Area:
Synaptic Plasticity
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High-probability grants
According to our matching algorithm, Adam Iliff is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2011 — 2013 |
Iliff, Adam James |
F31Activity Code Description: To provide predoctoral individuals with supervised research training in specified health and health-related areas leading toward the research degree (e.g., Ph.D.). |
Interaction of Opposing Forms of Synaptic Plasticity in Hippocampal Circuits
DESCRIPTION (provided by applicant): The mammalian hippocampus is known to be critical for the formation of long-term memories, yet this brain region is highly vulnerable to epilepsy. Long-term potentiation and depression (LTP and LTD) - two forms of "Hebbian" synaptic plasticity- are widely regarded as likely cellular mechanisms of information storage in hip- pocampal circuits. A different form of synaptic plasticity at hippocampal synapses - homeostatic synaptic plasticity -drives compensatory changes at synapses to stabilize network function when overall circuit activity changes. Since Hebbian forms of synaptic plasticity are long-lasting, how these changes in synaptic efficacy endure in the face of homeostatic mechanisms that would be predicted to reverse them is unknown. Theories have been proposed regarding how these ostensibly conflicting plasticity processes could be interacting but experimental support for these theories is scarce, largely because the conventional preparations and time- course over which homeostatic plasticity is often studied differ from those most widely used (acute hippocampal slices) to study Hebbian plasticity. To address this issue empirically, our laboratory has characterized a rapid form of homeostatic plasticity at CA3-CA1 synapses in acute hippocampal slices, and my preliminary data reveals that one form of Hebbian plasticity (LTD) constrains such homeostatic compensation in an input- specific fashion. Given that recent work has linked homeostatic overcompensation with the development of epileptoform activity in hippocampal circuits, alterations in this inhibitory regulation of homeostatic plasticity may play an important role in the pathogenesis of temporal lobe epilepsy. This proposal will now test the hypothesis that local protein synthesis in dendrites, in addition to allowing for long-lasting information storage, plays a novel role in allowing Hebbian plasticity to constrain local homeostatic compensation at hippocampal synapses. This hypothesis will be tested in two specific aims. The objective of aim #1 is to examine how Hebbian plasticity interacts with homeostatic plasticity at the same synaptic inputs. I will ex- amine whether this interaction reflects an inhibition of the homeostatic activity sensor that detects changes in activity or reflects modulation of the compensation process directly. The goal of aim #2 is to determine whether local dendritic protein synthesis mediates the ability of Hebbian plasticity to constrain homeostatic plasticity at the same synaptic inputs. This proposed research is significant and innovative because it provides the first experimental approach to define how homeostatic and Hebbian processes influence one another in a defined neural circuit prone to epileptogenesis. PUBLIC HEALTH RELEVANCE: Alterations in synaptic connections between neurons in the hippocampus are thought to contribute to learning and memory, yet this brain region is also highly susceptible to epilepsy. More recent work has identified a novel class of synaptic modification - termed homeostatic synaptic plasticity - that is thought to stabilize activity within neural networks, but how this form of synaptic plasticity interacts with modifications important for learning is not known. The proposed work will examine how homeostatic forms of synaptic plasticity interact with synaptic modifications important for learning and memory, and will thus critically inform future studies that target homeostatic plasticity as a novel therapeutic option for epilepsy with the potential for permanently restoring stable patterns of activity in seizure-prone circuits.
|
0.958 |
2016 — 2018 |
Iliff, Adam James |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Neural and Molecular Mechanisms Underlying Sound-Evoked Behavior in C. Elegans
? DESCRIPTION (provided by applicant): Hearing loss is one of the most common sensory impairments impacting human health, with both genetic and environmental etiologies. The central mediators of hearing are mechanosensitive channels capable of transducing a sound stimulus into electrical activity of sensory neurons. Despite decades of intense investigation using vertebrate models, the identity of the mechanotransduction channel for mammalian hearing remains unknown. The use of genetically tractable invertebrate systems, such as the popular genetic model Caenorhabditis elegans, has proven to be an indispensable platform for identifying the mechanisms and machinery underlying mechanotransduction. C. elegans has a compact nervous system amenable to neural circuit analyses and a completely sequenced genome with sophisticated genetic tools available, but the ability to perceive sound in this organism hasn't been observed until now. Despite the lack of an overt specialized sound-sensing organ, I find that C. elegans is strongly responsive to sound, suggesting this organism possesses a simple auditory system. Multiple lines of evidence indicate that C. elegans can directly transduce airborne sounds over a range of frequencies. Pilot experiments indicate that sound detection in C. elegans involves transduction channels distinct from classical touch receptors, suggesting that studies of sound transduction in C. elegans have great potential to reveal a novel sound-sensitive channel, which may be conserved as the elusive channel underlying hearing in mammals. This proposal will test the hypothesis that sound is transduced by mechanosensitive channels expressed in sensory neurons that functionally couple the detection of sound with escape locomotion circuits. The objective of Aim 1 is to identify the neural circuit underlying the auditory response and characterize neuronal activity to further our understanding of how sensory input is transformed into behavioral responses. The goal of Aim 2 is to identify and characterize the molecular mechanisms responsible for transducing sound. By pursuing this project, I will gain training in both classic C. elegans methods and cutting-edge functional circuit analysis, as well as in the topic of sensory neurobiology. The proposed research is significant because it provides the first experimental approach to study hearing in C. elegans and is expected to yield novel insights into the molecular nature of the mechanosensitive channels mediating hearing in humans.
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0.958 |