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The Journal of Neuroscience, December 3, 2008, 28(49):13331-13340; doi:10.1523/JNEUROSCI.3013-08.2008

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Cellular/Molecular
Tuning Thalamic Firing Modes via Simultaneous Modulation of T- and L-Type Ca²⁺ Channels Controls Pain Sensory Gating in the Thalamus

Eunji Cheong, Sukchan Lee, B. Jiwon Choi, Minjeong Sun, C. Justin Lee, and Hee-Sup Shin

Center for Neural Science, Korea Institute of Science and Technology, Seoul 136-791, Korea

Correspondence should be addressed to Dr. Hee-Sup Shin, Center for Neural Science, Korea Institute of Science and Technology, 39-1 Hawolgok-dong, Seongbuk-gu, Seoul 136-791, Korea. Email: shin{at}kist.re.kr

Two firing modes of thalamocortical (TC) neurons, tonic and burst firings, are thought to reflect the divergent states of sensory signal transmission from the thalamus to the cortex. However, the behavioral consequences of changes in the thalamic firing between the two modes have not been well demonstrated. Moreover, although the firing modes of TC neurons are known to be affected by corticothalamic inputs via thalamic metabotropic glutamate receptor type 1 (mGluR1)–phospholipase C β4 (PLCβ4) pathway, its molecular mechanisms have not been well elucidated. We addressed these questions using PLCβ4-deficient mice, which show decreased visceral pain responses. We demonstrate that burst and tonic firings of TC neurons are concomitantly regulated by PLCβ4 pathway. Blocking of this pathway by the mutation simultaneously increases bursting and decreases tonic firing of TC neurons through concurrent upregulation of T- and L-type Ca²⁺ currents. The mice with increased bursting and decreased tonic firing of TC neurons showed reduced visceral pain responses. Furthermore, we show that modulation of the Ca²⁺ channels or protein kinase C (PKC), a downstream molecule of PLCβ4, altered the firing modes of TC neurons and pain responses in the predicted ways. Our data demonstrate the molecular mechanism and behavioral consequences of altered firing modes of TC neurons in relaying the visceral pain signals. Our study also highlights the thalamic PLCβ4–PKC pathway as a "molecular switch" for the firing modes of TC neurons and thus for pain sensory gating.

Key words: thalamus; Ca²⁺ channels; phospholipase Cβ4; visceral pain; sensory gating; knock-out mice

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Received June 30, 2008; revised Oct. 1, 2008; accepted Oct. 8, 2008.

Correspondence should be addressed to Dr. Hee-Sup Shin, Center for Neural Science, Korea Institute of Science and Technology, 39-1 Hawolgok-dong, Seongbuk-gu, Seoul 136-791, Korea. Email: shin{at}kist.re.kr

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