Timothy Bliss

Last updated

Tim Bliss
Born
Timothy Vivian Pelham Bliss

(1940-07-27) 27 July 1940 (age 83) [1]
Education Dean Close School
Alma mater McGill University
Awards
Scientific career
Institutions

Timothy Vivian Pelham Bliss FRS (born 27 July 1940) is a British neuroscientist. [1] He is an adjunct professor at the University of Toronto, and a group leader emeritus at the Francis Crick Institute, London.

Contents

In 2016 Professor Tim Bliss shared with Professors Graham Collingridge and Richard Morris the 2016 Brain Prize, one of the world's most coveted science prizes. [3]

Life

Born in England he was educated at Dean Close School and McGill University (BSc, 1963; PhD, 1967). [1] In 1967 he joined the MRC National Institute for Medical Research in Mill Hill, London, where he was Head of the Division of Neurophysiology from 1988 till 2006. His work with Terje Lømo in Per Andersen's laboratory at the University of Oslo in the late 1960s established the phenomenon of long-term potentiation (LTP) as the dominant synaptic model of how the mammalian brain stores memories.

Career and research

In 1973, he and Terje Lømo published [4] the first evidence of a Hebb-like synaptic plasticity event induced by brief tetanic stimulation, known as long-term potentiation (LTP). [5] [6] [7] [8] His work has done much to provide a neural explanation for learning and memory. Studying the hippocampus – the memory centre of the brain – Tim showed that the strength of signals between neurons in the brain exhibits a long-term increase following brief but intense activation, a phenomenon known as long-term potentiation (LTP). [2]

Whilst LTP was discovered in Oslo in the lab of Per Andersen, Tim's subsequent research into the cellular properties of LTP and its relation to memory was conducted at London's National Institute for Medical Research where he worked from 1968 to 2006, becoming head of Neurosciences. [9] He is visiting professor at University College London.

Bliss is on the board of the Feldberg Foundation [10] and was trustee of Sir John Soane's Museum from 2004 to 2009. [11] From the years 2009 until 2013, Bliss worked as an adjunct professor in the South Korean university, Seoul National University. [12]

Awards and Honours [3]

Notable Contributions

Publications and Credits
YearTitleJournal
1969Lamellar Organization of Hippocampal Excitatory Pathways [14] Acta Physiologica Scandinavica
1970Plasticity in a Monosynaptic Cortical Pathway [15] The Journal of Physiology
1971Unit Analysis of Hippocampal Population Spikes [16] Experimental Brain Research
1971Long-Lasting Increases of Synaptic Influence in the Unanesthetized Hippocampus [17] The Journal of Physiology
1971Lamellar Organization of Hippocampal Pathways [18] Experimental Brain Research
1973Long-Lasting Potentiation of Synaptic Transmission in the Dentate Area of the Anaesthetized Rabbit Following Stimulation of the Perforant Path [19] [20] The Journal of Physiology
1979Synaptic Plasticity in the Hippocampus [21] Trends in Neurosciences

Related Research Articles

<span class="mw-page-title-main">Hippocampus</span> Vertebrate brain region involved in memory consolidation

The hippocampus is a major component of the brain of humans and other vertebrates. Humans and other mammals have two hippocampi, one in each side of the brain. The hippocampus is part of the limbic system, and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. The hippocampus is located in the allocortex, with neural projections into the neocortex in humans, as well as primates. The hippocampus, as the medial pallium, is a structure found in all vertebrates. In humans, it contains two main interlocking parts: the hippocampus proper, and the dentate gyrus.

<span class="mw-page-title-main">Long-term potentiation</span> Persistent strengthening of synapses based on recent patterns of activity

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

<span class="mw-page-title-main">Dentate gyrus</span> Region of the hippocampus in the brain

The dentate gyrus (DG) is part of the hippocampal formation in the temporal lobe of the brain, which also includes the hippocampus and the subiculum. The dentate gyrus is part of the hippocampal trisynaptic circuit and is thought to contribute to the formation of new episodic memories, the spontaneous exploration of novel environments and other functions.

David Courtenay Marr was a British neuroscientist and physiologist. Marr integrated results from psychology, artificial intelligence, and neurophysiology into new models of visual processing. His work was very influential in computational neuroscience and led to a resurgence of interest in the discipline.

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

<span class="mw-page-title-main">Excitatory postsynaptic potential</span> Process causing temporary increase in postsynaptic potential

In neuroscience, an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more likely to fire an action potential. This temporary depolarization of postsynaptic membrane potential, caused by the flow of positively charged ions into the postsynaptic cell, is a result of opening ligand-gated ion channels. These are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of negative ions into the cell or positive ions out of the cell. EPSPs can also result from a decrease in outgoing positive charges, while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

The induction of NMDA receptor-dependent long-term potentiation (LTP) in chemical synapses in the brain occurs via a fairly straightforward mechanism. A substantial and rapid rise in calcium ion concentration inside the postsynaptic cell is most possibly all that is required to induce LTP. But the mechanism of calcium delivery to the postsynaptic cell in inducing LTP is more complicated.

