scholarly journals Inhibition of electroacupuncture on nociceptive responses of dorsal horn neurons evoked by noxious colorectal distention in an intensity-dependent manner

2019 ◽  
Vol Volume 12 ◽  
pp. 231-242 ◽  
Author(s):  
Lingling Yu ◽  
Wei Wang ◽  
Liang Li ◽  
Qingguang Qin ◽  
Yutian Yu ◽  
...  
2005 ◽  
Vol 94 (6) ◽  
pp. 3788-3794 ◽  
Author(s):  
Gexin Wang ◽  
Bin Tang ◽  
Richard J. Traub

Previous studies suggest the lumbosacral (LS) spinal cord processes acute colorectal stimuli whereas the thoracolumbar (TL) and LS spinal segments process inflammatory stimuli. In this study, the effects of colorectal distention (CRD) on TL and LS dorsal horn neuronal activity were recorded in Nembutal-anesthetized male rats both with and without colonic inflammation. Both single cells (before and after inflammation) and populations (multiple cells from noninflamed or inflamed rats) were studied. CRD-responsive neurons had excitatory Abrupt (on–off with stimulus) or Sustained (prolonged after discharge) responses or were Inhibited by CRD. In noninflamed rats, a significantly greater percentage of LS neurons (63% Abrupt, 27% Sustained) were excited by CRD than TL neurons (61% Abrupt, 3% Sustained). The remaining cells were Inhibited (10% LS, 36% TL). LS Abrupt neurons had lower thresholds and greater response magnitudes to CRD compared with TL Abrupt neurons. After colonic inflammation, TL neurons became more excitable: the percentage of Inhibited neurons decreased, the response magnitude of Abrupt neurons increased, and the threshold decreased. In contrast, in single-cell recordings, the response of LS Sustained neurons increased, whereas LS Abrupt neurons decreased. These data suggest that in noninflamed rats, the net response to CRD of TL visceroceptive spinal sensory neurons is less than that of LS neurons. Colonic inflammation increases the net response of TL neurons and differentially modulates the response of LS neurons. These differences may contribute to the functional dichotomy between the TL and LS spinal segments in processing acute and inflammatory colorectal pain.


2010 ◽  
Vol 483 (1) ◽  
pp. 83
Author(s):  
Gerardo Rojas-Piloni ◽  
Rosalinda Mejía-Rodríguez ◽  
Guadalupe Martínez-Lorenzana ◽  
Miguel Condés-Lara

2010 ◽  
Vol 476 (1) ◽  
pp. 32-35 ◽  
Author(s):  
Rojas-Piloni Gerardo ◽  
Mejía-Rodríguez Rosalinda ◽  
Martínez-Lorenzana Guadalupe ◽  
Condés-Lara Miguel

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Takahiro Masuda ◽  
Yui Ozono ◽  
Satsuki Mikuriya ◽  
Yuta Kohro ◽  
Hidetoshi Tozaki-Saitoh ◽  
...  

2001 ◽  
Vol 95 (1) ◽  
pp. 139-143 ◽  
Author(s):  
Bao-Gang Liu ◽  
Xin-Liang Zhuang ◽  
Shi-Tong Li ◽  
Guo-Hui Xu ◽  
Sorin J. Brull ◽  
...  

