Expectations modulate long-term heat pain habituation.

Habituation to pain was shown to be a complex mechanism involving the pain encoding regions and the antinociceptive system in the brain. Pain perception can be modulated by cognitive factors; however it is unclear whether cognitive factors also influence habituation to pain. We used an established experimental design with repetitive moderate painful heat stimulation over eight consecutive days.

Insular cortex activity is associated with effects of negative expectation on nociceptive long-term habituation.

It is generally accepted that acute painful experience is influenced by context information shaping expectation and modulating attention, arousal, stress, and mood. However, little is known about the nature, duration, and extent of this effect, particularly regarding the negative expectation. We used a standardized longitudinal pain paradigm and painful heat test stimuli in healthy participants over a time course of 8 consecutive days, inducing nociceptive habituation over time.

Synaptic NR2A- but not NR2B-Containing NMDA Receptors Increase with Blockade of Ionotropic Glutamate Receptors.

NMDA receptors (NMDAR) are key molecules involved in physiological and pathophysiological brain processes such as plasticity and excitotoxicity. Neuronal activity regulates NMDA receptor levels in the cell membrane. However, little is known on which time scale this regulation occurs and whether the two main diheteromeric NMDA receptor subtypes in forebrain, NR1/NR2A and NR1/NR2B, are regulated in a similar fashion.

Contribution of hippocampal and extra-hippocampal NR2B-containing NMDA receptors to performance on spatial learning tasks.

Controversy revolves around the differential contribution of NR2A- and NR2B-containing NMDA receptors, which coexist in principal forebrain neurons, to synaptic plasticity and learning in the adult brain. Here, we report genetically modified mice in which the NR2B subunit is selectively ablated in principal neurons of the entire postnatal forebrain or only the hippocampus. NR2B ablation resulted in smaller NMDA receptor-mediated EPSCs with accelerated decay kinetics, as recorded in CA1 pyramidal cells.