A histologically derived stereotaxic atlas and substance P immunohistochemistry in the brain of the least shrew (Cryptotis parva) support its role as a model organism for behavioral and pharmacological research

Cysticercosis is an infection with larval cysts of the cestodeTaenia solium. Through pathways that are incompletely understood, dying parasites initiate a granulomatous reaction that, in the brain, causes seizures. Substance P (SP), a neuropeptide involved in pain-transmission, contributes to inflammation and previously was detected in granulomas associated with deadT. crassicepscysts. To determine if SP contributes to granuloma formation, we measured granuloma-size and levels of IL-1β, TNF-α, and IL-6 within granulomas inT. crassiceps-infected wild type (WT) mice and mice deficient in SP-precursor (SPP) or the SP-receptor (neurokinin 1, NK1). Granuloma volumes of infected SPP- and NK1-knockout mice were reduced by 31 and 36%, respectively, compared to WT mice (P<.05for both) and produced up to 5-fold less IL-1β, TNF-α, and IL-6 protein. Thus, SP signaling contributes to granuloma development and proinflammatory cytokine production inT. crassicepsinfection and suggests a potential role for this mediator in human cystercercosis.

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Effect of substance P on the content of catecholamines and on the enzymes of their synthesis in the brain of chronically alcoholized rats

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf02444370 ◽

1994 ◽

Vol 118 (1) ◽

pp. 728-730

Author(s):

I. P. Anokhina ◽

A. G. Veretinskaya ◽

A. A. Rodionov ◽

N. A. Khristolyubova

Keyword(s):

Substance P ◽

Chronically Alcoholized Rats ◽

The Brain

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Further Exploring the Brain–Skin Connection: Stress Worsens Dermatitis via Substance P-dependent Neurogenic Inflammation in Mice

Journal of Investigative Dermatology ◽

10.1038/sj.jid.5701079 ◽

2008 ◽

Vol 128 (2) ◽

pp. 434-446 ◽

Cited By ~ 92

Author(s):

Sanja Pavlovic ◽

Maria Daniltchenko ◽

Desmond J. Tobin ◽

Evelin Hagen ◽

Stephen P. Hunt ◽

...

Keyword(s):

Substance P ◽

Neurogenic Inflammation ◽

The Brain

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Vascular responses of dura mater

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.1.h157 ◽

1989 ◽

Vol 257 (1) ◽

pp. H157-H161 ◽

Cited By ~ 2

Author(s):

F. M. Faraci ◽

K. A. Kadel ◽

D. D. Heistad

Keyword(s):

Blood Flow ◽

Substance P ◽

Dura Mater ◽

Sympathetic Nerves ◽

Vascular Headache ◽

Vascular Responses ◽

Anesthetized Dogs ◽

High Level ◽

The Brain ◽

Increased Blood Flow

The goal of this study was to examine vascular responses of the dura mater. Microspheres were used to measure blood flow to the dura and brain in anesthetized dogs. Under control conditions, blood flow to the dura was 38 +/- 3 (SE) ml.min-1.100 g-1. Values for blood flow to the dura obtained with simultaneous injection of 15- and 50-microns microspheres were similar, which suggests that shunting of 15-microns spheres was minimal. Left atrial infusion of substance P (100 ng.kg-1.min-1) and serotonin (40 micrograms.kg-1.min-1), two agonists that have been reported to increase vascular permeability in the dura, increased blood flow to the dura two- to threefold. Adenosine (iv) produced vasodilatation in the dura. Adenosine and serotonin did not affect cerebral blood flow, but substance P increased blood flow to the brain by approximately 40%. Seizures, which produce pronounced dilatation of cerebral vessels despite activation of sympathetic nerves, produced vasoconstriction in the dura. Thus 1) the dura is perfused at a relatively high level of blood flow under normal conditions and is very responsive to vasoactive stimuli, and 2) substance P and serotonin, which have been implicated in the pathogenesis of vascular headache, produce pronounced vasodilator responses in the dura mater.

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Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder

Biochemistry and Cell Biology ◽

10.1139/bcb-2017-0122 ◽

2018 ◽

Vol 96 (2) ◽

pp. 88-97 ◽

Cited By ~ 17

Author(s):

Yohaan Fernandes ◽

Desire M. Buckley ◽

Johann K. Eberhart

Keyword(s):

Fetal Alcohol Spectrum Disorder ◽

Model Organism ◽

Spectrum Disorder ◽

Structural Defects ◽

Craniofacial Skeleton ◽

Fetal Alcohol ◽

Embryonic Exposure ◽

Fetal Alcohol Spectrum ◽

The Brain ◽

Insight Into

The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD.

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