Background Local anesthetics, such as bupivacaine, have been reported to block calcium currents in primary sensory neurons and to interfere with the release of neurotransmitters in central nervous system neurons. However, it is unknown whether local anesthetics affect the calcium current activity of central nervous system neurons. Methods Using a traditional whole cell voltage clamp technique, effects of bupivacaine and ropivacaine on high-voltage-activated calcium currents (HVA-Ic(a)) were investigated in enzymatically dissociated dorsal horn neurons of neonatal rats. Calcium currents were evoked by testing pulses from a holding potential of -90 to 0 mV. Results Bupivacaine significantly reduced HVA-Ic(a) in a dose-dependent manner. The peak HVA-Ic(a) decreased by 24.5+/-2.5, 32.0+/-6.8, 59.4+/-6.2, 88.3+/-1.5, and 91.6+/-1.1% in response to 10, 30, 50, 100 and 200 microM bupivacaine, respectively. Unlike bupivacaine, ropivacaine markedly increased HVA-Ic(a) at lower concentrations (< 50 microM) but decreased HVA-Ic(a) at higher concentrations (> or = 50 microM). The percent increases in peak HVA-Ic(a) induced by 10 and 30 microM ropivacaine were 95+/-19.1 and 41.6+/-8.3%, respectively. The percent decreases in response to 50, 100, and 200 microM ropivacaine were 21.1+/-2.1, 63.2+/-6.0 and 79.1+/-7.6%, respectively. Results indicate that the inhibitory potency of ropivacaine on HVA-Ic(a) was significantly lower than that of bupivacaine at the same concentrations. Conclusions The current study showed that bupivacaine inhibited HVA-Ic(a) recorded from dorsal horn neurons and that ropivacaine increased HVA-Ic(a) at lower concentrations but decreased HVA-Ic(a) at higher concentrations. The inhibitory potency of ropivacaine was lower than that of bupivacaine. Inhibition of calcium currents of central nervous system neurons may be related to the systemic neurotoxic effects of local anesthetics (e.g., convulsions, seizures).


Neuroscience ◽  
2013 ◽  
Vol 250 ◽  
pp. 275-281 ◽  
Author(s):  
K. Nishida ◽  
K. Takechi ◽  
T. Akiyama ◽  
M.I. Carstens ◽  
E. Carstens

Neuroreport ◽  
2001 ◽  
Vol 12 (4) ◽  
pp. 797-801 ◽  
Author(s):  
Jaakko Kalmari ◽  
Sirkku Niissalo ◽  
Yrjö T. Konttinen ◽  
Antti Pertovaara

1997 ◽  
Vol 77 (5) ◽  
pp. 2831-2835 ◽  
Author(s):  
B. J. Workman ◽  
B. M. Lumb

Workman, B. J. and B. M. Lumb. Inhibitory effects evoked from the anterior hypothalamus are selective for the nociceptive responses of dorsal horn neurons with high- and low-threshold inputs. J. Neurophysiol. 77: 2831–2835, 1997. The aim of the present study was to examine the selectivity of descending control of nociceptive information in the spinal dorsal horn following neuronal activation at “pressor” sites in the anterior hypothalamus. Extracellular single-unit activity was recorded from 11 dorsal horn neurons in the lower lumbar spinal cord of anesthetized rats. Neurons selected for investigation were those that responded to noxious (pinch and radiant heat >46°C) and nonnoxious (prod, stroke, and/or brush) stimulation within their cutaneous receptive fields on the ipsilateral hind paw. These are referred to as Class 2 neurons. Micropipettes were inserted stereotaxically into the anterior hypothalamus at sites where injection of the excitatory amino acidl-homocysteic acid (l-HCA) evoked increases in arterial blood pressure. The effects of microinjection of l-HCA at “pressor” sites in the anterior hypothalamus were then tested on the responses of Class 2 neurons to noxious and nonnoxious stimulation of their excitatory receptive fields. The high-threshold (pinch and/or radiant heat) responses of 7/7 Class 2 neurons tested were inhibited by an average of 66.3 ± 8.8% (mean ± SE) by neuronal activation at hypothalamic pressor sites. The low-threshold (prod) responses of 10/10 Class 2 neurons tested were not inhibited by neuronal activation at hypothalamic pressor sites; in 6 of these cells the response to low-intensity stimulation was increased by between 4 and 20%. Control injections of the inhibitory amino acid γ-aminobutyric acid (GABA) at the same hypothalamic pressor sites had no significant effects on arterial blood pressure or neuronal activity. With regard to sensory processing in the spinal cord, these data suggest that descending inhibitory control that originates from neurons in pressor regions of the anterior hypothalamus is highly selective for nociceptive inputs to Class 2 neurons.


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