Paul Patterson: In Memoriam

Caltech neuroscientist Paul Patterson, whose career spanned developmental neurobiology, behavioral neuroscience, and neuroimmunology, passed away on June 25 at the age of 70 from an aggressive brain tumor. Patterson was a pioneer and an iconoclast who was not afraid to work outside of the scientific mainstream; consequently, he made a number of important and seminal contributions that opened up entire fields of research. As his colleague of almost 30 years at Caltech, I watched his scientific evolution and transformations with curiosity, some skepticism, and ultimately admiration. Paul was a consummate scientist, in the sense that he was consumed with science. He was possessed of a restless imagination and a drive to find hard problems that others would be too timid or conservative to investigate. He pursued these challenges with vigor and passion to a degree that could strike some as bordering on the quixotic. Patterson’s ability to forge his path, without regard for mainstream opinion, was a continuing theme throughout his career. In this respect he was the clear inheritor of the scientific temperament of his uncle, Clair Patterson, a professor of geochemistry at Caltech who pursued a lifelong crusade to demonstrate the danger posed to public health by lead poisoning, despite initial skepticism from his colleagues. Paul’s friends, students, and close colleagues loved him, even as he occasionally exasperated them. Patterson initially achieved widespread recognition for his seminal work on the phenotypic plasticity of neurotransmitter identity, which he carried out at Harvard Medical School’s Department of Neurobiology in the mid-1970s. He pioneered methods for the primary culture of neonatal sympathetic neurons, one of the first types of isolated neuron to be grown in vitro. With his student Linda Chun, and working with Edwin Furshpan and David Potter, Patterson demonstrated that immature sympathetic neurons could, when cocultured with heart cells, switch their neurotransmitter phenotype from noradrenergic to cholinergic, a switch that was ultimately