M range are normally reached with therapeutic ASA doses and much higher concentrations have to be expected in acidic tissues. Our results may, thus, help to explain aspirin's antinociceptive action. The role of prostaglandin synthesis inhibition is discussed.
2 citations