Serena Dudek | |
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| Born | 1964 (age 59–60) Anaheim, California |
| Nationality | USA |
| Alma mater | University of California, Irvine Brown University |
| Spouse | Marc Sommer |
| Children | 1 |
| Awards | A.E. Bennett Research Award (2009) [1] |
Serena M. Dudek (born 1964; Anaheim, California), is an American neuroscientist known for her work on long-term depression [2] [3] and synaptic plasticity in the CA2 region of the hippocampus. [4]
Dudek's father was an English professor at Fullerton College, and her mother was a clinical cytologist and medical technologist. [5] In high school, she worked at Knott's Berry Farm, selling ice cream and popcorn. She was also on the drill team at Savanna High School. [5]
In 1982, Serena Dudek matriculated into the University of California, Irvine. [6] Dudek worked as an undergraduate researcher in the lab of Gary Lynch, studying the degradation of brain spectrin, also known as fodrin, by calpains. [5] [6]
Serena Dudek enrolled a Ph.D. program at Brown University where she joined Mark Bear's lab to study long-term depression in a collaboration with Leon Cooper. [5] Her work was used to support the BCM theory. [7] She finished her Ph.D. studies in 1992. [1]
After receiving her doctorate, Dudek did post-doctoral work at the University of Alabama at Birmingham. and with the National Institute of Child Health and Human Development. In 2001, Dudek started working at the NIEHS, where she is now a Senior Investigator. [1]
On August 26, 2007 with the Duke University Medical Center, Dudek et al published a paper on their research on brain proteins in mice related to Obsessive-compulsive disorder (OCD). The SAPAP3 protein plays a crucial role in nerve signals traveling to another across the synapse within the striatum. Additional gene mutations that are mirrored in humans are hypothesized to play a role within OCD in humans too. [8] On September 19, 2010 Dudek et al published a paper titled "Gene limits learning and memory in mice" which studied the effect of a specific gene deletion on cognitive performance in mice. [9]
In a Newsweek article called "Buff Your Brain" Serena Dudek and her colleagues' 2011 research on the effects of caffeine in lab rodents was highlighted. [10] Serena Dudek's research found that rats that were given an equivalent shot of two cups of coffee had stronger electrical activity between neurons in their hippocampus area called CA2. [10] [11]
In Laboratory News article named "Doh! Losing ‘Homer Simpson’ gene makes mice smart," Dudek was cited for her study on electrical currents on mice. The article highlights how mice with the disabled "Homer Simpson" gene were able to have stronger neuron connections in the hippocampus area called CA2.
In Scientific American Article titled "Knocking Out a 'Dumb' Gene Boosts Memory in Mice", [12] Dudek rationalizes why we would have a "dumb" gene, explaining that, "If the gene is conserved by natural selection, there must be some reason. Intuitively, it seems there should be a downside to having this gene knocked out, but we haven’t found it so far. It may be that these mice are hallucinating, and you just can’t tell."
In an article titled "Coffee for your thoughts: New study suggests caffeine can help learning, memory" [13] from the Columbia Chronicle, Dudek discussed her work on the CA2 region of the hippocampus. She discusses her work in which she observed the CA2 region in rats after administering caffeine. Her team then removed and observed the rat brains and found that caffeine improved synaptic strength in the CA2 region of the brain.
An article from The Pilot entitled, "UNC Pembroke Professor, Biotech Center Team Identify Dementia-Related Brain Alterations due to Military Blasts", [14] Dudek and other researchers are cited on their work concerning the neurological effects from explosive blasts.
In 2012, Dudek's work on caffeine's effect on neuronal connection was highlighted in Newsweek, supporting the research of electrical activity of neurons on cognitive functioning. [10]
Ever since 1987, Serena Dudek has been a part of the Society for Neuroscience: Washington, DC, US. From October, 2019 to October 2020, she served as the treasurer of the society. [15]
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 other 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.
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.
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.
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.
Pavlovian fear conditioning is a behavioral paradigm in which organisms learn to predict aversive events. It is a form of learning in which an aversive stimulus is associated with a particular neutral context or neutral stimulus, resulting in the expression of fear responses to the originally neutral stimulus or context. This can be done by pairing the neutral stimulus with an aversive stimulus. Eventually, the neutral stimulus alone can elicit the state of fear. In the vocabulary of classical conditioning, the neutral stimulus or context is the "conditional stimulus" (CS), the aversive stimulus is the "unconditional stimulus" (US), and the fear is the "conditional response" (CR).
