| First Author | Youn DH | Year | 2005 |
| Journal | Brain Res Mol Brain Res | Volume | 142 |
| Issue | 1 | Pages | 9-18 |
| PubMed ID | 16219388 | Mgi Jnum | J:104051 |
| Mgi Id | MGI:3611088 | Doi | 10.1016/j.molbrainres.2005.09.004 |
| Citation | Youn DH, et al. (2005) Altered long-term synaptic plasticity and kainate-induced Ca2+ transients in the substantia gelatinosa neurons in GLU(K6)-deficient mice. Brain Res Mol Brain Res 142(1):9-18 |
| abstractText | Functional kainate receptors are expressed in the spinal cord substantia gelatinosa region, and their activation contributes to bi-directional regulation of excitatory synaptic transmission at primary afferent synapses with spinal cord substantia gelatinosa neurons. However, no study has reported a role(s) for kainate receptor subtypes in long-term synaptic plasticity phenomena in this region. Using gene-targeted mice lacking glutamate receptor 5 (GLU(K5)) or GLU(K6) subunit, we here show that GLU(K6) subunit, but not GLU(K5) subunit, is involved in the induction of long-term potentiation of excitatory postsynaptic potentials, evoked by two different protocols: (1) high-frequency primary afferent stimulation (100 Hz, 3 s) and (2) low-frequency spike-timing stimulation (1 Hz, 200 pulses). In addition, GLU(K6) subunit plays an important role in the expression of kainate-induced Ca2+ transients in the substantia gelatinosa. On the other hand, genetic deletion of GLU(K5) or GLU(K6) subunit does not prevent the induction of long-term depression. These results indicate that unique expression of kainate receptors subunits is important in regulating spinal synaptic plasticity and thereby processing of sensory information, including pain. |
