The overall objective of these experiments is to advance our understanding of the neurophysiological mechanisms that underlie responses of the sympathetic nervous system to emotional stressors in an animal model. Project 4 focuses upon two integrated autonomic/behavioral responses to emotional stressors in which the sympathetic nervous system predominates; the defense reaction and the vigilance reaction: This project seeks to delineate the functional efferent pathways that mediate the cardiovascular components of the defense and vigilance reactions and to determine how critical CNS sites interact to produce these integrated patterns of response to stressors. Although attenuation of cardiovascular reactivity is a goal of many clinical interventions, the CNS mechanisms involved in the modulation of the gain of affective response systems are poorly understood. Accordingly, one of the objectives of the current proposal is to assess the mechanisms by which sensory information from chemoreceptor and baroreceptors modulate cardiovascular reactivity associated with the defense reaction and the vigilance reaction. By using electrophysiological, neuroanatomical, and behavioral techniques the following specific aims will be addressed; 1) to continue the line of inquiry initiated during the previous funding period which will use a retrograde analysis to trace the efferent pathways that mediate athe defense reaction and the vigilance reaction. 2) to use the lidocaine reversible lesioning technique and single cell recording techniques to determine the function of integrative sites located ina the amygdala, hypothalamus and periaqueductal grey (PAG) ina the organization and regulation the defense reaction; 3) to use lidocaine lesions and single cells recording techniques to asses mechanisms of feedback regulation of cardiovascular reactivity by information from baroreceptor and chemoreceptive afferents; 4) to use a retrograde analysis to map pathways from baroreceptors to CNS sites that mediate feedback regulation of the defense reaction.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
2P01HL036588-11
Application #
5213606
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
11
Fiscal Year
1996
Total Cost
Indirect Cost
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