Area:
Learning and Memory
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High-probability grants
According to our matching algorithm, Cedric L. Williams is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1997 — 2001 |
Williams, Cedric L |
K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Neurobiological Contribution to Memory Formation @ University of Virginia Charlottesville
DESCRIPTION (Adapted from applicant's abstract): The objective of this project is to correlate performance on memory-related behavioral tasks with neurotransmitter changes occurring in brain regions that process memory. Hormones released from the adrenals during emotionally arousing events influence cell groups in the lateral parabrachial nucleus (PB) and central amygdala (AMY) to encode new experiences more effectively. Since some adrenal hormones do not enter the brain, their effects on anatomical structures must be mediated by some intervening mechanism. Brainstem nuclei in the nucleus of the solitary tract (NTS) receive input regarding changes in peripheral autonomic and neuroendocrine states via the vagus nerve and convey this information to neurons in the PB and AMY. The proposed experiments are based on the hypothesis that the intervening mechanism by which epinephrine influences the AMY or PB during memory storage involves activation of catecholaminergic nuclei in the NTS. This hypothesis will be tested by determining if the reported effects of a peripheral injection of epinephrine on influencing amygdala neurotransmitter levels or facilitating memory storage processes are altered by removing the contribution of the NTS. In these experiments, the involvement of the NTS will be reduced by blocking noradrenergic receptors in this nucleus or interrupting neural transmission with the use of local anesthetics. The second set of experiments will test the hypothesis by examining whether stimulation of NTS noradrenergic neurons mimics, or produces comparable effects on memory and central amygdala norepinephrine activity as that produced by peripheral epinephrine. The final series of experiments will determine if there are corresponding increases in extracellular levels of norepinephrine in both the NTS and central amygdala after epinephrine injection, and if the changes are mediated by the PB. These findings are expected to have implications in the treatment of memory disorders by increasing understanding of the interactions between brain structures and neurotransmitter systems that regulate memory.
|
1 |
2001 — 2005 |
Williams, Cedric L |
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. |
Noradrenergic Modulation of Memory Storage @ University of Virginia Charlottesville
Memory dysfunction is an increased important problem among Americans, especially in those who are either aging , experiencing depression or exposed to emotional trauma. The factors contributing to memory disorder involve either a reduced or exaggerated capacity to experience arousal, which results in impaired neurotransmitter release in limbic structures that process memory. Hormones released from the adrenals after exposure to arousing events facilitate encoding and storage of memory traces by stimulating norepinephrine secretion in the brain. However, most hormones have limited capacity to enter the brain and therefore do not produce direct effects on structures that actively encode and store memory. The objective of this application is to reveal the neural pathways that arousal-related hormones utilize to affect brain regions such as the nucleus of the solitary tract (NTS), which in turn, influence norepinephrine release in limbic regions that process memory. The central hypothesis of this application proposes that regulation of memory formation by arousal- related hormones involves activation of NTS noradrenergic neurons which in turn, influence norepinephrine output in the amygdala and hippocampus. This hypothesis will be tested by 1) examining the neural pathway that mediates epinephrine's mnemonic effects on brainstem and limbic structures, 2) delineating the class of receptors in the NTS that initiate the cascade of intracellular events to increase impulse flow from this nucleus to limbic structures, and 3) by determining the neural pathways brainstem neurons utilize to influence neural activity associated with memory consolidation in both of the amygdala and hippocampus. The proposed investigations are expected to provide a better understanding of the involvement of norepinephrine in regulating memory formation and also expand current knowledge by characterizing the neural events which lead to optimal memory performance following the endogenous release of peripheral hormones. Information gained from these studies will be beneficial in identifying the underlying causes of memory disorders.
|
1 |
2007 — 2012 |
Williams, Cedric Erisir, Alev (co-PI) [⬀] |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Peripheral & Central Correlates of Arousal & Memory @ University of Virginia Main Campus
The scope of this project is to understand how physiological changes induced by emotionally arousing events improve the degree to which affective experiences are stored into long term memory. This research is driven by the hypothesis that the vagus nerve and brainstem neurons that they synapse upon serve as an interface between autonomic arousal, produced by hormone secretion in the periphery, and accompanying changes in neurotransmitter release in the brain that then accelerates memory storage processing. The project will obtain electrophysiological recordings from the vagus nerve to assess how fluctuations in visceral signals regulate the release of the neurotransmitter norepinephrine in brain areas where affective and contextual components of newly learned events are encoded. Other experiments will use behavioral, neurochemical and immunocytochemical endpoints to identify how experiences of an emotional nature increase central noradrenergic transmission. They will also identify how potentiated norepineprhine initiates intracellular signaling cascades that convert novel experiences from labile traces into more permanent long term memory. The overall project is expected to reveal neural and molecular systems that permit arousal-induced changes in peripheral autonomic activity to regulate the strength in which new events are encoded into memory. This project will also provide extensive research training for undergraduate students majoring in Psychology, Cognitive Science and Neuroscience as well as provide an avenue for undergraduates to develop independent thesis projects prior to graduation. These types of opportunities have proven beneficial in not only training the next generation of behavioral neuroscientists, but also in ensuring their entry into productive graduate psychology or neuroscience graduate programs.
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0.915 |