TY - JOUR
T1 - Direct presynaptic regulation of GABA/glycine release by kainate receptors in the dorsal horn
T2 - An ionotropic mechanism
AU - Kerchner, Geoffrey A.
AU - Wang, Guo Du
AU - Qiu, Chang Shen
AU - Huettner, James E.
AU - Zhuo, Min
N1 - Funding Information:
We wish to thank Timothy J. Wilding for technical assistance as well as Joe Henry Steinbach and Charles F. Zorumski for helpful discussions. This work was supported by NIH grants NS38680 and NS30888.
PY - 2001/11/8
Y1 - 2001/11/8
N2 - In the spinal cord dorsal horn, excitatory sensory fibers terminate adjacent to interneuron terminals. Here, we show that kainate (KA) receptor activation triggered action potential-independent release of GABA and glycine from dorsal horn interneurons. This release was transient, because KA receptors desensitized, and it required Na+ entry and Ca2+ channel activation. KA modulated evoked inhibitory transmission in a dose-dependent, biphasic manner, with suppression being more prominent. In recordings from isolated neuron pairs, this suppression required GABAB receptor activation, suggesting that KA-triggered GABA release activated presynaptic GABAB autoreceptors. Finally, glutamate released from sensory fibers caused a KA and GABAB receptor-dependent suppression of inhibitory transmission in spinal slices. Thus, we show how presynaptic KA receptors are linked to changes in GABA/glycine release and highlight a novel role for these receptors in regulating sensory transmission.
AB - In the spinal cord dorsal horn, excitatory sensory fibers terminate adjacent to interneuron terminals. Here, we show that kainate (KA) receptor activation triggered action potential-independent release of GABA and glycine from dorsal horn interneurons. This release was transient, because KA receptors desensitized, and it required Na+ entry and Ca2+ channel activation. KA modulated evoked inhibitory transmission in a dose-dependent, biphasic manner, with suppression being more prominent. In recordings from isolated neuron pairs, this suppression required GABAB receptor activation, suggesting that KA-triggered GABA release activated presynaptic GABAB autoreceptors. Finally, glutamate released from sensory fibers caused a KA and GABAB receptor-dependent suppression of inhibitory transmission in spinal slices. Thus, we show how presynaptic KA receptors are linked to changes in GABA/glycine release and highlight a novel role for these receptors in regulating sensory transmission.
UR - http://www.scopus.com/inward/record.url?scp=0035829686&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(01)00479-2
DO - 10.1016/S0896-6273(01)00479-2
M3 - Article
C2 - 11709158
AN - SCOPUS:0035829686
SN - 0896-6273
VL - 32
SP - 477
EP - 488
JO - Neuron
JF - Neuron
IS - 3
ER -