, 2009) to compensate
for the individual differences using a nonrigid mapping software, JIP. Data were analyzed as described above for individual monkeys. Two ROIs were then defined in left and right TEpv between A0 and A4 in or on the lateral bank of the OTS, by taking all the voxels selectively more active for Learned symbols than for Untrained shapes and Faces within this subregion (114 voxels). Software for stimulus presentation BMS-754807 price and reward delivery was developed in-house and was written in C++. All experiments were done in accordance with procedures approved by the Harvard Medical School Standing Committee on Animals. This work was supported by NIH grant EY16187. We thank Wim Vanduffel for much help developing scanning technology, Tristram Savage for monkey training, and Winrich Freiwald, Doris Tsao, and Heather Sternshein for advice and comments. “
“(Neuron 68, 473–487; November 4, 2010) In the Supplemental Experimental Procedures related to this article, we erroneously stated that the patch-pipette solution
used for Ca2+-uncaging experiments contained, among other ingredients, 110 mM Cs-glutamate and 20 mM Cs-HEPES. This is incorrect. Instead, we used 110 mM K-gluconate and 20 mM K-HEPES. We apologize for this error. “
“(Neuron 73, 35–43; January 12, 2012) In the legend of Figure 4E, the statement “Values above 0 represent higher expression in PV than SST” should have been “Values above 0 represent higher expression in C59 wnt SST than PV.” This has now been corrected in the article online, and we regret the error. “
“The treatment of schizophrenia has relied heavily on antipsychotic drugs (APDs) that primarily impact on the dopaminergic system, principally at D2 receptors (Strange, 2001). APDs act with high affinity (in the low nanomolar
range) with clinical efficacy closely matching their published potency at D2 receptors (Strange, 2001). However, some aspects of APD action are difficult to explain based solely on their action at D2 receptors. For example, the therapeutic benefit of APDs increases slowly during treatment, Calpain an occurrence which correlates with their accumulation in tissue (Agid et al., 2003). APDs also inhibit voltage-gated sodium (Ogata and Narahashi, 1989) and calcium channels (Sah and Bean, 1994), implicating them in the control of neurotransmitter release. However, the clinical relevance of this potential presynaptic mechanism of action was largely dismissed, since it requires micromolar concentrations of APDs. It has been known for years that APDs such as clozapine and haloperidol exhibit increased accumulation in brain (Strange, 2001). This phenomenon has been ascribed to the fact that many APDs are weak bases, allowing them to accumulate in acidic intracellular compartments such as endosomes or synaptic vesicles (SVs) (Rayport and Sulzer, 1995).