The correlation analysis between spiking in BLA cue-responsive neurons and LFPs from GC was measured for a 125 ms-wide bin either preceding (control) or following the onset of the tone. Eight, simultaneously recorded GC LFPs were used for each cell. The cross-correlation was computed on a trial-to-trial basis between the continuous LFPs and the rate histogram using a bin size of 1 ms.

The average cross-correlogram was computed for each cell-LFP pairing. To eliminate the influence from stimulus-induced covariation, a cross-correlogram was performed on pairs of signals coming from different trials (trial shuffle) and was subtracted from the average cross-correlogram on same trials. The peak occurring within buy SCH 900776 a ±50 ms lag of the resulting cross-correlogram was measured for both pre- and post-tone segments, and the values were compared with a t test. See Supplemental Experimental Procedures. See Supplemental Experimental Procedures. The authors

would like to thank Dr. Craig Evinger, Dr. Ahmad Jezzini, Dr. Giancarlo La Camera, learn more Dr. Lorna Role, Haixin Liu, and Martha Stone for the very helpful comments and discussions. A.F. would like to add a special acknowledgement to Drs. Don Katz and Arianna Maffei for their always insightful feedback. This work was supported by National Institute of Deafness and Other Communication Disorders Grants R01-DC010389 and R03-DC008885 and by a Klingenstein Foundation Fellowship (to A.F.). “
“We frequently hear that we are at the cusp of realizing the promise of molecular medicine. Nowhere is that promise closer to being realized than in the case of fragile X syndrome (FXS). FXS is now considered the gold standard for neurodevelopmental research because it has been barely 20 years from the identification of the gene responsible for the disorder to a putative molecular Liothyronine Sodium mechanism, resulting in multiple drugs undergoing clinical trials for treatment of patients. However, a concern of clinicians and hopeful parents has been “what if it’s too late”? Autism and related disorders such as FXS always have been thought to be irreversibly set

within a critical window during early childhood development between birth and 3 years of age. Often times, by the time FXS is diagnosed unambiguously, that window already has passed, which limits intervention options considerably. In the current issue of Neuron, Michalon et al. (2012) offer a bright ray of hope by comprehensively demonstrating the reversal of a wide variety of FXS phenotypes in adult mice with CTEP, a new selective antagonist of mGluR5 ( Figure 1). One of the most enduring hypotheses in FXS research has been the “mGluR theory,” which posits that many abnormalities associated with FXS are caused by excessive metabotropic glutamate receptor 5 (mGluR5) signaling. This excessive signaling results in exaggerated protein synthesis, which triggers an array of abnormal synaptic plasticity and behaviors (Bear et al., 2004).