Cutaneous Afferent Stimulation for the Relief of Pain

Author(s):  
D. M. Long
Keyword(s):  
2003 ◽  
Vol 94 (1) ◽  
pp. 220-226 ◽  
Author(s):  
Weirong Zhang ◽  
Paul W. Davenport

It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
K. Agashkov ◽  
V. Krotov ◽  
M. Krasniakova ◽  
D. Shevchuk ◽  
Y. Andrianov ◽  
...  

AbstractLamina I spino-parabrachial neurons (SPNs) receive peripheral nociceptive input, process it and transmit to the supraspinal centres. Although responses of SPNs to cutaneous receptive field stimulations have been intensively studied, the mechanisms of signal processing in these neurons are poorly understood. Therefore, we used an ex-vivo spinal cord preparation to examine synaptic and cellular mechanisms determining specific input-output characteristics of the neurons. The vast majority of the SPNs received a few direct nociceptive C-fiber inputs and generated one spike in response to saturating afferent stimulation, thus functioning as simple transducers of painful stimulus. However, 69% of afferent stimulation-induced action potentials in the entire SPN population originated from a small fraction (19%) of high-output neurons. These neurons received a larger number of direct Aδ- and C-fiber inputs, generated intrinsic bursts and efficiently integrated a local network activity via NMDA-receptor-dependent mechanisms. The high-output SPNs amplified and integrated the nociceptive input gradually encoding its intensity into the number of generated spikes. Thus, different mechanisms of signal processing allow lamina I SPNs to play distinct roles in nociception.


Neonatology ◽  
1978 ◽  
Vol 34 (3-4) ◽  
pp. 187-198 ◽  
Author(s):  
P.M. Gootman ◽  
N.M. Buckley ◽  
N. Gootman ◽  
L.A. Crane ◽  
B.J. Buckley

1999 ◽  
Vol 277 (4) ◽  
pp. H1311-H1316 ◽  
Author(s):  
David C. Merrill ◽  
Jeffrey L. Segar ◽  
Oliva J. McWeeny ◽  
Jean E. Robillard

Previous work in our laboratory has demonstrated impairment of cardiopulmonary reflex control of renal sympathetic nerve activity (RSNA) during the newborn period. The present study was designed to test the hypothesis that this delayed maturation is secondary to incomplete central integration of vagal afferent input. Term fetal (135–140 days; n = 6), newborn (3–7 days of age; n = 8), and young adult (6–8 wk old; n = 8) sheep anesthetized with α-chloralose underwent vagal afferent nerve stimulation. All animals had undergone prior sinoaortic denervation to eliminate influences from the arterial baroreceptors. After determination of optimal stimulation parameters, RSNA responses to gradual increases in stimulation frequency (1.0–16 Hz) were recorded and compared by one-way ANOVA. RSNA decreased progressively with increased frequency of stimulation in all three groups of animals. When comparing the three groups at any given frequency of stimulation, reflex withdrawal of RSNA tended to be more pronounced in newborn lambs ( P< 0.05 for 1 and 4 Hz). Heart rate (HR) was also noted to decrease significantly with vagal afferent stimulation in each of the groups, but no significant differences in the reflex decreases in HR were noted among the three groups of animals. These results demonstrate that central integration of vagal afferent input is intact in fetal and newborn sheep. These results suggest that the delayed maturation of cardiopulmonary reflex-mediated changes in RSNA seen early in development appears to depend on intrinsic alterations in baroreceptor function rather than incomplete central integration.


2004 ◽  
Vol 91 (6) ◽  
pp. 2413-2421 ◽  
Author(s):  
Yu-Zhen Pan ◽  
Hui-Lin Pan

Spinal lamina II (substantia gelatinosa) neurons play an important role in processing of nociceptive information from primary afferent nerves. Anatomical studies suggest that neurons in the outer (lamina IIo) and inner (lamina IIi) zone of lamina II receive distinct afferent inputs. The functional significance of this preferential afferent termination in lamina II remains unclear. In this study, we examined the differential synaptic inputs to neurons in lamina IIo and IIi in response to primary afferent stimulation. Whole cell voltage-clamp recordings were performed on neurons in lamina IIo and IIi of the rat spinal cord slice under visual guidance. Capsaicin (1 μM) significantly increased the frequency of glutamatergic miniature excitatory postsynaptic currents (mEPSCs) in all 27 lamina IIo neurons and significantly increased the amplitude of mEPSCs in 12 of 27 lamina IIo neurons. However, capsaicin only significantly increased the frequency of mEPSCs in 9 of 22 (40.9%) lamina IIi neurons and increased the amplitude of mEPSCs in 6 of these 9 neurons. Furthermore, the peak amplitude of EPSCs, evoked by electrical stimulation of the attached dorsal root, in 40 lamina IIo neurons was significantly greater than that [160.5 ± 16.7 vs. 87.0 ± 10.4 (SE) pA] in 37 lamina IIi neurons. On the other hand, the peak amplitude of evoked inhibitory postsynaptic currents (IPSCs) in 40 lamina IIo neurons was significantly smaller than that (103.1 ± 11.6 vs. 258.4 ± 24.4 pA) in 37 lamina IIi neurons. In addition, the peak amplitudes of both EPSCs and IPSCs, evoked by direct stimulation of lamina II, were similar in lamina IIo and IIi neurons. This study provides new information that stimulation of primary afferents differentially potentiates synaptic inputs to neurons in lamina IIo and IIi. The quantitative difference in excitatory and inhibitory synaptic inputs to lamina IIo and IIi neurons may be important for integration of sensory information from primary afferent nerves.


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