Abstract
Itch and pain share similar mechanisms. It has been well documented that the anterior cingulate cortex (ACC) is important for pain-related perception. ACC has also been approved to be a potential pruritus-associated brain region. However, the mechanism of sensitization in pruriceptive neurons in the ACC is not clear. In current study, a chronic itch model was established by diphenylcyclopropenone (DCP) application. We found that both the frequency and amplitude of miniature excitatory postsynaptic currents in the ACC were enhanced after the formation of chronic itch. The paired-pulse ratio in ACC neurons recorded from the DCP group were smaller than those recorded in control group at the 50-ms interval. We also observe a significant increase in the AMPA/NMDA ratio in the DCP group. Moreover, an increased inward rectification of AMPARs in ACC pyramidal neurons was observed in the DCP group. Interestingly, the calculated ratio of silent synapses was significantly reduced in the DCP group compared with controls. Taken together, we conclude that a potentiation of synaptic transmission in the ACC can be induced by chronic itch, and unsilencing silent synapses, which probably involved recruitment of AMPARS, contributed to the potentiation of postsynaptic transmission.
Highlights
Itch is an uncomfortable sensation and emotional experience that strongly evokes a desire to scratch [1]
The DCP group showed significantly more scratching compared with the control group during the 7 days of treatment (Control group: 13.21 ± 1.26 bouts, n = 24 rats; DCP group: 40.14 ± 2.63 bouts, n = 28 rats, Mann-Whitney, rank sum test, p < 0.001; Fig. 1c)
We recorded Miniature excitatory postsynaptic currents (mEPSCs) of pyramidal neurons in layers II/III of the anterior cingulate cortex (ACC), and found an obvious increase in the frequency of mEPSCs in the DCP group compared with the control group (Control: 1.56 ± 0.14 Hz, n = 12 neurons/5 rats; DCP: 2.87 ± 0.30 Hz, n = 12 neurons/5 rats, p < 0.001, t test; Fig. 2b, c)
Summary
Itch is an uncomfortable sensation and emotional experience that strongly evokes a desire to scratch [1]. Itch is caused by skin disease and systemic, neuropathic, psychogenic and cutaneous disorders [2]. Neuroimaging studies in humans have confirmed the anterior cingulate cortex (ACC), along with other cortical structures, are activated by itch [7, 8]. Descalzi et al showed that itching enhanced spontaneous excitatory post-synaptic currents in ACC pyramidal neurons [9]. Itch can be classified as either acute or chronic according to the course duration. Acute itch is a daily experience that can usually be abolished by briefly scratching near the
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