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Altered long-term synaptic plasticity and kainate-induced Ca 2+ transients in the substantia gelatinosa neurons in GLU K6 -deficient mice

Molecular Brain Research, ISSN: 0169-328X, Vol: 142, Issue: 1, Page: 9-18
2005
  • 12
    Citations
  • 0
    Usage
  • 10
    Captures
  • 0
    Mentions
  • 0
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    12
    • Citation Indexes
      12
  • Captures
    10

Article Description

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 Ca 2+ 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.

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