Biography:Arnold Eskin

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Short description: American chronobiologist (died 2019)
Arnold Eskin
Born(1940-11-08)November 8, 1940
DiedDecember 22, 2019(2019-12-22) (aged 79)
Alma mater
Known for
Scientific career
FieldsChronobiology, neurobiology
Websitewww.bchs.uh.edu/people/detail/?155622-961-5=aeskin#info_research

Arnold Eskin was a professor of chronobiology at the University of Houston in Houston, Texas. He attended Vanderbilt University, where he received a degree in physics. He later attended University of Texas at Austin, where he received his Ph.D. in zoology in 1969.[1] He is recognized in the term Eskinogram, and has been a leader in the discovery of mechanisms underlying entrainment of circadian clocks.

Research

Aplysia californica

Menaker lab

In his early scientific career, Eskin studied circadian rhythms in the house sparrow, while working in chronobiologist Michael Menaker's lab at the University of Texas at Austin.

Eskin's most cited paper while in Menaker's lab concerns his research of non-ocular entraining cues in house sparrows.[2] In it, Eskin and Menaker showed the scientific community the ability of house sparrows to entrain to auditory cues as opposed to previously shown light cues.[2]

Ongoing research

Eskin's current research focuses on long-term memory formation. His lab focuses on the role of the circadian clock and the regulation of glutamate uptake in synaptic plasticity, using aplysia and rats as model organisms primarily.[1]

Role of glutamate transporters in memory formation

Eskin's lab has extensively studied the role of glutamate transporters in synaptic plasticity in aplysia. Specifically, his group has shown that glutamate uptake increases during long-term sensitization in Aplysia, long-term potentiation (LTP) in the hippocampus of rats, and morphine addiction and withdrawal in rats.[3] Deficiencies in glutamate uptake during changes in synaptic efficacy have also been linked to diseases such as Amyotrophic lateral sclerosis (ALS), Alzheimer's disease, and Epilepsy.[4] Blockage of NMDA receptors prevents glutamate from binding, which prevents the formation of long-term memory.[5] Eskin's group believes that the mechanism for glutamate uptake is phylogenetically conserved for multiple types of synaptic plasticity. They currently study the mechanism by which this process takes place.[1]

Role of circadian clocks in memory formation

Eskin has also researched the role of the circadian clock in glutaminergic synaptic plasticity. Although it was known that the brain's circadian clock could influence physiological outputs such as sleep and wakefulness, metabolic rate, and body temperature, Eskin suggested that the circadian clock may play another role as a regulator for memory formation.[6] He and his lab have shown that an aplysia's ability to form long-term memory is dependent on the time of day, namely that aplysia are able to form long-term memories during the day, but are unable to at night. This was done via regulation of several factors, including neurotransmitter release, MAPK signaling, and immediate early gene expression. Short-term memory, however, has not been shown to vary based on time of day.[7] The mechanism by which this occurs is not currently understood, but Eskin and his lab have continued to study the circadian characteristics of glutamate uptake in synaptic plasticity in order to learn more about the mechanism by which memory formation is controlled by a circadian clock.[6] Furthermore, such information will be useful for chronobiology as a whole in helping explain how a biological clock regulates its outputs to produce rhythm.[1]

Eskinogram

The three components of an Eskinogram: Input, Oscillator, and Output.

Eskin developed the Eskinogram as a heuristic that provides a mechanism for understanding circadian clock pathways. It presents a clock pathway as having three components: input, oscillator, and output. Further modifications to this core model can be made for more complex systems. For example, one oscillator may be able to control multiple outputs.[8]

Model use

The Eskinogram has notably been used to model how the suprachiasmatic nucleus (SCN) acts as a master oscillator for the human biological clock. A group of photoreceptors called the intrinsically photosensitive retinal ganglion cells (ipRGCs) act as the input for the clock mechanism. These cells then use a pathway dependent on melanopsin to signal to the SCN. The SCN then uses a transcription-translation feedback loop, consisting of a set of clock genes that regulate their own expression, to act as a complete oscillator and signal locomotor outputs accordingly.[8]

Impact

The Eskinogram is regarded as a central dogma for circadian researchers. This has led to Eskin's work being influential to later researchers in chronobiology. For example, Eskin worked closely with Dr. Samer Hattar on his thesis on circadian rhythms.[9]

Awards and honors

For his contributions to the Department of Biology and Biochemistry, Eskin received the 25th Esther Farfel Award from the University of Houston in 2003. Serving as department chair from 1994 to 2000, he established a focus on research in neuroscience, biological clocks, and infectious disease and tripled research grants to the department.[10] In the same year, Eskin also received the John and Rebecca Moores Professors Award from the University of Houston.[11]

References

  1. 1.0 1.1 1.2 1.3 "Arnold Eskin". 2021-11-09. https://uh.edu/nsm/biology-biochemistry/people/faculty/memoriam/arnold-eskin/. 
  2. 2.0 2.1 Menaker, M.; Eskin, A. (Dec 23, 1966). "Entrainment of circadian rhythms by sound in Passer domesticus". Science 154 (3756): 1579–1581. doi:10.1126/science.154.3756.1579. ISSN 0036-8075. PMID 5924929. Bibcode1966Sci...154.1579M. 
  3. Levenson, Jonathan (2002). "Glutamate uptake in synaptic plasticity: from mollusc to mammal.". Current Molecular Medicine 2 (7): 593–603. doi:10.2174/1566524023362069. PMID 12420799. http://www.eurekaselect.com/64502/article. Retrieved 2015-04-07. 
  4. Lin, Chien-Liang Glenn; Kong, Qiongman; Cuny, Gregory D; Glicksman, Marcie A (September 2012). "Glutamate transporter EAAT2: a new target for the treatment of neurodegenerative diseases". Future Medicinal Chemistry 4 (13): 1689–1700. doi:10.4155/fmc.12.122. ISSN 1756-8919. PMID 22924507. 
  5. Rosenegger, David; Lukowiak, Ken (2010-08-31). "The participation of NMDA receptors, PKC, and MAPK in the formation of memory following operant conditioning in Lymnaea". Molecular Brain 3 (1): 24. doi:10.1186/1756-6606-3-24. ISSN 1756-6606. PMID 20807415. 
  6. 6.0 6.1 "BIOLOGICAL CLOCK MAY SHUT DOWN LONG-TERM MEMORY AT NIGHT". University of Houston. February 15, 2005. http://www.uh.edu/news-events/archive/nr/2005/02feb/021805aeskin.html. 
  7. Michels, Maxamilian; Lyons, Lisa (August 4, 2014). "Unraveling the complexities of circadian and sleep interactions with memory formation through invertebrate research". Front Syst Neurosci 8 (133): 133. doi:10.3389/fnsys.2014.00133. PMID 25136297. 
  8. 8.0 8.1 Van Gelder R (2004). "Resetting the Clock: Dexras 1 Defines a Path". Neuron 43 (5): 603–604. doi:10.1016/j.neuron.2004.08.029. PMID 15339641. 
  9. "Why Many of Us Suffer Seasonal Affective Disorder" Brain Science Institute [1]. Retrieved 2014-04-22.
  10. "The Esther Farfel Award." University of Houston [2]. Retrieved 2015-04-07.
  11. "Biologist gets two top honors." The Daily Cougar [3]. Retrieved 2015-04-07.