In vivo patch-clamp analysis of sensory neuronal circuit in the rat superficial spinal dorsal horn

2004 ◽  
Vol 1269 ◽  
pp. 69-72 ◽  
Author(s):  
Hidemasa Furue ◽  
Go Kato ◽  
Ji Hoon Kim ◽  
Byung-Il Min ◽  
Toshihiko Katafuchi ◽  
...  
2019 ◽  
Vol Volume 12 ◽  
pp. 1269-1278 ◽  
Author(s):  
Motoki Sonohata ◽  
Atsushi Doi ◽  
Toshiharu Yasaka ◽  
Daisuke Uta ◽  
Masaaki Mawatari ◽  
...  

2000 ◽  
Vol 84 (4) ◽  
pp. 2171-2174 ◽  
Author(s):  
Keita Narikawa ◽  
Hidemasa Furue ◽  
Eiichi Kumamoto ◽  
Megumu Yoshimura

To know a functional role of inhibitory synaptic responses in transmitting noxious and innoxious information from the periphery to the rat spinal dorsal horn, we examined inhibitory postsynaptic currents (IPSCs) elicited in substantia gelatinosa (SG) neurons by mechanical stimuli applied to the skin using the newly developed in vivo patch-clamp technique. In the majority (80%) of SG neurons examined, a brush stimulus applied to the ipsilateral hind limb produced a barrage of IPSCs that persisted during the stimulus, while a pinch stimulus evoked IPSCs only at its beginning and end. The pinch-evoked IPSCs may have been caused by a touch that occurs at the on/off time of the pinch. The evoked IPSCs were blocked by either a glycine-receptor antagonist, strychnine (4 μM), or a GABAA-receptor antagonist, bicuculline (20 μM). All SG neurons examined received inhibitory inputs from a wide area throughout the thigh and lower leg. When IPSCs were examined together with excitatory postsynaptic currents (EPSCs) in the same neurons, a brush evoked a persistent activity of both IPSCs and EPSCs during the stimulus while a pinch evoked such an activity of EPSCs but not IPSCs. It is suggested that innoxious mechanical stimuli activate a GABAergic or glycinergic circuitry in the spinal dorsal horn. This inhibitory transmission may play an important role in the modulation of noxious information in the SG.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Miyuki Kurabe ◽  
Hidemasa Furue ◽  
Tatsuro Kohno

Abstract Intravenous lidocaine administration produces an analgesic effect in various pain states, such as neuropathic and acute pain, although the underlying mechanisms remains unclear. Here, we hypothesized that intravenous lidocaine acts on spinal cord neurons and induces analgesia in acute pain. We therefore examined the action of intravenous lidocaine in the spinal cord using the in vivo patch-clamp technique. We first investigated the effects of intravenous lidocaine using behavioural measures in rats. We then performed in vivo patch-clamp recording from spinal substantia gelatinosa (SG) neurons. Intravenous lidocaine had a dose-dependent analgesic effect on the withdrawal response to noxious mechanical stimuli. In the electrophysiological experiments, intravenous lidocaine inhibited the excitatory postsynaptic currents (EPSCs) evoked by noxious pinch stimuli. Intravenous lidocaine also decreased the frequency, but did not change the amplitude, of both spontaneous and miniature EPSCs. However, it did not affect inhibitory postsynaptic currents. Furthermore, intravenous lidocaine induced outward currents in SG neurons. Intravenous lidocaine inhibits glutamate release from presynaptic terminals in spinal SG neurons. Concomitantly, it hyperpolarizes postsynaptic neurons by shifting the membrane potential. This decrease in the excitability of spinal dorsal horn neurons may be a possible mechanism for the analgesic action of intravenous lidocaine in acute pain.


2009 ◽  
Vol 13 (S1) ◽  
Author(s):  
M. Gassner ◽  
M. Wagner ◽  
H. Fischer ◽  
R. Drdla ◽  
T. Jäger ◽  
...  

1999 ◽  
Vol 4 (2) ◽  
pp. 192-200 ◽  
Author(s):  
Henrik Gustafsson ◽  
Guilherme de Araujo Lucas ◽  
Eva Schött ◽  
Carl-Olav Stiller ◽  
Pawel Alster ◽  
...  

2012 ◽  
Vol 120 (2) ◽  
pp. 129-132 ◽  
Author(s):  
Alba Vidal-Torres ◽  
Alicia Carceller ◽  
Daniel Zamanillo ◽  
Manuel Merlos ◽  
Jos^|^eacute; Miguel Vela ◽  
...  

1996 ◽  
Vol 118 (8) ◽  
pp. 1875-1877 ◽  
Author(s):  
L.C. Stanfa ◽  
V. Chapman ◽  
N. Kerr ◽  
A.H. Dickenson

2021 ◽  
Vol 13 ◽  
Author(s):  
Austin Kearns ◽  
Jazmine Jayasi ◽  
Xin Liu ◽  
Jigong Wang ◽  
Yuqiang Shi ◽  
...  

Opioids are widely used for pain relief; however, chronic opioid use causes a paradoxical state of enhanced pain sensitivity, termed “Opioid-induced hyperalgesia (OIH).” Despite the clinical importance of OIH, the detailed mechanism by which it enhances pain sensitivity remains unclear. In this study, we tested whether repeated morphine induces a neuronal circuit polarization in the mouse spinal dorsal horn (SDH). Transgenic mice expressing GFP to neurokinin 1 receptor-expressing neurons (sNK1Rn) and GABAergic interneurons (sGABAn) that received morphine [20 mg/kg, once daily for four consecutive days (i.p.)] developed mechanical hypersensitivity. Repeated morphine altered synaptic strengths in the SDH as a specific cell-type but not in a gender-dependent manner. In sNK1Rn and non-tonic firing neurons, repeated morphine treatment significantly increased frequency of spontaneous excitatory postsynaptic current (sEPSC) and evoked EPSC (eEPSC). In addition, repeated morphine treatment significantly decreased evoked inhibitory postsynaptic current (eIPSC) in sNK1Rn. Conversely, in sGABAn and tonic firing neurons, repeated morphine treatment significantly decreased sEPSC frequency and eEPSC, but had no change of eIPSC in sGABAn. Interestingly, repeated morphine treatment significantly decreased neuronal rheobase of sNK1Rn but had no effect on sGABAn. These findings suggest that spinal neuronal circuit polarization maybe the mechanism of OIH and identify a potential therapeutic mechanism to prevent or treat opioid-induced pain.


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