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High-probability grants
According to our matching algorithm, Matthew JM Rowan is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2014 — 2016 |
Rowan, Matthew J.m. |
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. |
Local Control of the Action Potential in Axons @ Max Planck Florida Corporation
DESCRIPTION (provided by applicant): In axons, the action potential (AP) waveform determines the timing and strength of neurotransmission. Although the AP is classically thought of as a stereotyped all or none signal, recent studies have shown that the axonal AP waveform is more malleable then once thought. One explanation is that a non-uniform distribution of voltage-sensitive potassium (Kv) channels exists within different axonal compartments. The relative inaccessibility of axons to electrophysiology has hampered exploration of this topic. This is especially true with respect to the small axons of interneurons, in which the axonal AP waveform has not been directly observed. To study the AP in interneuron axons, I developed a 2-photon (2P) voltage imaging technique to accurately report fast voltage changes with high spatial and temporal resolution. The compact cerebellar stellate cell was chosen, as these interneurons provide the sole source of inhibition within the cerebellum and play a vital role in the temporal integration of cerebellar output. Preliminary results show APs are shaped at individual boutons by locally expressed Kv channels, allowing AP waveform changes to occur at one bouton without perturbing the AP at nearby boutons. In addition, activity-dependent broadening of the AP occurred at boutons but not in connecting axon shafts, suggesting that inactivating Kv channels expressed at boutons were responsible for this effect. This proposal will explore local AP control in more detail. The 1st aim will determine which Kv subtypes are locally expressed at boutons as well as how local control influences synaptic strength within axons, utilizing patch-clamp recordings and 2P voltage and Ca2+ imaging/uncaging Kv inhibitor. The 2nd aim will uncover which Kv subtypes allow for rapid activity-dependent broadening and the impact of this phenomenon on synaptic transmission. Results from these aims will present new data on how interneuron axons perform complex computations in a site-specific manner, leading to a more complete understanding of neuronal processing.
|
0.903 |
2021 |
Rowan, Matthew J.m. |
R56Activity Code Description: To provide limited interim research support based on the merit of a pending R01 application while applicant gathers additional data to revise a new or competing renewal application. This grant will underwrite highly meritorious applications that if given the opportunity to revise their application could meet IC recommended standards and would be missed opportunities if not funded. Interim funded ends when the applicant succeeds in obtaining an R01 or other competing award built on the R56 grant. These awards are not renewable. |
Neuronal Mechanisms of Altered Circuit Excitability in Early Alzheimer's
14 million Americans are projected to be living with dementia by 2050. Alzheimer?s disease (AD) is the most common form of dementia, responsible for ~70% of all cases. A hallmark feature of Alzheimer?s disease (AD) is progressive synaptic and neuronal pathology- factors that ultimately result in cognitive decline. While there is increasing confidence that specific biomarkers can predict the occurrence of AD in individuals, the molecular and cellular mechanisms contributing to the initiation of the disease remain poorly understood. Gaining a greater understanding of these mechanisms is crucial if we hope to halt neurodegeneration early enough to preserve memory and cognition. Interestingly, a common phenomenon has now been observed in both humans with mild cognitive impairment, as well as in animal models during the early stages of AD. These observations agree that neuronal circuits affected by AD become more active during the early stages of the disease. In addition, evidence exists that hyperactive neurons become vulnerable to synaptic degradation- a hallmark feature of AD. Our objective is to uncover neuronal mechanisms that result in this early-stage circuit dysfunction. Evidence exists that inhibitory interneurons are vulnerable to changes in activity during early AD. For example, action potential (AP) firing is modified in interneurons, but less so in other cell types, in prodromic AD mouse models. AP firing in interneurons is controlled by a unique subset of ion channels, and it has been suggested that the expression of particular ion channels change in interneurons during AD. However, what changes in the expression, subcellular trafficking, or biophysical properties of ion channels occur in early AD remain unclear. Using human APP-expressing mouse models and cutting-edge molecular, electrophysiological, and 2-photon imaging techniques, we propose to uncover changes in specific ion channels in these GABAergic interneurons in depth. Based on our preliminary data, we hypothesize that modification of a particular class of Kv channels in interneurons directly contributes to cortical hyperexcitability in early AD. Importantly, studies will be performed ex vivo early on in the disease process (i.e., before plaque formation or synapse loss). Findings from this proposal will help us better understand the initiating factors of circuit pathology during early AD and could lead directly to the development of molecular and cellular therapies that halt synaptic and neuronal pathology.
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0.936 |