Area:
Neuroscience Biology
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High-probability grants
According to our matching algorithm, W Michael Panneton is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1988 — 1995 |
Panneton, W Michael |
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. |
Trigeminal Modulation of Autonomic Behavior
Stimulating the nasal cavity exerts a powerful and abrupt alteration of respiratory and cardiovascular rhythms. This remarkable behavior is present in all vertebrates, including man, and commonly is called the diving reflex. The control is mediated through the central nervous system, which possesses the neuronal circuits directing cardiorespiratory function. However, no information is available regarding the specific central neural circuits driving this behavior. My long-term objective is to establish the brainstem reflex pathways utilized in the diving reflex in mammals. The general aim of this proposal is to establish the trigeminal component of these circuits; it specifically aims to 1) determine the locus within the trigeminal sensory complex which receives sensory fibers from the nose and upper respiratory passages using transganglionic transport methods; 2) validate the importance of this area as the trigeminal mediator of cardiorespiratory function using both reversible blocking agents (lidocaine and muscimol) and electrical and chemical (glutamate) stimulation; 3) determine the projections of neurons in this area to brainstem autonomic nuclei using conventional neuroanatomical techniques (HRP, PHA-L, tritiated amino acids); 4) specifically determine the role of the trigeminoparabrachial pathway in the response using blocking agents and if this pathway uses opiates as a chemical messenger (double labeling techniques and naloxone injections). The powerful inhibition of respiration and heart resulting from upper respiratory stimulation may provide a neurogenic basis for the tragedy of the Sudden Infant Death Syndrome (SIDS) and the cardiorespiratory alterations seen in simple intubation procedures. Understanding the brainstem circuitry of the diving response could aid in the diagnosis and remedy of these problems. Knowledge of these same brainstem circuits will serve as a substrate for future investigations of how a simple somatic stimulus could be designed to modulate autonomic behavior and how higher levels of the brain (i.e. limbic) influence cardiorespiratory activity usually controlled at lower levels.
|
1.009 |
2001 — 2004 |
Panneton, W Michael |
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. |
The Cpa: Somatic and Autonomic Systems
DESCRIPTION (Verbatim from the application): The long-term goal of my research is to establish the brainstem circuits through which trigeminal neurons modulate cardiovascular and respiratory activity in mammals. The cardiorespiratory depression (the diving response) seen after stimulation of he upper respiratory tract (URT) has served as my model. The aims for this proposal are directed towards elucidating the control of blood pressure, specifically in regard to both nasal and muscle stimulation. We shall focus our attention on the interplay between the caudal pressor area (CPA) and its interaction with the premotor sympathetic bulbospinal neurons of the rostroventrolateral medulla RVLM). Since the CPA is basically undefined in the rat, two of our aims are directed to locating it and demonstrating its connections, especially with the RVLM. Two other aims will define its role in blood pressure regulation in general as well as to nasal nd muscle stimulation. A fifth aim will define the primary afferent termination of sensory fibers innervating the triceps sure muscle in the rat. We propose specifically to 1) localize the CPA in the caudal medulla; 2) define the input/output of the CPA; 3) define the central termination of sensory fibers to the triceps sure muscle; 4) determine the role of the CPA during the diving esponse and muscle stimulation; and, 5) characterize the responses of individual neurons in the CPA to hypertensive, hypotensive, oxious, and nasal and muscle stimuli. The CPA has been defined in variable positions within the caudal medulla depending on the species in question. Aim I specifically will identify its location in the rat. Blood pressure will be recorded after stimulating the caudal medulla; such a procedure should localize the pressor areas there. Two complimentary neuroanatomical methodologies will determine the output/input of the PA, especially to the RVLM, as outlined in Aim II The orthogradely transported tracer biotinylated dextrin amine and the retrogradely transported tracer fluorogold will elucidate projections from/to the CPA. There is some controversy regarding the input o the dorsal horn of primary afferent fibers from muscle. Aim III will use transganglionic transport of HRP to investigate this roblem and correlate this data to that seen in Aim II. In Aim IV, the CPA will be tested to determine its role in controlling blood pressure to both nasal and muscle stimulation. Chemical lesions using ibotenic acid will be made in the CPA and changes in cardiovascular behavior to such stimulation determined. Finally, neurons in the CPA will be monitored electrophysiologically in Aim V and their responses recorded to hypertensive, hypotensive, noxious, and nasal and muscle stimuli. This study will provide the most complete study of the CPA, about which little is known. Stimulation of the URT or large muscles in man causes an increase in sympathetic discharge and hypertension. Understanding the brainstem mechanisms governing he vascular constriction after either of these somatic stimuli may provide a neurological explanation for this. Such knowledge may lead to an understanding of essential hypertension.
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1.009 |