cached image
We are testing a new system for linking grants to scientists.
The funding information displayed below comes from the
NIH Research Portfolio Online Reporting Tools and the
NSF Award Database.
The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
You can help! If you notice any innacuracies, please
sign in and mark grants as correct or incorrect matches.
Sign in to see low-probability grants and correct any errors in linkage between grants and researchers.
High-probability grants
According to our matching algorithm, Robert W. Stackman Jr is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2005 — 2009 |
Stackman, Robert William |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Ethanol's Influence On Neural Mechanisms of Navigation @ Oregon Health and Science University
DESCRIPTION (provided by applicant): This is a 2-yr proposal of research examining the influence of ethanol on the neural mechanisms that control higher cognitive functions, in particular spatial navigation. Spatial navigation is a fundamental behavior that is essential for accurate moving about our environment and for efficiently changing routes to goal locations in the face of environmental changes. Navigation requires a number of higher cognitive functions including perception, attention, planning, judgment, and memory. In humans, acute alcohol intoxication impairs several higher cognitive functions including navigation, memory and attention. Alcohol intoxication is a leading contributor to motor vehicle accidental deaths, sports accidents, impairments in complex behaviors, and ataxia in the United States. Acute alcohol intoxication limits the ability to form new memories, and impairs the ability to effectively use established spatial memories. The brain mechanisms responsible for these effects of alcohol are not known. Understanding the neurobiological mechanisms that are responsible for the detrimental behavioral actions of acute alcohol is essential for developing effective strategies to treat or prevent problems associated with alcohol abuse. The long term goal of this research is to define the brain mechanisms responsible for alcohol's effects on navigation. Previous behavioral studies have shown that acute ethanol disrupts spatial memory in rats and mice. In contrast, acute ethanol has minimal effects on the spatial firing of hippocampal neurons (place cells). Thus, there is a disconnection between the behavioral and electrophysiological influences of ethanol. This discrepancy suggests that ethanol's effect on spatial cognition may result from actions of the drug on brain systems other than the hippocampus. The dose-dependent effects of acute ethanol on hippocampal-dependent and anterior thalamicdependent spatial navigation will be determined in C57BL/6J mice in Aim 1. Aim 2 will determine the dose dependent effects of acute ethanol on hippocampal place cells and anterior thalamic head direction cell responses. This second aim will provide an indication of the consequences of ethanol on the neurobiological correlates of spatial information processing. Aim 3 is designed to examine the simultaneous effect of ethanol on the firing patterns of multiple neurons recorded in parallel from the anterior thalamus and hippocampus of mice engaged in navigation tasks. This innovative research coupling electrophysiological and cognitive measures will provide important data regarding the neural networks that are responsible for ethanol's influence on spatial cognition.
|
0.958 |
2005 — 2011 |
Stackman Jr, Robert |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Influence of Sk Channels On Hippocampal Memory @ Florida Atlantic University
Small conductance calcium-activated potassium (SK) channels influence the excitability of neurons and regulate synaptic plasticity, physiological processes that are fundamental for higher cognitive functions such as learning and memory. Brain circuitry that includes the hippocampus is essential for forming explicit memories, such as memory for facts, personal history and events. This project tests the influence of SK channels on brain and behavioral mechanisms of explicit memory. The central hypothesis is that SK2 channels restrict the functional output of hippocampal neurons that may be necessary for synaptic plasticity and memory. The specific aims of the studies to test this hypothesis are to: Determine the individual contributions of SK1, SK2, and SK3 channels to hippocampal learning and memory using transgenic mice strains (Aim 1). Mice that selectively lack SK2 channels are expected to have improved memory, while mice that overexpress SK2 channels are expected to have impaired memory. Determine the specific influence of hippocampal SK channels on the memory processes of encoding, retention and retrieval (Aim 2). This will be determined by direct administration of SK channel blockers or activators into the hippocampus of C57BL/6J mice. Blocking SK channels is expected to improve memory encoding, while activation of SK channels is expected to impair memory encoding. Defining how SK channels regulate hippocampal memory will improve the understanding of the behavioral and brain mechanisms of learning and memory. This project will provide opportunities for postdoctoral, graduate and undergraduate students to gain expertise in the science of learning and memory. The research will also serve as a focus for scientific outreach programs directed to the broader community.
|
0.915 |
2009 — 2013 |
Stackman, Robert William |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Memory Modulation by Sk Channels @ Florida Atlantic University
DESCRIPTION (provided by applicant): Treating the devastating loss of memory associated with aging or neurodegenerative disease requires that we first understand the basic cellular mechanisms of memory. Small conductance calcium-activated potassium (SK) channels play a fundamental role in shaping the responses of neurons in brain regions known to be critical for memory. SK channels are also functionally coupled to a well recognized cellular mechanism of memory, the NMDA-type glutamate receptor. NMDA receptor activity is considered by many to be essential for synaptic changes that underlie memory formation. Activation of SK channels reduces excitatory NMDA receptor responses and shunts NMDA receptor-dependent synaptic plasticity. Therefore, SK channels are in a unique position to influence memory processes. The goals of this application are to understand: A) the distinct influence of SK channels in the hippocampus and in the lateral amygdala on the processes of memory encoding, retention, retrieval and extinction;B) the consequence of specific blockade of SK2 channels, or the specific activation of SK3 and SK2 channels on hippocampal and amygdala memory processes;C) the efficacy of SK channel blockers to rescue the memory deficits found in mice that overexpress SK2 channels;and D) the potential for dendritic SK2 channels in the lateral amygdala to be internalized after the encoding of new fear memories. These experiments combine Pavlovian fear conditioning paradigms with region-specific intracranial microinfusions to define the influence of brain SK channels on memory processes. The final aim involves a collaborative effort with Dr. John Adelman (Co- Investigator) to conduct ultrastructural analyses of synapses of lateral amygdala neurons after fear conditioning. Our preliminary findings indicate that the SK channel blocker, apamin enhances memory, while the SK channel activator, 1-EBIO impairs memory. Evidence also suggests that memory encoding or the formation of new memory is uniquely sensitive to SK channel blockers and activators. The lack of effect of SK channel drugs on later stages of memory suggests that SK channels may undergo a form of plasticity during learning - perhaps removal from the dendritic spine surface. Together, the proposed studies will provide insights into the relatively underdeveloped field of memory modulation. The studies will improve knowledge of the mechanisms involved in distinct memory processes, including extinction of memory. These studies will also contribute to defining targets for novel therapies to combat impairments of memory that result from aging and neurological disorders, a well as treatments for fear and anxiety disorders. PUBLIC HEALTH RELEVANCE: The proposed studies will provide insights into the fundamental basic biology of memory. The project will highlight mechanisms of several memory processes and aid the development of novel therapies to combat impairments of memory that result from aging, neurodegenerative disorders, and fear or anxiety disorders.
|
0.958 |