In this excerpt from his introduction to Violence and Public Memory, editor Martin Blatt discusses his family history connected to the Holocaust and how this history propelled him to a lifelong commitment to social justice through the telling of history in public contexts. He then identifies how the relationship of violence to public memory has been a central theme throughout his professional career as a public historian. Blatt proceeds to define how he employs the terms “violence” and “public memory” in this book. He examines contemporary literature and the public history arena to highlight exemplary works focused on violence and public memory. Subsequently, he highlights a range of publications that examine this connection. Blatt explores the contents of this edited volume regarding geography, types of memorialization, and historical timeframe. He stresses his belief that the measure of the integrity of a nation or culture is the degree to which there is an unflinching examination of the violent past and its meaning for contemporary society. He has organized the book into five thematic sections—genocide; slavery; racial and sexual hatred in the United States; apartheid; and fascism and war. Each section includes multiple chapters tied to the specific theme. Blatt concludes the introduction by summarizing each section and chapter (these summaries are not included here).

Fragile X syndrome, the most commonly known genetic cause of autism, is due to loss of the fragile X mental retardation protein, which regulates signal transduction at metabotropic glutamate receptor-5 in the brain. Fragile X mental retardation protein deletion in mice enhances metabotropic glutamate receptor-5-dependent long-term depression in the hippocampus and cerebellum. Here we show that a distinct type of metabotropic glutamate receptor-5-dependent long-term depression at excitatory synapses of the ventral striatum and prefrontal cortex, which is mediated by the endocannabinoid 2-arachidonoyl-sn-glycerol, is absent in fragile X mental retardation protein-null mice. In these mutants, the macromolecular complex that links metabotropic glutamate receptor-5 to the 2-arachidonoyl-sn-glycerol-producing enzyme, diacylglycerol lipase-α (endocannabinoid signalosome), is disrupted and metabotropic glutamate receptor-5-dependent 2-arachidonoyl-sn-glycerol formation is compromised. These changes are accompanied by impaired endocannabinoid-dependent long-term depression. Pharmacological enhancement of 2-arachidonoyl-sn-glycerol signalling normalizes this synaptic defect and corrects behavioural abnormalities in fragile X mental retardation protein-deficient mice. The results identify the endocannabinoid signalosome as a molecular substrate for fragile X syndrome, which might be targeted by therapy.