Stephen F. Heinemann

Stephen F. Heinemann (1939–2014) was a professor of neuroscience at the Salk Institute. He was an early researcher in the field of molecular neuroscience, contributing to the current knowledge of how nerves communicate with each other, and the role of neurotransmitters. Stephen Heinemann died August 6, 2014, of kidney failure. He joined the Salk Institute in 1970, where he founded the department of molecular neurobiology, which soon became known as one of the world's top research centers in the field. He did pioneering work in the subject of motor neurons and the neuromuscular junction. He remained at Salk until his retirement. alt=Courtyard of the Salk Institute for Biological Studies, La Jolla, California. 360 degree panorama in the courtyard of the Salk Institute for Biological Studies, La Jolla, California. Heinemann researched at the Salk Institute from 1970 until his retirement. Photographed on an August morning by Gregg M. Erickson.

Research Stephen F. Heinemann's research focus was acetylcholine and glutamate receptors. As shown by Heinemann, NMDA receptors differ in that they allow significant amounts of calcium to enter the cell rather than just sodium. Heinemann's research also illuminated the role of the metabotropic glutamate receptor 5 in learning and unlearning information using a rodent model. Metabotropic receptors differ from ionotropic receptors in that they activate other internal cell signaling pathways. Heinemann and his team also discovered the differences between kainate and AMPA receptors, which were previously thought to make up one family of glutamate receptors. Heinemann's most notable contribution to the study of glutamate as a major excitatory neurotransmitter was to identify and replicate the DNA sequences for each of many of these receptors and their subunits. This allowed for further research of the function and dysfunction of communication between neurons through neurotransmitter receptors.

Neurological disorders Stephen Heinemann's research contributed largely to the understanding and treatment of neurological disorders. Much of his research focused on the idea that disorders can occur when connectivity is disrupted between cells. His work with glutamate receptors showed that malfunctions can contribute to disorders such as schizophrenia and bipolar disorder. In doing so, his team discovered the cause of paralysis in the neuromuscular disorder, myasthenia gravis. the Institute of Medicine, and the American Academy of Arts and Sciences. He also served as president of the Society for Neuroscience in 2005–2006. For his outstanding efforts in research and his dedication to neuroscience, Heinemann was awarded the Bristol-Myers Squibb Distinguished Achievement in Neuroscience Research Award, the McKnight Award for Research. Additionally, he was awarded the Julius Axelrod Prize from the Society for Neuroscience in 2010 because of his research involving neuropharmacology, as well as his commitment to mentoring future scientists.

Notable publications +Bevan S, Kullberg RW, Heinemann SF. Human myasthenic sera reduce acetylcholine sensitivity of human muscle cells in tissue culture. Nature. 267: 263–5. PMID 865619Hume RI, Dingledine R, Heinemann SF. Identification of a site in glutamate receptor subunits that controls calcium permeability. Science. 253: 1028–31. PMID 1653450Hollmann M, Heinemann S. Cloned glutamate receptors. Annual Review of Neuroscience. 17: 31–108. PMID 8210177 DOI: 10.1146/annurev.ne.17.030194.000335Contractor A, Swanson G, Heinemann SF. Kainate receptors are involved in short- and long-term plasticity at mossy fiber synapses in the hippocampus. Neuron. 29: 209–16. PMID 11182092 DOI: 10.1016/S0896-6273(01)00191-XKayadjanian N, Lee HS, Piña-Crespo J, Heinemann SF. Localization of glutamate receptors to distal dendrites depends on subunit composition and the kinesin motor protein KIF17. Molecular and Cellular Neurosciences. 34: 219–30. PMID 17174564 DOI: 10.1016/j.mcn.2006.11.001Talantova M, Sanz-Blasco S, Zhang X, Xia P, Akhtar MW, Okamoto SI, Dziewczapolski G, Nakamura T, Cao G, Pratt AE, Kang YJ, Tu S, Molokanova E, McKercher SR, Hires SA... ... Heinemann SF, et al. Correction to supporting information for "Aβ induces astrocytic glutamate release, extrasynaptic NMDA receptor activation, and synaptic loss," Proceedings of the National Academy of Sciences of the United States of America. 112: E3751-E3752. DOI: 10.1073/pnas.1511282112