Pain
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Comparative Study
Social networks and pain interference with daily activities in middle and old age.
Social networks have emerged as important in the development and progression of disability in aging cohorts. We have previously reported that pain that interferes with daily activities is common and increases incrementally from middle age into later life. The current study has investigated whether pain interference in this age group is related to social network characteristics. 5215 community-dwelling adults aged 50 years and over participating in the North Staffordshire Osteoarthritis Project (NorStOP) and identified as currently experiencing pain formed the sample for the present analysis. ⋯ The associations with close friends and children were reduced but remained significant after adjusting for sociodemographic factors. The association with close friends became non-significant after adjusting for depression suggesting this may form part of the pathway linking close friends networks and pain interference. Pain-related interference shows similar associations with social networks as all-cause disability and may benefit similarly from a public health perspective.
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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.