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.[1]
Stephen Heinemann was born February 11, 1939, in Boston, Massachusetts, to Robert Heinemann and Christel Fuchs. He grew up in Cambridge, Massachusetts and attended Buckingham Browne & Nichols secondary school. Heinemann met his wife, Ann Reischauer Heinemann, in Cambridge. They were married for 54 years and had five children.[2] His uncle, Emil Julius Klaus Fuchs, a physicist and spy who contributed to the development of the atomic bomb, influenced Heinemann's interest in science.[1]
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.
Researchedit
Stephen F. Heinemann's research focus was acetylcholine and glutamate receptors.[1] A majority of the excitatory neurons in the central nervous system communicate via these two chemical signaling molecules known as neurotransmitters. Heinemann's work included identifying the key structural elements of the receptor proteins that allow them to recognize signal molecules and enact change in the cell. The understanding of their structures has furthered research in cognition and neurological disorders. His research has illuminated the cognitive function of several receptors. Heinemann has also researched the application of dysfunction in these neurotransmitter receptors on human diseases including addiction and Alzheimers.[5]
Glutamate receptorsedit
Glutamate is an excitatory neurotransmitter. In humans and other vertebrate's brains, glutamate controls over 90% of excitatory connections. Receptors for glutamate are found throughout the brain. One contribution Heinemann made to neuroscience includes discovering and cloning the first DNA sequences of glutamate receptors. There are 3 ionotropic glutamate receptors that Heinemann contributed to differentiating: AMPA receptors, NMDA receptors, and kainate receptors.[6] 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.[7]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.[8] This allowed for further research of the function and dysfunction of communication between neurons through neurotransmitter receptors.
Neurological disordersedit
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.[1] In addition, he studied acetylcholine and nicotine receptors in the brain, especially their involvement with Alzheimer's and Parkinson's.[9] In doing so, his team discovered the cause of paralysis in the neuromuscular disorder, myasthenia gravis.[1]
Bevan S, Kullberg RW, Heinemann SF. Human myasthenic sera reduce acetylcholine sensitivity of human muscle cells in tissue culture. Nature. 267: 263–5. PMID 865619
Hume RI, Dingledine R, Heinemann SF. Identification of a site in glutamate receptor subunits that controls calcium permeability. Science. 253: 1028–31. PMID 1653450
Contractor 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-X
Kayadjanian 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.2006.11.001
Talantova 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
Referencesedit
^ abcdef"Stephen F. Heinemann, pioneering Salk neuroscientist, dies at 75". Salk Institute for Biological Studies. Retrieved 19 April 2019.
^ abcdStevens, Charles F.; Lipton, Stuart A. (9 October 2014). "Stephen F. Heinemann 1939–2014". Cell. 159 (2): 231–232. doi:10.1016/j.cell.2014.09.042. ISSN 0092-8674. PMID 25436266.
^ ab"Stephen F. Heinemann | The Gruber Foundation". gruber.yale.edu. Retrieved 19 April 2019.
^Julius, David; Lemke, Greg (7 October 2014). "Stephen F. Heinemann: A true original". Proceedings of the National Academy of Sciences. 111 (40): 14314–14315. Bibcode:2014PNAS..11114314L. doi:10.1073/pnas.1416208111. ISSN 0027-8424. PMC4209978. PMID 25258411.
^ ab"Stephen Heinemann". www.nasonline.org. Retrieved 19 April 2019.
^. 2009-02-13. Archived from the original on 2009-02-13. Retrieved 2020-03-30.
^"Forget It! A Biochemical Pathway For Blocking Your Worst Fears?". ScienceDaily. 26 March 2009. Retrieved 2020-03-30.
^Contractor, Anis; Mulle, Christophe; Swanson, Geoffrey T (20 Jan 2011). "Kainate receptors coming of age: milestones of two decades of research". Trends in Neurosciences. 34 (3): 154–163. doi:10.1016/j.tins.2010.12.002. ISSN 0166-2236. PMC3051042. PMID 21256604.
^"Nicotinic Receptor May Help Trigger Alzheimer's Disease". Salk Institute for Biological Studies. Retrieved 2020-03-30.
