Area:
neurochemistry, behavior
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High-probability grants
According to our matching algorithm, Janet Finlay is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1999 — 2002 |
Finlay, Janet M |
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. |
Model of Schizophrenia--Role of Cortical Dopamine @ Western Washington University
Postmortem studies indicate that the dopamine (DA) innervation of prefrontal cortex (PFC) is diminished in schizophrenic subjects. Furthermore, neurodevelopmental disruptions involving mesoprefrontal DA neurons are thought to contribute to the pathophysiology of schizophrenia and could, in part, account for the emergence of symptoms as the individual matures. To determine the potential functional consequences of this structural abnormality, I will examine whether partial loss of DA axons in the prefrontal cortex (PFC) sustained early in development (12 days of age) differentially affect function of PFC in the prepubertal and adult rat. First, we will examine the effect of partial loss of DA axons sustained early in development on local extracellular DA in PFC of the prepubertal and adult rat (Aim 1). Our recent studies indicate that 60% loss of DA axons in PFC sustained immediately prior to puberty (40 days of age), decreased basal and stress- evoked extracellular DA in PFC of the adult rat (68 days of age). Thus, moderate loss of DA fibers as recently observed in PFC of schizophrenic subjects, may be sufficient to impair the function of PFC. I will also examine the effects of partial loss of DA axons in PFC sustained early in development on the ability of the PFC to regulate the neurochemical activity of a subcortical target area, the mesoaccumbens DA projection (Aim 2). Previously, it has been suggested that diminished activity of mesoprefrontal DA neurons augments the activity of subcortical DA neurons and that both events contribute to the pathophysiology of schizophrenia. Our own studies indicate that partial loss of DA axons in PFC sustained immediately prior to puberty, increased stress-evoked DA release in the NAS shell of adult rats. Finally, we will examine the impact of partial loss of DA axons in PFC sustained early in development on behaviors thought to be modulated by mesoprefrontal and mesoaccumbens DA neurons in the prepubertal and adult rat (Aim 3). It has been suggested that dysfunction of mesoprefrontal and mesoaccumbens DA neurons together give rise to some of the behavioral symptoms of schizophrenia. Previously, we reported that partial loss of DA axons in PFC sustained immediately prior to puberty attenuated amphetamine-evoked DA release in the NAS core and amphetamine-induced motor behavior in adult rats. Together, the latter findings suggest that neurochemical interactions between mesocortical and mesoaccumbens DA neurons ultimately play a role in the expression of behavior. The present studies will correlate changes in the activity of mesoprefrontai and mesoaccumbens DA neurons with performance on a delayed response task, motor behavior, and the behavioral response to appetitive and aversive stimuli.
|
0.958 |
2010 |
Finlay, Janet M |
R15Activity Code Description: Supports small-scale research projects at educational institutions that provide baccalaureate or advanced degrees for a significant number of the Nation’s research scientists but that have not been major recipients of NIH support. The goals of the program are to (1) support meritorious research, (2) expose students to research, and (3) strengthen the research environment of the institution. Awards provide limited Direct Costs, plus applicable F&A costs, for periods not to exceed 36 months. This activity code uses multi-year funding authority; however, OER approval is NOT needed prior to an IC using this activity code. |
Behavioral and Neurochemical Effects of Cortical Nmda Receptor Dysfunction: Impli @ Western Washington University
DESCRIPTION (provided by applicant): Altered function of cortical glutamate afferent and efferent projections is thought to contribute to the pathophysiology of schizophrenia. In particular, attention has focused on possible alterations in glutamate N-methyl-D-aspartate (NMDA) receptors in the prefrontal cortex (PFC). Individual NMDA receptors are comprised of a common NR1 subunit (necessary for functional NMDA receptors) together with a combination of NR2A-D subunits. Recent postmortem studies have found evidence of decreased NR1 transcript in the PFC of schizophrenic subjects. A goal of our research is to examine whether regionally restricted loss of NR1 function in the PFC contributes to cognitive and neurochemical deficits associated with the illness. The present studies will be performed in a mouse model in which loxP sites flank a functionally requisite exon of the NR1 subunit (fNR1 mice). Gene deletions will be performed by local administration of adeno-associated-virus Cre recombinase. Our previous studies indicate that impaired function of the NR1 subunit in the medial PFC and CA3 hippocampus of fNR1 mice differentially disrupts sustained attention and working memory, respectively. Aim 1 of the present proposal is to further explore the effects of localized disruptions of the NR1 subunit in the PFC and CA3 hippocampus on cognitive function in adult fNR1 mice. Cognitive function will be examined using delayed spatial win-shift, non-delayed random foraging, and visual sustained attention tasks. Aim 2 will assess whether NR1 dysfunction in the PFC results in secondary disruptions in the neurochemical activity of mesoprefrontal dopamine (DA) neurons. Dysfunction of mesoprefrontal DA neurons has long been thought to contribute to cognitive deficits in schizophrenia. Furthermore, considerable experimental evidence supports the existence of a glutamate-DA interaction in the PFC and, in turn, our hypothesis that chronic NR1 dysfunction will impair the functional capacity of mesocortical DA neurons. The effects of localized PFC NR1 dysfunction on regulation of local extracellular DA will be examined using in vivo microdialysis. Preliminary data from our lab supports the feasibility of performing microdialysis in fNR1 mice. The overall goal of the proposed research is to examine the behavioral and neurochemical effects of dysfunction of glutamate N-methyl-D-aspartate (NMDA) receptors in the prefrontal cortex (PFC) in an effort to further understand the neurobiological basis of cognitive deficits associated with schizophrenia. Consistent with the objective of the AREA grant mechanism, all preliminary and future experiments described in this proposal have involved and will continue to involve undergraduate students in our newly established behavioral neuroscience major at Western Washington University. PUBLIC HEALTH RELEVANCE: Schizophrenia is a debilitating disease affecting ~1% of the population. Cognitive deficits associated with the disease are the most disruptive and unfortunately, the least responsive to currently available treatments. The proposed research endeavors to further our understanding of the neurobiological basis of these deficits in the hopes of ultimately, contributing to ongoing efforts to develop novel treatments for the cognitive impairment.
|
0.958 |