Altered long-term synaptic plasticity and kainate-induced Ca super(2) super(+) transients in the substantia gelatinosa neurons in GLU sub(K) sub(6)-deficient mice

• Published in: Brain research. Molecular brain research. 2005-12, Vol.142 (1), p.9-18
• Main Authors: Youn, D H, Voitenko, N, Gerber, G, Park, Y K, Galik, J, Randic, M
• Format: Article
• Language: English
• ISSN: 0169-328X
• DOI: 10.1016/j.molbrainres.2005.09.004

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 sub(K) sub(5)) or GLU sub(K) sub(6) subunit, we here show that GLU sub(K) sub(6) subunit, but not GLU sub(K) sub(5) 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 sub(K) sub(6) subunit plays an important role in the expression of kainate-induced Ca super(2) super(+) transients in the substantia gelatinosa. On the other hand, genetic deletion of GLU sub(K) sub(5) or GLU sub(K) sub(6) 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.