Area:
Neuroscience Biology, Molecular Biology, Cell Biology
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High-probability grants
According to our matching algorithm, Jerry J. Buccafusco is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1985 — 1991 |
Buccafusco, Jerry J |
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. |
Mechanism of Centrally-Acting Antihypertensive Drugs @ Medical College of Georgia (McG)
Several clinically available antihypertensive drugs are known to act within the central nervous system to produce a reduction in arterial pressure. Clonidine and methyldopa typify this class of drugs and both compounds are central alpha-adrenergic agonists although their structure and neuronal metabolism are quite different. While central alpha-adrenergic receptors are important for their antihypertensive action brain catecholaminergic neurons are not required, and the maintenance of experimental hypertension may not be dependent on this central neuronal system. Recent studies in this laboratory have suggested an alternate hypothesis. We have found that both clonidine and methylopa produce marked inhibition of central cholinergic neuronal activity in the spontaneously hypertensive rat (SHR). Also, it appears that cholinergic neuronal activity is enhanced in certain brain regions of this model. The purpose of this project is to provide further evidence for the role of central cholinergic neurons in mediating the antihypertensive action of drugs like clonidine and methyldopa. This will be accomplished by 1) examining the ability of clonidine and methyldopa to inhibit the synthesis of regional brain acetylcholine (ACh) in other models of experimental hypertension, DOCA-salt hypertension, Grollman renal hypertension, and salt induced hypertension in the Dahl, salt-sensitive strain; 2) examining the effects on brain ACh metabolism of other clonidine-like drugs, i.e., guanfacine and xylazine; 3) comparing the relative rates of ACh biosynthesis in the models of hypertension and their respective normotensive controls and 4) examining the effects of pharmacologic inhibition of presynaptic central cholinergic activity through the formation of a cholinergic 'false neurotransmitter'. In all studies arterial pressure will be measured directly from unanesthetized rats. ACh biosynthesis will be estimated biochemically by tracer injection of the precursor 3H-choline with subsequent measurement of the rate of formation of labeled ACh. Correlation of both neurochemical and neuropharmacological data will be employed to test our central cholinergic hypothesis of experimental hypertension. This study will aid in understanding the nature of central adrenergic-cholinergic interactions in hypertensive disease and in the mechanism of action of clonidine and related drugs.
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1 |
2007 — 2008 |
Buccafusco, Jerry J |
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. |
Cotinine For Cognitive Impairment in Neurological and Neuropsychiatric Disorders @ Medical College of Georgia (McG)
[unreadable] DESCRIPTION (provided by applicant): In recent years our research findings have provided a new appreciation for the potential pharmacological properties of cotinine, the principal metabolite of nicotine produced after using tobacco products. We now provide compelling evidence that cotinine is indeed a pharmacologically active compound having a number of actions that suggest that it might mediate some of the beneficial effects of nicotine, as well as exhibiting some unique properties of its own. Cotinine was shown to have full efficacy (relative to nicotine) in protecting neural-like cells in culture from a cytotoxic insult. The drug was active in a rat model that predicts antipsychotic-like potential. Cotinine also improved working memory accuracy by non-human primates, and the drug exhibited ability to enhance attention in a distractor version of the same task. Finally we demonstrated that unlike nicotine, cotinine failed to stimulate autonomic ganglionic transmission in the awake rat, but it partly desensitized ganglionic receptors without affecting resting blood pressure. We propose to extend these findings by studying the potential neuroprotective properties of cotinine in a transgenic mouse model of Alzheimer's disease. The potential of cotinine as a prototypical agent to improve cognition in schizophrenia will be studied in a rat model of sustained attention and in monkeys in a working memory task by evaluating the ability of the compound to attenuate or reverse the impairing effects of low doses of psychotomimetic agents. Finally, the relative ability of cotinine to desensitize nicotinic receptors will be determined in of acetylcholine release from relevant regions of rat and monkey CNS. We expect at the completion of these studies to show that cotinine has exploitable therapeutic potential relevant to human diseases that feature behavioral and cognitive impairment and neurodegeneration. Based on its cognition-enhancing and antipsychotic potential, cotinine also could prove useful in the difficult to treat cognitive deficits associated with schizophrenia. Perhaps even more importantly cotinine has the potential to serve as a prototypical agent by which new drug entities may be compared. The partly translational design of the study will provide results leading to eventual clinical trials with cotinine or a relevant analog. [unreadable] [unreadable] [unreadable] [unreadable]
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