Schaffer collaterals are axon collaterals given off by CA3 pyramidal cells in the hippocampus. These collaterals project to area CA1 of the hippocampus and are an integral part of memory formation and the emotional network of the Papez circuit, and of the hippocampal trisynaptic loop. It is one of the most studied synapses in the world and named after the Hungarian anatomist-neurologist Károly Schaffer.

Sensitization is a non-associative learning process in which repeated administration of a stimulus results in the progressive amplification of a response. Sensitization often is characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated. For example, repetition of a painful stimulus may make one more responsive to a loud noise.

Metaplasticity is a term originally coined by W.C. Abraham and M.F. Bear to refer to the plasticity of synaptic plasticity. Until that time synaptic plasticity had referred to the plastic nature of individual synapses. However this new form referred to the plasticity of the plasticity itself, thus the term meta-plasticity. The idea is that the synapse's previous history of activity determines its current plasticity. This may play a role in some of the underlying mechanisms thought to be important in memory and learning such as long-term potentiation (LTP), long-term depression (LTD) and so forth. These mechanisms depend on current synaptic "state", as set by ongoing extrinsic influences such as the level of synaptic inhibition, the activity of modulatory afferents such as catecholamines, and the pool of hormones affecting the synapses under study. Recently, it has become clear that the prior history of synaptic activity is an additional variable that influences the synaptic state, and thereby the degree, of LTP or LTD produced by a given experimental protocol. In a sense, then, synaptic plasticity is governed by an activity-dependent plasticity of the synaptic state; such plasticity of synaptic plasticity has been termed metaplasticity. There is little known about metaplasticity, and there is much research currently underway on the subject, despite its difficulty of study, because of its theoretical importance in brain and cognitive science. Most research of this type is done via cultured hippocampus cells or hippocampal slices.

Ca<sup>2+</sup>/calmodulin-dependent protein kinase II

Ca2+
/calmodulin-dependent protein kinase II is a serine/threonine-specific protein kinase that is regulated by the Ca2+
/calmodulin complex. CaMKII is involved in many signaling cascades and is thought to be an important mediator of learning and memory. CaMKII is also necessary for Ca2+
 homeostasis and reuptake in cardiomyocytes, chloride transport in epithelia, positive T-cell selection, and CD8 T-cell activation.

Denise Manahan-Vaughan is an Irish neuroscientist and neurophysiologist. She is head of the Department of Neurophysiology, dean of studies and director of the International Graduate School of Neuroscience and co-founder of the Research Department of Neuroscience of the Ruhr University Bochum. Her research focuses on elucidation of the cellular and synaptic mechanisms underlying the acquisition and long-term maintenance of associative memories. She uses a multidisciplinary approach to study how spatial experiences, sensory input, neuromodulation, or brain disease impacts on, and provide insight into, the function of the hippocampus in enabling long-term memory.

Coincidence detection is a neuronal process in which a neural circuit encodes information by detecting the occurrence of temporally close but spatially distributed input signals. Coincidence detectors influence neuronal information processing by reducing temporal jitter and spontaneous activity, allowing the creation of variable associations between separate neural events in memory. The study of coincidence detectors has been crucial in neuroscience with regards to understanding the formation of computational maps in the brain.

The spine apparatus (SA) is a specialized form of endoplasmic reticulum (ER) that is found in a subpopulation of dendritic spines in central neurons. It was discovered by Edward George Gray in 1959 when he applied electron microscopy to fixed cortical tissue. The SA consists of a series of stacked discs that are connected to each other and to the dendritic system of ER-tubules. The actin binding protein synaptopodin is an essential component of the SA. Mice that lack the gene for synaptopodin do not form a spine apparatus. The SA is believed to play a role in synaptic plasticity, learning and memory, but the exact function of the spine apparatus is still enigmatic.

Graham Leon Collingridge is a British neuroscientist and professor at the University of Toronto and at the University of Bristol. He is also a senior investigator at the Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital in Toronto.

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Addiction is a state characterized by compulsive engagement in rewarding stimuli, despite adverse consequences. The process of developing an addiction occurs through instrumental learning, which is otherwise known as operant conditioning.

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Early long-term potentiation (E-LTP) is the first phase of long-term potentiation (LTP), a well-studied form of synaptic plasticity, and consists of an increase in synaptic strength. LTP could be produced by repetitive stimulation of the presynaptic terminals, and it is believed to play a role in memory function in the hippocampus, amygdala and other cortical brain structures in mammals.

