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High-probability grants
According to our matching algorithm, John P. Christianson is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2016 — 2017 |
Christianson, John Paul |
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.) |
Stressor Controllability, Resilience and Prefrontal Endocannabinoids
ABSTRACT The ability to control the onset, offset or intensity of a stressor is one of the most important factors in determining the physiological and psychological consequences of the stressor. Across species, control over stress leads to resilience while uncontrollable stressors predispose one to psychiatric disease. Control over stress operates via a neural circuit that includes the ventromedial prefrontal cortex (vmPFC). In published and pilot studies we have established that control over stress increases the intrinsic excitability of the vmPFC and propose to test here the role of endogenous cannabinoids (eCBs) in this phenomenon. eCBs are known to alter vmPFC excitability by modulation of local inhibitory interneurons. Our working hypothesis that the experience of control over stress triggers eCB release which blunts activity of GABAergic interneurons within the vmPFC leading to stress resilience. This project incorporates a study of sex differences in stress coping mechanisms, which will help fill the massive gap in our understanding of stress and resilience in women. In a set of discovery experiments we seek to quantify eCB levels in the vmPFC after controllable or uncontrollable stress using LC-MS/MS and quantify prefrontal GABAergic inhibitory activity using acute slice electrophysiology and immunuohistochemistry. The prediction is that controllable stress elevates eCBs, reduces GABAergic synaptic transmission and GABAergic neuronal activation. In mechanistic studies we will knock down or elevate vmPFC eCBs by targeting the eCB degredation enzymes using a combination of viral overexpression and pharmacology. By combining these manipulations with exposure to controllable or uncontrollable stress we can determine whether eCBs are necessary and sufficient for stress resilience in later behavioral tests of social anxiety and fear.
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1 |
2017 — 2018 |
Christianson, John Paul |
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. |
Insular Cortex Oxytocin and Social Affective Behavior
Project Abstract Disorders involving social behaviors such as autism spectrum disorder are increasingly prevalent, yet the pathophysiological bases for these conditions elude researchers and current treatments are woefully inadequate. The insular cortex and the neuropeptide oxytocin are highly implicated in both normal and pathological social affective processes such as empathy. Importantly, the oxytocin receptor is concentrated in the insular cortex, providing a link between these neural systems. Using a simple test of social affect in rat, we propose a multidisciplinary approach to determine the contribution and interaction of these systems in primitive, empathy-like processes. We hypothesize that social affective behavior in rodents involves axonal release of oxytocin acting at insular cortex oxytocin receptors and communication between the insula and other nodes in the social emotional circuit, namely the ventromedial prefrontal cortex. We seek to test this hypothesis in a number of ways. First, we will determine if insular cortex oxytocin receptors are necessary to social affective behavior using behavioral pharmacology and chemogenetics, quantify socially evoked oxytocin release within insula using in vivo microdialysis, identify the consequences of OT on the intrinsic excitability of prefrontal cortex-projecting insular pyramidal neurons and a generate a functional map of neuronal activation resulting from social affect using immunohistochemistry. Next we will chemogenetically manipulate the oxytocinergic input to the insula to determine if axonal release of oxytocin is sufficient to modulate social behaviors. Finally, we will utilize a multi-site, pathway specific chemogenetic strategy to dissect the contribution of insular cortex outputs to the prefrontal cortex in social affect, and their dependency on oxytocin. The expected contribution of this work will be to link release of oxytocin and action at insular cortex oxytocin receptors to social affective behaviors, via modulation of the insular cortex output to the prefrontal cortex. This work can have a transformative impact on our understanding of fundamental social behaviors, inform the development of new treatments of social disorders, and provide mechanistic support for theoretical models of the social brain.
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1 |
2019 — 2021 |
Christianson, John Paul |
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. |
Insular Cortex and Social Affect
Abstract Disorders involving social behaviors such as autism spectrum disorder are increasingly prevalent, yet the pathophysiological bases for these conditions elude researchers and current treatments are woefully inadequate. The insular cortex is highly implicated in both normal and pathological social affective processes such as emotion recognition and empathy. The insular cortex receives a major input from the amygdala and so it is likely a site of integration for social and emotional information leading to modulation of social approach and avoidance behaviors via insular projections to the nucleus accumbens. Using a simple rodent social behavioral test in which rats display approach behaviors to conspecifics in distress, we hypothesize that an amygdala to insula to accumbens circuit mediates social responses to stressed individuals. We will use tract specific descriptive and mechanistic methods to establish the necessity and sufficiency of insula-projecting amygdala neurons and accumbens-projecting insula neurons in social decision making. Using activity dependent genetic labeling of insular cortex neurons we will address whether insula-dependent approach and avoidant behaviors are mediated by the same or distinct subsets of insula neurons. This work will inform the development of new treatments of social disorders and provide mechanistic tests of major theoretical models of the social brain.
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