Impairment of afferent synaptic inputs for mechanical and cold sensation to substantia gelatinosa neurons of the rat spinal dorsal horn through cadherin-8 expressing synaptic glomeruli

2007 ◽  
Vol 58 ◽  
pp. S71
Author(s):  
Hidemasa Furue ◽  
Sachihiro S.C. Suzuki ◽  
Kohei Koga ◽  
Mitsuo Nohmi ◽  
Masatoshi Takeichi ◽  
...  
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.


Neuroscience ◽  
2005 ◽  
Vol 134 (2) ◽  
pp. 595-604 ◽  
Author(s):  
A. Miyakawa ◽  
H. Furue ◽  
T. Katafuchi ◽  
N. Jiang ◽  
T. Yasaka ◽  
...  

2017 ◽  
Vol 380 ◽  
pp. 205-211 ◽  
Author(s):  
Daisuke Uta ◽  
Du-Jie Xie ◽  
Tsuyoshi Hattori ◽  
Ken-ichi Kasahara ◽  
Megumu Yoshimura

Pain ◽  
2000 ◽  
Vol 85 (3) ◽  
pp. 385-393 ◽  
Author(s):  
Minako Iyadomi ◽  
Ikuo Iyadomi ◽  
Eiichi Kumamoto ◽  
Katsumaro Tomokuni ◽  
Megumu Yoshimura

2009 ◽  
Vol 101 (4) ◽  
pp. 2041-2051 ◽  
Author(s):  
Hui Nie ◽  
Han-Rong Weng

Activation of N-methyl-d-aspartate (NMDA) receptors in the spinal dorsal horn neurons is a key process related to sensory transmission, neural plasticity, and pathogenesis of pain. In this study, we investigated how activation of NMDA receptors in spinal substantia gelatinosa neurons is regulated by glutamate re-uptake through glutamate transporters located in the astrocytic and neuronal plasma membranes. Using visualized whole cell patch recording techniques, NMDA excitatory postsynaptic currents evoked by graded peripheral inputs in spinal substantia gelatinosa neurons of spinal slices from young adult rats were analyzed before and after combined inhibition of glial and neuronal glutamate transporters by d-threo-β-benzyloxyaspartate (TBOA). Blockade of glutamate transporters increased the number and duration of NMDA receptors activated by weak and by strong primary afferent inputs as well as by exogenous glutamate. The enhancement in activation of NMDA receptors induced by TBOA was greater in neurons that have weaker synaptic input at baseline. Impaired glutamate uptake increased the open probability of NMDA channels and caused glutamate spillover outside the active synapses, leading to activation of extrasynaptic NMDA receptors and/or receptors located in neighboring synapses. Finally, blockade of glutamate transporters resulted in an increased proportion of NR2B subunit activation induced by peripheral input, and this increase was further augmented by stronger afferent input. These data indicate that glutamate transporters regulate spatiotemporal and intensity coding for sensory input and prevent excessive activation of glutamate receptors in the spinal dorsal horn. It is suggested that remedying dysfunctional glutamate transporters may be a potential new avenue to prevent the pathogenesis of pain.


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