L
Lawrence P. Schramm
Researcher at Johns Hopkins University
Publications - 80
Citations - 2839
Lawrence P. Schramm is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Spinal cord & Spinal cord injury. The author has an hindex of 31, co-authored 79 publications receiving 2740 citations. Previous affiliations of Lawrence P. Schramm include Johns Hopkins University School of Medicine & University of Minnesota.
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Peripheral and central pathways regulating the kidney: a study using pseudorabies virus
TL;DR: The paucity of infected propriospinal neurons in the presence of infected brainstem neurons, even in lightly infected rats, is discussed in reference to the relative importance of descending vs spinal regulation of the sympathetic outflow to the kidney.
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Maximum likelihood identification of neural point process systems
TL;DR: In this paper, a method is presented whereby functional relationships between neurons can be detected and modeled using the theory of random point processes, based on a point process characterization involving stochastic intensities and an additive rate function model.
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Preganglionic innervation of the adrenal gland of the rat: a study using horseradish peroxidase.
TL;DR: Adrenal medullae of 15-day-old and adult rats were injected with a solution of horseradish peroxidase. as discussed by the authors showed that the perikarya and dendrites exhibited a predominately transverse orientation.
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Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.
Pitayadet Jumrussirikul,Jay L. Dinerman,Ted M. Dawson,Valina L. Dawson,Ulf Ekelund,Dimitrios Georgakopoulos,Lawrence P. Schramm,Hugh Calkins,Solomon H. Snyder,Joshua M. Hare,Ronald D. Berger +10 more
TL;DR: It is suggested that the absence of nNOS activity leads to reduced baseline parasympathetic tone, but does not prevent baroreflex-mediated cardioinhibition unless inhibitory G proteins are also inactivated, serving as parallel pathways to mediate autonomic slowing of heart rate in the mouse.
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Sensitivity of sympathetically correlated spinal interneurons, renal sympathetic nerve activity, and arterial pressure to somatic and visceral stimuli after chronic spinal injury.
TL;DR: The results suggest that spinal circuits undergo significant plastic changes in the chronic stage of spinal cord injury, and they provide a mechanism for the observation, in some human patients, that many stimuli applied caudal to the site of spinal injury increase sympathetic activity and arterial pressure.