Pain
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Comparative Study
In vivo recruitment by painful stimuli of AMPA receptor subunits to the plasma membrane of spinal cord neurons.
The persistent increase in pain sensitivity observed after injury, known as hyperalgesia, depends on synaptic plasticity in the pain pathway, particularly in the spinal cord. Several potential mechanisms have been proposed, including post-synaptic exocytosis of the AMPA subclass of glutamate receptors (AMPA-R), which is known to play a critical role in synaptic plasticity in the hippocampus. AMPA-R trafficking has been described in spinal neurons in culture but it is unknown if it can also occur in spinal neurons in vivo, or if it can be induced by natural painful stimulation. ⋯ Brefeldin-A, an antibiotic that inhibits exocytosis of proteins, not only prevented GluR1 trafficking to the membrane but also inhibited referred hyperalgesia in capsaicin-treated mice. Our results show that delivery of GluR1 AMPA receptor subunits to the cell membrane through a CaMKII activity-dependent exocytotic regulated pathway contributes to the development of hyperalgesia after a painful stimulus. We conclude that AMPA-R trafficking contributes to the synaptic strengthening induced in the pain pathway by natural stimulation.
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Comparative Study
The effects of acute and chronic restraint stress on activation of ERK in the rostral ventromedial medulla and locus coeruleus.
Extracellular signal-regulated kinase (ERK) is a key molecule in numerous cellular and physiological processes in the CNS. Exposure to stressors causes substantial effects on the perception and response to pain. The rostral ventromedial medulla (RVM) and the locus coeruleus (LC) play crucial roles in descending pain modulation system. ⋯ Protein levels of tryptophan hydroxylase were significantly increased in the RVM region in the 3-week restraint rats. On the other hand, the chronic restraint stress significantly decreased p-ERK-IR in the LC [P<0.05]. These findings suggest that chronic restraint stress-induced activation of ERK in the RVM and the suppression in the LC may be involved in the modulation of the pain threshold by chronic stress.