January 01, 1970
stephen, heinemann, stephen, heinemann, 1939, 2014, professor, neuroscience, salk, institute, early, researcher, field, molecular, neuroscience, contributing, current, knowledge, nerves, communicate, with, each, other, role, neurotransmitters, died, august, 20. 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 1 Stephen F HeinemannBornFebruary 11 1939Boston Massachusetts USDiedAugust 6 2014Alma materCaltech Harvard UniversitySpouseAnn ReischauerChildren5Scientific careerFieldsneuroscienceInstitutionsSalk Institute MIT Stanford University Contents 1 Early life 2 Education and career 3 Research 3 1 Glutamate receptors 3 2 Neurological disorders 4 Awards 5 Notable publications 6 ReferencesEarly life editStephen Heinemann was born February 11 1939 in Boston Massachusetts to Robert Heinemann and Christel Fuchs He grew up in Cambridge Massachusetts and attended Buckingham Browne amp Nichols secondary school Heinemann met his wife Ann Reischauer Heinemann in Cambridge They were married for 54 years and had five children 2 His uncle Emil Julius Klaus Fuchs a physicist and spy who contributed to the development of the atomic bomb influenced Heinemann s interest in science 1 Education and career editHeinemann graduated from Caltech with a bachelor s degree in 1962 and in 1967 he earned a PhD in biochemistry at Harvard University under the mentorship of Matt Meselson a well known geneticist and molecular biologist 2 He then did research as a postdoctoral fellow at Massachusetts Institute of Technology and Stanford University His work at MIT was alongside A Dale Kaiser They focused on how transcription is related to the phage lambda repressor synthesis During his time at Stanford he worked with Ethan Royal Signer 1 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 3 2 He did pioneering work in the subject of motor neurons and the neuromuscular junction He remained at Salk until his retirement 4 nbsp 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 editStephen F Heinemann s research focus was acetylcholine and glutamate receptors 1 A majority of the excitatory neurons in the central nervous system communicate via these two chemical signaling molecules known as neurotransmitters Heinemann s work included identifying the key structural elements of the receptor proteins that allow them to recognize signal molecules and enact change in the cell The understanding of their structures has furthered research in cognition and neurological disorders His research has illuminated the cognitive function of several receptors Heinemann has also researched the application of dysfunction in these neurotransmitter receptors on human diseases including addiction and Alzheimers 5 Glutamate receptors edit Glutamate is an excitatory neurotransmitter In humans and other vertebrate s brains glutamate controls over 90 of excitatory connections Receptors for glutamate are found throughout the brain One contribution Heinemann made to neuroscience includes discovering and cloning the first DNA sequences of glutamate receptors There are 3 ionotropic glutamate receptors that Heinemann contributed to differentiating AMPA receptors NMDA receptors and kainate receptors 6 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 7 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 8 This allowed for further research of the function and dysfunction of communication between neurons through neurotransmitter receptors Neurological disorders edit 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 1 In addition he studied acetylcholine and nicotine receptors in the brain especially their involvement with Alzheimer s and Parkinson s 9 In doing so his team discovered the cause of paralysis in the neuromuscular disorder myasthenia gravis 1 Awards editHeinemann received a number of rewards and honors for his achievements in science He was an elected member of the National Academy of Sciences 5 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 3 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 2 Notable publications editBevan S Kullberg RW Heinemann SF Human myasthenic sera reduce acetylcholine sensitivity of human muscle cells in tissue culture Nature 267 263 5 PMID 865619 Hume RI Dingledine R Heinemann SF Identification of a site in glutamate receptor subunits that controls calcium permeability Science 253 1028 31 PMID 1653450 Hollmann M Heinemann S Cloned glutamate receptors Annual Review of Neuroscience 17 31 108 PMID 8210177 DOI 10 1146 annurev ne 17 030194 000335 Contractor 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 X Kayadjanian N Lee HS Pina 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 11 001 Talantova 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 Ab 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 1511282112References edit a b c d e f Stephen F Heinemann pioneering Salk neuroscientist dies at 75 Salk Institute for Biological Studies Retrieved 19 April 2019 a b c d Stevens Charles F Lipton Stuart A 9 October 2014 Stephen F Heinemann 1939 2014 Cell 159 2 231 232 doi 10 1016 j cell 2014 09 042 ISSN 0092 8674 PMID 25436266 a b Stephen F Heinemann The Gruber Foundation gruber yale edu Retrieved 19 April 2019 Julius David Lemke Greg 7 October 2014 Stephen F Heinemann A true original Proceedings of the National Academy of Sciences 111 40 14314 14315 Bibcode 2014PNAS 11114314L doi 10 1073 pnas 1416208111 ISSN 0027 8424 PMC 4209978 PMID 25258411 a b Stephen Heinemann www nasonline org Retrieved 19 April 2019 The Glutamate Receptor Ion Channels Dingledine et al 51 1 7 Pharmacological Reviews 2009 02 13 Archived from the original on 2009 02 13 Retrieved 2020 03 30 Forget It A Biochemical Pathway For Blocking Your Worst Fears ScienceDaily 26 March 2009 Retrieved 2020 03 30 Contractor Anis Mulle Christophe Swanson Geoffrey T 20 Jan 2011 Kainate receptors coming of age milestones of two decades of research Trends in Neurosciences 34 3 154 163 doi 10 1016 j tins 2010 12 002 ISSN 0166 2236 PMC 3051042 PMID 21256604 Nicotinic Receptor May Help Trigger Alzheimer s Disease Salk Institute for Biological Studies Retrieved 2020 03 30 Retrieved from https en wikipedia org w index php title Stephen Heinemann amp oldid 1203897546, wikipedia, wiki, book, books, library,
