Aparticularly intense painful stimulus enhances the sensation evoked by subsequent noxious stimuli. This hyperalgesia may result from facilitation of sensory neurotransmission in the spinal cord, perhaps by mechanisms similar to synaptic plasticity in other pathways. In this week's Journal, Larsson and Broman used immunolabeling of calcium/calmodulin-dependent kinase II (CaMKII) to track the associated modulation of spinal cord pathways. The translocation of autophosphorylated CaMKII to the postsynaptic density makes it one marker of synaptic plasticity. The authors injected rat hindpaws with capsaicin to induce hyperalgesia. Transganglionic tracing of the capsaicin injection site marked the nonpeptidergic class of nociceptors, but not peptidergic nociceptive neurons that express substance P and calcitonin generelated peptide. Phosphorylated CaMKII more than doubled in dorsal horn synapses formed by peptidergic neurons and fell by about one-half in synapses formed by labeled, nonpeptidergic neurons. In low-threshold mechanoreceptor neurons, CaMKII expression did not change with capsaicin treatment.
2. D1, GAD, and Working Memory
Nobuhide Kobori and Pramod K. Dash
Kobori and Dash examined deficits in working memory after a mild concussive brain injury that did not cause overt neuronal loss. The authors targeted the medial prefrontal cortex (mPFC), known to be important for working memory (WM). Rats performed a delay match-to-place task, in which they escaped a water maze to a hidden platform (the location trial), were removed from the maze, and then relocated the platform (the match trial). Brain-injured rats displayed a random search pattern during the match trial indicative of impaired WM. The memory deficits were associated with neurochemical changes in mPFC, including higher levels of D1 dopamine receptors and more neurons detected by immunola
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