References

  1. 1 2 3 "BLISS, Dr Timothy Vivian Pelham" . Who's Who . Vol. 2016 (online Oxford University Press  ed.). Oxford: A & C Black.(Subscription or UK public library membership required.)
  2. 1 2 "Dr Timothy Bliss FMedSci FRS". London: Royal Society. Archived from the original on 17 November 2015. One or more of the preceding sentences incorporates text from the royalsociety.org website where:
    "All text published under the heading 'Biography' on Fellow profile pages is available under Creative Commons Attribution 4.0 International License." -- "Royal Society Terms, conditions and policies". Archived from the original on 25 September 2015. Retrieved 9 March 2016.{{cite web}}: CS1 maint: bot: original URL status unknown (link)
  3. 1 2 "Biography Timothy Bliss – Grete Lundbeck European Brain Research Foundation". thebrainprize.org. Retrieved 2 March 2023.
  4. ↑ Bliss, T. V.; Lomo, T (1973). "Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path". The Journal of Physiology. 232 (2): 331–56. doi:10.1113/jphysiol.1973.sp010273. PMC   1350458 . PMID   4727084.
  5. ↑ Dolphin, A. C.; Errington, M. L.; Bliss, T. V. P. (1982). "Long-term potentiation of the perforant path in vivo is associated with increased glutamate release". Nature. 297 (5866): 496–497. Bibcode:1982Natur.297..496D. doi:10.1038/297496a0. ISSN   0028-0836. PMID   6123949. S2CID   4255128.
  6. ↑ Tim V. P. Bliss, Graham L. Collingridge, Richard G. Morris, Long-term potentiation: enhancing neuroscience for 30 years, Oxford University Press, 2004, ISBN   978-0-19-853030-5
  7. ↑ Per Andersen, Richard Morris, David Amaral, Tim Bliss and John O'Keefe (eds), The hippocampus book. Oxford University Press, 2007. ISBN   978-0-19-510027-3
  8. ↑ Bliss, T. V. P.; Collingridge, G. L. (1993). "A synaptic model of memory: Long-term potentiation in the hippocampus". Nature. 361 (6407): 31–39. Bibcode:1993Natur.361...31B. doi:10.1038/361031a0. PMID   8421494. S2CID   4326182.
  9. ↑ The Committee Office, House of Commons. "House of Commons – Science and Technology Committee – Written Evidence". Parliament of the United Kingdom. Retrieved 21 December 2012.
  10. ↑ "Board members of the Feldberg Foundation". Feldbergfoundation.org. Retrieved 21 December 2012.
  11. ↑ "Dr T V P Bliss, FRS Authorised Biography – Debrett's People of Today, Dr T V P Bliss, FRS Profile". www.debretts.co.uk. Archived from the original on 31 March 2012. Retrieved 13 January 2022.
  12. ↑ "Academy of Europe: Bliss Timothy". www.ae-info.org. Retrieved 29 November 2022.
  13. ↑ "Tim Bliss | The Lundbeck Foundation". lundbeckfonden.com. Retrieved 29 November 2022.
  14. ↑ Andersen, P; Bliss, TV; Lomo, T; Olsen, LI; Skrede, KK (May 1969). "Lamellar organization of hippocampal excitatory pathways". Acta Physiologica Scandinavica. 76 (1): 4A–5A. doi:10.1111/j.1748-1716.1969.tb04499.x. PMID   5823402 . Retrieved 28 November 2022.
  15. ↑ Bliss, TV; Lomo, T (April 1970). "Plasticity in a monosynaptic cortical pathway". The Journal of Physiology. 207 (2): 61P. PMID   5511138 . Retrieved 28 November 2022.
  16. ↑ Andersen, P.; Bliss, T. V. P.; Skrede, K. K. (1 August 1971). "Unit analysis of hippocampal population spikes". Experimental Brain Research. 13 (2): 208–221. doi:10.1007/BF00234086. PMID   5123965. S2CID   7160894 . Retrieved 28 November 2022.
  17. ↑ Bliss, TV; Gardner-Medwin, AR (July 1971). "Long-lasting increases of synaptic influence in the unanesthetized hippocampus". The Journal of Physiology. 216 (1): 32P–33P. PMID   5558363 . Retrieved 28 November 2022.
  18. ↑ Andersen, P; Bliss, TV; Skrede, KK (1971). "Lamellar organization of hippocampal pathways". Experimental Brain Research. 13 (2): 222–38. doi:10.1007/BF00234087. PMID   5570425. S2CID   12075886 . Retrieved 28 November 2022.
  19. ↑ Bliss, TV; Lomo, T (July 1973). "Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path". The Journal of Physiology. 232 (2): 331–56. doi:10.1113/jphysiol.1973.sp010273. PMC   1350458 . PMID   4727084. S2CID   2983008.
  20. ↑ Bliss, TV; Gardner-Medwin, AR (July 1973). "Long-lasting potentiation of synaptic transmission in the dentate area of the unanaestetized rabbit following stimulation of the perforant path". The Journal of Physiology. 232 (2): 357–74. doi:10.1113/jphysiol.1973.sp010274. PMC   1350459 . PMID   4727085. S2CID   21559512.
  21. ↑ Bliss, T. V. P. (1 January 1979). "Synaptic plasticity in the hippocampus". Trends in Neurosciences. 2: 42–45. doi:10.1016/0166-2236(79)90019-5. S2CID   53151887 . Retrieved 29 November 2022.
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