Thalamic decoupling softens the blow

Low-voltage–activated T-type Ca²⁺ channels facilitate pain signaling in both peripheral pain receptors and in the spinal cord. They also stimulate thalamic burst firing, but whether these channels enhance or suppress nociceptive signal processing has been unclear. In October 3 Science, Daesoo Kim and colleagues from the Korea Institute of Science and Technology report a series of experiments indicating that T-type Ca²⁺ channels in the thalamus are activated by visceral pain signals and then inhibit the processing of these signals, thereby suppressing pain responses (Science, 302:117-119, October 3, 2003).

Kim et al. applied a range of sensory stimuli to mice lacking α1G-type Ca2+ channels (α1G-/-) and observed no difference between mutants and their wildtype littermates in response to thermal or mechanical stimuli, or in hyperalgesia to cutaneous pain. The authors then induced visceral pain by intraperitoneal (IP) injection of acetic acid or MgSO4 and observed stronger writhing responses, signifying pain, in ...