Area:
Nicotinic Receptors
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High-probability grants
According to our matching algorithm, Jim Boulter is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1997 — 2002 |
Boulter, Jim |
P50Activity Code Description: To support any part of the full range of research and development from very basic to clinical; may involve ancillary supportive activities such as protracted patient care necessary to the primary research or R&D effort. The spectrum of activities comprises a multidisciplinary attack on a specific disease entity or biomedical problem area. These grants differ from program project grants in that they are usually developed in response to an announcement of the programmatic needs of an Institute or Division and subsequently receive continuous attention from its staff. Centers may also serve as regional or national resources for special research purposes. |
Core--Molecular Biology Core @ University of California Los Angeles
opioid receptor; molecular biology; biomedical facility; polymerase chain reaction; genetically modified animals; laboratory mouse;
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1 |
1998 — 1999 |
Boulter, Jim |
R03Activity Code Description: To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
Transgenic Approaches to Acetylcholine Receptor Function @ University of California Los Angeles
DESCRIPTION (Applicant's Abstract): The long term goal of this proposal is to use a molecular genetic approach to investigate the function of nicotinic acetylcholine receptors (nAChR) in the vertebrate central nervous system. Although considerable molecular data regarding the structure and function of nAChR subunits is available, far less is known about neural circuitry or roles subserved by the individual receptors. Moreover, little is known about the physiological consequences of mutations within these genes, the precise roles of receptor subtypes in the normal ontogeny and modulation of central nervous system synapses, or in the establishment of nicotine-induced dependence, tolerance and withdrawal among habitual tobacco users. As a first step towards addressing these issues, this proposal outlines experiments which use homologous recombination to introduce null or altered-function mutations of selected nAChR subunit genes into mice. The rationale for these exploratory studies rests on the assumption that deficits or alterations in targeted genes can, upon analysis of subject animals, reveal or clarify the function of the mutated gene. Specifically, the extant application proposes to utilize recombinant DNA methodologies to construct two strains of mice, the first of which will harbor a deletion of the alpha6 nAChR subunit gene. Since the alpha6 subunit gene is actively transcribed in catecholaminergic nuclei (ventral segmental area, substantia nigra, and locus coeruleus), it is anticipated that null mutants will help to define central nicotinic cholinergic circuits which modulate locomotion. Likewise, an alpha6 null mutation is anticipated to have profound effects on behaviors which originate in the mesolimbic dopamine system and are relevant to the reinforcing properties of nicotine, or to basic motivational processes which underlie learning and cognitive behavior. The second genetically engineered mouse will harbor a specific mutation (Ser248Phe) in the alpha4 nAChR subunit gene. In vitro this mutation potentiates onset and slows recovery from receptor desensitization, while in vivo this mutation is responsible for a human, brain-specific phenotype known as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). The purpose of this part of the proposal is to provide an animal model to analyze the molecular pathology of partial epilepsy, and to offer a paradigm for the development and evaluation of cholinergic therapeutic strategies.
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1 |
2005 — 2006 |
Boulter, Jim |
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.) |
A Mouse Model of Inherited Frontal Lobe Epilepsy @ University of California Los Angeles
DESCRIPTION (provided by applicant): One (1) widely accepted benchmark in epilepsy research is to achieve a cure for an inherited form of epilepsy by developing a therapy that is based on understanding the effects of the causative mutation. Towards this end, we have genetically engineered mutant mouse strains that genocopy a human disorder known as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). Patients with this idiopathic partial epilepsy syndrome become symptomatic during the second decade of life. Audiovisual monitoring and polysomnography reveals brief clusters of hyperkinetic motor seizures and vocalizations that begin during non-rapid eye movement sleep. Currently, several mutations have been linked to ADNFLE, all of which map to the pore-forming domain of the nicotinic acetylcholine receptor (nAChR) a4 or B2 subunit genes. We have created 2 lines of 'knockin' mice that contain ADNFLE mutations in the nAChR a4 subunit gene. The principal objective of this proposal is to establish the degree to which these mutant mice phenocopy human ADNFLE and thereby validate this animal model of inherited partial epilepsy. In Specific Aim 1, we propose experiments that seek to characterize recurrent seizure activity in ADNFLE mice. In particular, we will determine the age of seizure onset, estimate penetrance, and evaluate seizure semiology and frequency. Combined video-polysomnographic and electroencephalographic (EEC) analyses will be used to measure ictal and interictal EEG patterns, localize the neuroanatomical origin of epileptiform activity, and explore the relationship between sleep and seizure onset. In Specific Aim 2, we outline studies using mouse brain slices and electrophysiology to test the hypothesis that mutant a4B2 nAChRs alter y-aminobutyric acid-mediated events leading to disinhibition of excitatory, glutamatergic systems and seizures. The objective of these experiments is to examine possible synaptic mechanisms underlying epileptogenesis and to determine the effects of ADNFLE mutations on a4a2receptor-mediated function in vivo.
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1 |