An apical dendrite is a dendrite that emerges from the apex of a pyramidal cell. Apical dendrites are one of two primary categories of dendrites, and they distinguish the pyramidal cells from spiny stellate cells in the cortices. Pyramidal cells are found in the prefrontal cortex, the hippocampus, the entorhinal cortex, the olfactory cortex, and other areas. Dendrite arbors formed by apical dendrites are the means by which synaptic inputs into a cell are integrated. The apical dendrites in these regions contribute significantly to memory, learning, and sensory associations by modulating the excitatory and inhibitory signals received by the pyramidal cells.
Glutamate receptors are synaptic and non synaptic receptors located primarily on the membranes of neuronal and glial cells. Glutamate is abundant in the human body, but particularly in the nervous system and especially prominent in the human brain where it is the body's most prominent neurotransmitter, the brain's main excitatory neurotransmitter, and also the precursor for GABA, the brain's main inhibitory neurotransmitter. Glutamate receptors are responsible for the glutamate-mediated postsynaptic excitation of neural cells, and are important for neural communication, memory formation, learning, and regulation.
Brian R. Christie is a Professor of Medicine and Neuroscience at The University of Victoria. He helped found the Neuroscience Graduate Program at the University of Victoria and served as its director from 2010–2017. He is a Michael Smith Senior Scholar Award winner. Christie received his PhD in 1992 from the University of Otago before doing postdoctoral work with Daniel Johnston at Baylor College of Medicine and Terrence Sejnowski at the Salk Institute for Biological Studies, and then became Assistant Professor at the University of British Columbia. Promoted to Associate Professor in 2007. Full Professor in 2013.
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.
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.
Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules during increased neuronal activity.
Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.
The cellular transcription factor CREB helps learning and the stabilization and retrieval of fear-based, long-term memories. This is done mainly through its expression in the hippocampus and the amygdala. Studies supporting the role of CREB in cognition include those that knock out the gene, reduce its expression, or overexpress it.
The relationship between sleep and memory has been studied since at least the early 19th century. Memory, the cognitive process of storing and retrieving past experiences, learning and recognition, is a product of brain plasticity, the structural changes within synapses that create associations between stimuli. Stimuli are encoded within milliseconds; however, the long-term maintenance of memories can take additional minutes, days, or even years to fully consolidate and become a stable memory that is accessible. Therefore, the formation of a specific memory occurs rapidly, but the evolution of a memory is often an ongoing process.
While the cellular and molecular mechanisms of learning and memory have long been a central focus of neuroscience, it is only in recent years that attention has turned to the epigenetic mechanisms behind the dynamic changes in gene transcription responsible for memory formation and maintenance. Epigenetic gene regulation often involves the physical marking of DNA or associated proteins to cause or allow long-lasting changes in gene activity. Epigenetic mechanisms such as DNA methylation and histone modifications have been shown to play an important role in learning and memory.
Mark Firman Bear is an American neuroscientist. He is currently the Picower Professor of Neuroscience at The Picower Institute for Learning and Memory at Massachusetts Institute of Technology. He is a former Howard Hughes Medical Institute Investigator; an Elected Fellow of the American Association for the Advancement of Science and the American Academy of Arts and Sciences; and a Member of the National Academy of Medicine.
Rosemary C. Bagot is a Canadian neuroscientist who researches the mechanisms of altered brain function in depression. She is an assistant professor in behavioral neuroscience in the Department of Psychology at McGill University in Montreal, Canada. Her focus in behavioral neuroscience is on understanding the mechanisms of altered brain circuit function in depression. Employing a multidisciplinary approach, Bagot investigates why only some people who experience stress become depressed.
Cristina Maria Alberini is an Italian neuroscientist who studies the biological mechanisms of long-term memory. She is a Professor in Neuroscience at the Center for Neural Science in New York University, and adjunct professor at the Departments of Neuroscience, Psychiatry, and Structural and Chemical Biology at the Icahn School of Medicine at Mount Sinai in New York.
Hey-Kyoung Lee is a neuroscience professor at Johns Hopkins University. She studies cross-modal plasticity between visual and auditory systems.
Nicole Calakos is an American neuroscientist and neurologist. She is the Lincoln Financial Group Distinguished Professor of Neurobiology at Duke University. She is an elected Member of the American Association for the Advancement of Science, American Society for Clinical Investigation, and National Academy of Medicine for her "pioneering work in optogenetic approaches, and substantial contributions in the area of synaptic plasticity with a focus on striatal circuity of the basal ganglia."
| Authority control databases: Academics |
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