Stephen F. Heinemann

from Wikipedia, the free encyclopedia

Stephen "Steve" Fox Heinemann (born February 11, 1939 in Boston , Massachusetts , USA ; † August 6, 2014 in San Diego , California , USA) was an American biochemist and neurobiologist . He was Professor of Neuroscience at the Salk Institute for Biological Studies and the University of California, San Diego . He is one of the fathers of molecular neuroscience and is a pioneer in research into neurotransmitter receptors.

Life

Stephen Fox Heinemann, son of the teacher Robert B. Heinemann and Christel Fuchs Holtzer, grew up in Cambridge , Massachusetts. Here he attended secondary school at Buckingham Browne & Nichols School. He received his first chemistry kit from his uncle Klaus Fuchs , a theoretical physicist who was involved in the development of the atomic bomb as part of the Manhattan Project and who later confessed to spying for the Soviet Union . At that time he already met his wife Ann, daughter of Edwin Reischauer , a renowned Harvard professor of East Asian studies who was US ambassador to Japan in the 1960s . Heinemann received his bachelor's degree from the California Institute of Technology (CalTech) in 1962 and received his doctorate in biochemistry from Harvard University in 1967 with Matthew Meselson with work on DNA structure . As a postdoc at the Massachusetts Institute of Technology (MIT) and Stanford University , his work contributed to the elucidation of the genetics of the life cycle of the bacteriophage lambda . Soon his interest in neurobiology grew. In 1970 Heinemann accepted an appointment as a faculty member at the Salk Institute for Biological Studies in La Jolla . This made him one of the first neuroscientists here. He made a significant contribution to the fact that the discipline of Molecular Neurobiology at the Salk already had the highest ranking of all comparable programs worldwide at the end of the 1980s. From 2005 to 2006 he was elected President of the Society for Neuroscience . In this capacity he supported the Dalai Lama's controversial lecture "Dialogues Between Neuroscience and Society" at the Society's annual meeting in 2005. He left behind his wife Ann, a daughter, four sons, four sisters, twelve grandchildren and countless colleagues who were in his Laboratory received their training.

research

After his colleagues at the Salk Institute, Jim Patrick and Jon Lindstrom, discovered that immunizing rabbits with nicotinic acetylcholine receptors (nAChR) induces symptoms similar to myasthenia gravis , Heinemann was able to show with others that the serum of patients increased the sensitivity to acetylcholine in Muscles lowers. The discovery that myasthenia gravis is an autoimmune disease , often triggered by antibodies against the nicotinic acetylcholine receptor (nAChR) of the neuromuscular endplate , increased interest in cloning these receptors. After his Japanese colleague Shōsaku Numa was the first to succeed in isolating the cDNA for a nicotinic acetylcholine receptor (from the electrical organ of the California electric ray ), Steve Heinemann turned to neural nAChR with his colleagues Jim Boulter and Jim Patrick. They succeeded in isolating the first subunit of nAChR, alpha-3, from mammals using a homology screen. This was followed by the cloning of further subunits and the characterization of the receptor.

Heinemann was also successful in trying to clone the glutamate receptors . In his laboratory, functional expression cloning was used to isolate a subunit of the AMPA receptor , followed by further subunits of the AMPA and kainate receptors . This made the biochemical characterization and the establishment of mouse models , such as knockout mutants , possible.

With his work, Steve Heinemann laid the basis for a better understanding of synaptic mechanisms, but also for the development of therapies for so-called "synaptopathies" such as stroke , epilepsy , Parkinson's disease and Alzheimer's disease , as well as various neuropsychiatric diseases .

Honors and memberships

Web links

Individual evidence

  1. ^ J. Patrick, J. Lindstrom: Autoimmune response to acetylcholine receptor. In: Science. Volume 180, Number 4088, May 1973, pp. 871-872, PMID 4706680 .
  2. ^ S. Bevan, RW Kullberg, SF Heinemann: Human myasthenic sera reduce acetylcholine sensitivity of human muscle cells in tissue culture. In: Nature. Volume 267, Number 5608, May 1977, pp. 263-265, PMID 865619 .
  3. Jim Boulter, Karen Evans, Dan Goldman, Gary Martin, Doug Treco, Steve Heinemann, Jim Patrick: Isolation of a cDNA clone coding for a possible neural nicotinic acetylcholine receptor α-subunit. In: Nature. 319, 1986, p. 368, doi : 10.1038 / 319368a0 .
  4. ES Deneris, J. Boulter, J. Connolly, E. Wada, K. Wada, D. Goldman, LW Swanson, J. Patrick, S. Heinemann: Genes encoding neuronal nicotinic acetylcholine receptors. In: Clinical chemistry. Volume 35, Number 5, May 1989, pp. 731-737, PMID 2655998 (review).
  5. M. Hollmann, A. O'Shea-Greenfield, SW Rogers, S. Heinemann: Cloning by functional expression of a member of the glutamate receptor family. In: Nature. Volume 342, Number 6250, December 1989, pp. 643-648, doi : 10.1038 / 342643a0 , PMID 2480522 .
  6. B. Bettler, J. Boulter, I. Hermans-Borgmeyer, A. O'Shea-Greenfield, ES Deneris, C. Moll, U. Borgmeyer, M. Hollmann, S. Heinemann: Cloning of a novel glutamate receptor subunit, GluR5: expression in the nervous system during development. In: Neuron. Volume 5, Number 5, November 1990, pp. 583-595, PMID 1977421 .
  7. J. Boulter, B. Bettler, R. Dingledine, J. Edgebjerg, M. Hartley, I. Hermans-Borgmeyer, M. Hollmann, RI Hume, S. Rogers, S. Heinemann: Molecular biology of the glutamate receptors. In: Clinical neuropharmacology. Volume 15 Suppl 1 Pt A, 1992, pp. 60A-61A, PMID 1323407 .
  8. ^ A. Contractor, G. Swanson, SF Heinemann: Kainate receptors are involved in short- and long-term plasticity at mossy fiber synapses in the hippocampus. In: Neuron. Volume 29, Number 1, January 2001, pp. 209-216, PMID 11182092 .