Fig. 7: Optogenetic activation of the ACC induced pain behavior in the contralateral hind paw in nerve-injured mice, whereas inhibition relieved pain. | Communications Biology

Fig. 7: Optogenetic activation of the ACC induced pain behavior in the contralateral hind paw in nerve-injured mice, whereas inhibition relieved pain.

From: Activation of the glutamatergic cingulate cortical-cortical connection facilitates pain in adult mice

Fig. 7: Optogenetic activation of the ACC induced pain behavior in the contralateral hind paw in nerve-injured mice, whereas inhibition relieved pain.The alternative text for this image may have been generated using AI.

a Schematic of bilateral ACC injection of AAV-hSyn-ChR2-EYFP and implantation of optic fibers in mice. b Blue light activation of right ACC significantly decreased left hind paw withdrawal threshold, and activation of left ACC significantly decreased right hind paw withdrawal threshold in mice (n = 8 mice, p < 0.05 for BL versus right ACC-ChR2 of left hind paw, p < 0.05 for BL versus left ACC-ChR2 of right hind paw). c Blue light activation of left or right ACC significantly decreased response latency of hot plate test in mice (n = 8 mice, p < 0.01 for BL versus left ACC-ChR2, p < 0.001 for BL versus left ACC-ChR2). d Schematic of bilateral ACC injection of AAV-hSyn-eNpHR-mCherry and implantation of optic fibers in mice. e Yellow light inhibition of right ACC significantly increased the left hind paw withdrawal threshold, and inhibition of left ACC significantly increased the right hind paw withdrawal threshold in mice (n = 6 mice, p < 0.01 for BL versus right ACC-eNpHR of left hind paw, p < 0.01 for BL versus left ACC-eNpHR of right hind paw). f Yellow light inhibition of left or right ACC significantly increased response latency of hot plate test in mice (n = 6 mice, p < 0.05 for BL versus left ACC-eNpHR, p < 0.05 for BL versus left ACC-eNpHR). g Experimental timeline of the nerve injury and behavior tests in mice. h Schematic diagram of the pain model of spared nerve injury in mice. i Compared with the sham group, the mechanical threshold of the ipsilateral hind paw with injury was significantly reduced in the nerve injury group (Sham, n = 8 mice, Nerve injury, n = 11 mice, for Sham versus Nerve injury, p < 0.001 for 3 d, 7 d, 14 d, and 28 d). j Blue light evoked-activation of ipsilateral or contralateral ACC after nerve injury did not affect the withdrawal threshold of the ipsilateral hind paw (n = 11 mice). k Yellow light inhibition of right ACC significantly increased the withdrawal threshold of the ipsilateral hind paw 3, and 7 days after nerve-injured in mice (n = 5 mice, for Nerve injury versus Nerve injury + right ACC-eNpHR, p < 0.05 for 3d and 7 d). l Compared with the sham group, the mechanical threshold of the contralateral hind paw with injury was significantly reduced in the nerve injury group (Sham, n = 8 mice; Nerve injury, n = 11 mice, for Sham versus Nerve injury, p < 0.05 for 7 d, 14 d, and 28 d). m Blue light activation of ipsilateral ACC significantly decreased the contralateral hind paw withdrawal threshold 14, and 28 days after nerve-injured in mice (n = 11 mice, for Nerve injury versus Nerve injury + left ACC-ChR2, p < 0.05 for 14 d, p < 0.01 for 28 d). n Yellow light inhibition of ipsilateral ACC significantly increased the withdrawal threshold of the contralateral hind paw 3, 7, 14, and 28 days after nerve-injured in mice (n = 5 mice, for Nerve injury versus Nerve injury + left ACC-eNpHR, p < 0.05 for 3 d, 7 d, 14 d, and 28 d). Error bars represent SEM, *indicates significant difference (*p < 0.05, **p < 0.01, ***p < 0.001). ACC anterior cingulate cortex, BL baseline.

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