Table 1 Studies performed on chronic pain in the ACC of mice
Chronic pain | ACC | References |
|---|---|---|
Inflammatory pain | Increased synaptic GluA1 subunits | Bie et al., 2011 |
Activation of mu opioid receptor inhibits the excitatory glutamatergic transmission | Zheng, 2010 | |
GluA1 but not GluA2 contributes to LTP | Toyoda et al., 2009 | |
Increased transmitter release and number of available vesicles | Toyoda et al., 2009 | |
Enhanced presynaptic glutamate release and neuronal cAMP | Wu et al., 2008 | |
Enhanced presynaptic neurotransmitter release | Zhao et al., 2006 | |
Inflammatory pain & Neuropathic pain | Long-term temporal imprecision of information coding | Li et al., 2014 |
Activation of Erk | Wei et al., 2008 | |
Neuropathic pain | Postsynaptic GluA1 accumulation | Chen et al., 2014 |
Long-term enhancement of cortical-spinal projecting cells | Chen et al., 2014 | |
Disinhibition of the ACC | Blom et al., 2014 | |
Long-term changes in spontaneous membrane-potential oscillations | Ning et al., 2013 | |
LTD impairment | Kang et al., 2012 | |
Activation of PKMζ | Li et al., 2010 | |
Reduced cannabinoid receptor 1 activity | Hoot et al., 2010 | |
Increased transmitter release | Toyoda et al., 2009 | |
Presynaptic and postsynaptic amplifications | Xu et al., 2008 | |
Bone cancer pain | LTD impairment | Chiou et al., 2012 |
Visceral pain | Facilitation of synaptic transmission | Wang et al., 2013 |
Increased expression of Fos in the CNS | Zhang et al., 2014 | |
Long-term enhancement of AMPA receptors in the ACC | This study |