Catecholaminergic neurons of treefrog isthmotrigeminal tegmentum

1980 ◽  
Vol 39 (2) ◽  
Author(s):  
R.S. Schmidt
Keyword(s):  
Catecholaminergic Neurons

Catecholaminergic neurons in the brain-stem and sleep apnea in SIDS victims

2004 ◽  
Vol 10 (3-4) ◽  
pp. 173-178 ◽  
Author(s):  
Toshiko Sawaguchi ◽  
Yuri Ozawa ◽  
Patricia Franco ◽  
Hazim Kadhim ◽  
Jose Groswasser ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Brain Stem ◽  
Catecholaminergic Neurons ◽  
The Brain

Long-term modulation of tyrosine hydroxylase activity and expression by endothelin-1 and -3 in the rat anterior and posterior hypothalamus

2008 ◽  
Vol 294 (3) ◽  
pp. R905-R914 ◽  
Author(s):  
Guadalupe Perfume ◽  
Sabrina L. Nabhen ◽  
Karla Riquelme Barrera ◽  
María G. Otero ◽  
Liliana G. Bianciotti ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Cardiovascular Effects ◽  
Receptor Activation ◽  
Catecholaminergic Neurons ◽  
Endothelin System ◽  
Catecholaminergic Transmission ◽  
Underlying Mechanisms ◽  
G Protein Coupled ◽  
The Brain

Brain catecholamines are involved in the regulation of biological functions, including cardiovascular activity. The hypothalamus presents areas with high density of catecholaminergic neurons and the endothelin system. Two hypothalamic regions intimately related with the cardiovascular control are distinguished: the anterior (AHR) and posterior (PHR) hypothalamus, considered to be sympathoinhibitory and sympathoexcitatory regions, respectively. We previously reported that endothelins (ETs) are involved in the short-term tyrosine hydroxylase (TH) regulation in both the AHR and PHR. TH is crucial for catecholaminergic transmission and is tightly regulated by well-characterized mechanisms. In the present study, we sought to establish the effects and underlying mechanisms of ET-1 and ET-3 on TH long-term modulation. Results showed that in the AHR, ETs decreased TH activity through ETB receptor activation coupled to the nitric oxide, phosphoinositide, and CaMK-II pathways. They also reduced total TH level and TH phosphorylated forms (Ser 19 and 40). Conversely, in the PHR, ETs increased TH activity through a G protein-coupled receptor, likely an atypical ET receptor or the ETC receptor, which stimulated the phosphoinositide and adenylyl cyclase pathways, as well as CaMK-II. ETs also increased total TH level and the Ser 19, 31, and 40 phosphorylated sites of the enzyme. These findings support that ETs are involved in the long-term regulation of TH activity, leading to reduced sympathoinhibition in the AHR and increased sympathoexcitation in the PHR. Present and previous studies may partially explain the cardiovascular effects produced by ETs when applied to the brain.

Electron microscopic localization of substance P and enkephalin in axon terminals related to dendrites of catecholaminergic neurons

1979 ◽  
Vol 160 (3) ◽  
pp. 387-400 ◽  
Author(s):  
Virginia M. Pickel ◽  
Tong H. Joh ◽  
Donald J. Reis ◽  
Susan E. Leeman ◽  
Richard J. Miller
Keyword(s):  
Substance P ◽  
Electron Microscopic ◽  
Catecholaminergic Neurons ◽  
Axon Terminals ◽  
Microscopic Localization ◽  
Electron Microscopic Localization

Nicotine activates NPY and catecholaminergic neurons in brainstem regions involved in ACTH secretion

1997 ◽  
Vol 759 (2) ◽  
pp. 259-269 ◽  
Author(s):  
Shannon G Matta ◽  
James D Valentine ◽  
Burt M Sharp
Keyword(s):  
Acth Secretion ◽  
Catecholaminergic Neurons

scholarly journals Intermittent severe hypoxia induces plasticity within serotonergic and catecholaminergic neurons in the neonatal rat ventrolateral medulla

2016 ◽  
Vol 120 (11) ◽  
pp. 1277-1287 ◽  
Author(s):  
Scott A. Givan ◽  
Kevin J. Cummings
Keyword(s):  
Tyrosine Hydroxylase ◽  
Tryptophan Hydroxylase ◽  
Neonatal Rat ◽  
Severe Hypoxia ◽  
Autonomic Response ◽  
Ventrolateral Medulla ◽  
Dopa Decarboxylase ◽  
Catecholaminergic Neurons ◽  
Catecholaminergic System ◽  
Rat Pups

5-HT neurons contribute to autoresuscitation and survival during intermittent severe hypoxia (IsH). In adults, catecholaminergic neurons in the ventrolateral medulla (VLM) contribute to the autonomic response to hypoxia. We hypothesized that 1) catecholaminergic neurons in the neonatal VLM are activated following IsH, 2) this activation is compromised following an acute loss of brain stem 5-HT, and 3) IsH induces cellular and/or transcriptomic plasticity within catecholaminergic and serotonergic neurons that are within or project to the VLM, respectively. To test these hypotheses, we treated rat pups with 6-fluorotryptophan, a tryptophan hydroxylase (TPH) inhibitor, and then exposed treated and vehicle controls to IsH or air. Along with immunohistochemistry to detect tyrosine hydroxylase (TH)- or Fos-positive neurons, we used RNA sequencing to resolve the effects of IsH and 5-HT deficiency on the expression of serotonergic and catecholaminergic system genes in the VLM. 5-HT deficiency compromised autoresuscitation and survival. IsH significantly increased the number of identifiable TH-positive VLM neurons, an effect enhanced by 5-HT deficiency ( P = 0.003). Contrary to our hypothesis, 5-HT-deficient pups had significantly more Fos-positive neurons following IsH ( P = 0.008) and more activated TH-positive neurons following IsH or air ( P = 0.04). In both groups the expression of the 5-HT transporter and TPH2 was increased following IsH. In 5-HT-deficient pups, the expression of the inhibitory 5-HT1A receptor was decreased following IsH, while the expression of DOPA decarboxylase was increased. These data show that the serotonergic and catecholaminergic systems in the VLM of the neonatal rat are dynamically upregulated by IsH, potentially adapting cardiorespiratory responses to severe hypoxia.

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