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
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...