For feature-based magnitude coding, we calculated ARed – ABlue, where ARed and ABlue indicate the activity Bioactive Compound Library rates for trials when the red or blue stimuli, respectively, appeared farther from the reference point. Analogous differences were calculated for the duration task. In the matching task, we calculated only ARed – ABlue. Figure S4 presents normalized preference indices in the form of contrast ratios: (ARed – ABlue)/(ARed + ABlue) or (AS2 – AS1)/(AS2 + AS1). We also used population activity averages to assess the magnitude of coding. We designated the condition associated

with the highest discharge rate (e.g., S2 longer or farther) as the preferred condition and the one with the lowest activity as the antipreferred condition, and we calculated the population averages as the means of separately calculated single-cell averages, along with the SEM. Near the end of recording, we made electrolytic marking lesions (15 μA for 10 s). Ten days later, the monkeys were deeply anesthetized selleck chemicals and perfused with 10% formol saline. We plotted recording sites on coronal Nissl-stained sections, by reference to the recovered marking lesions, pins inserted during the perfusion, and structural magnetic resonance images. Although the entry points for more posterior recordings (Figure 1D) make it appear that many cells were located in the postarcuate cortex, track reconstructions based on the

angle and depth of penetrations indicated

that nearly all recordings in caudal PF came from Fossariinae the prearcuate cortex, which corresponds to area 8. This work was supported by the Division of Intramural Research of the NIMH (Z01MH-01092) and by Grants-in-Aid to S.T. from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) (23119714) and the Japanese Society for the Promotion of Science (JSPS) (22700340) in Japan. We thank Dr. Andrew Mitz, Mr. James Fellows, and Ms. Ping-yu Chen for technical support. “
“Loss of spinal cord dorsal horn inhibitory circuits, many of which involve interneurons that express gamma aminobutyric acid (GABA), is one of the major contributors to the persistent neuropathic pain that can follow nerve injury. The loss of inhibition contributes not only to the development of spontaneous pain but also to the hyperexcitability that underlies the mechanical hypersensitivity (allodynia) and exacerbated pain (hyperalgesia). For example, partial sciatic nerve injury reduces spinal GABA release and expression of the GABA-synthesizing enzyme glutamic acid decarboxylase (GAD; Moore et al., 2002). The consequence of this is a loss of inhibitory tone in the dorsal horn. It is not clear, however, whether the reduced GABAergic inhibition results from injury-induced degeneration of GABAergic interneurons (Scholz et al., 2005 and Sugimoto et al., 1990), reduced primary afferent input to these interneurons (Kohno et al.