scholarly journals Expression of (pro)renin receptor and angiotensin II type 1 receptor on bone marrow‐related neurons in the central nervous system

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Christie Diane Kimball ◽  
Wencheng Li ◽  
Andrea Zsombok ◽  
Andrei Derbenev ◽  
Joseph Francis ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Bone Marrow ◽  
Nervous System ◽  
Angiotensin Ii ◽  
The Central Nervous System

Angiotensin II Type 1 receptor (AT1) signaling in astrocytes regulates synaptic degeneration-induced leukocyte entry to the central nervous system

2011 ◽  
Vol 25 (5) ◽  
pp. 897-904 ◽  
Author(s):  
L. Füchtbauer ◽  
M. Groth-Rasmussen ◽  
T.H. Holm ◽  
M. Løbner ◽  
H. Toft-Hansen ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Synaptic Degeneration ◽  
The Central Nervous System

Mammalian Bone Marrow Acetylcholinesterase

1982 ◽  
Vol 40 ◽  
pp. 44-45
Author(s):  
Ezzatollah Keyhani
Keyword(s):  
Central Nervous System ◽  
Bone Marrow ◽  
Nervous System ◽  
Common Property ◽  
Extracellular Medium ◽  
The Central Nervous System ◽  
The Common ◽  
Mammalian Bone

Acetylcholinesterase (EC 3.1.1.7) (ACHE) has been localized at cholinergic junctions both in the central nervous system and at the periphery and it functions in neurotransmission. ACHE was also found in other tissues without involvement in neurotransmission, but exhibiting the common property of transporting water and ions. This communication describes intracellular ACHE in mammalian bone marrow and its secretion into the extracellular medium.

scholarly journals Non-Oncological Neuroradiological Manifestations in NF1 and Their Clinical Implications

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1831
Author(s):  
Camilla Russo ◽  
Carmela Russo ◽  
Daniele Cascone ◽  
Federica Mazio ◽  
Claudia Santoro ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Structural Organization ◽  
Neurofibromatosis Type ◽  
Review Article ◽  
Tumor Suppressor Protein ◽  
Clinical Implications ◽  
Nf1 Gene ◽  
The Central Nervous System

Neurofibromatosis type 1 (NF1), the most frequent phakomatosis and one of the most common inherited tumor predisposition syndromes, is characterized by several manifestations that pervasively involve central and peripheral nervous system structures. The disorder is due to mutations in the NF1 gene, which encodes for the ubiquitous tumor suppressor protein neurofibromin; neurofibromin is highly expressed in neural crest derived tissues, where it plays a crucial role in regulating cell proliferation, differentiation, and structural organization. This review article aims to provide an overview on NF1 non-neoplastic manifestations of neuroradiological interest, involving both the central nervous system and spine. We also briefly review the most recent MRI functional findings in NF1.

Central site for pressor action of blood-borne angiotensin in rat

1980 ◽  
Vol 239 (3) ◽  
pp. R358-R361 ◽  
Author(s):  
G. D. Fink ◽  
J. R. Haywood ◽  
W. J. Bryan ◽  
W. Packwood ◽  
M. J. Brody
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Third Ventricle ◽  
Central Component ◽  
The Third ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
The Difference

A previous study demonstrated that the threshold dose of intra-arterial angiotensin II required to induce a pressor response in the rat was significantly lower when the drug was administered into the carotid artery than when administered into the abdominal aorta. This result was interpreted to indicate that part of the increase in arterial pressure produced by low concentrations of blood-borne angiotensin in this species was the result of an effect on structures in the central nervous system selectively accessible via the carotid vascular bed. The purpose of the present study was to establish more precisely the site of the pressor action of angiotensin within the central nervous system. The central component of the pressor effect of angiotensin was quantified as the difference in pressor responses to intracarotid and intra-aortic infusions of angiotensin II (delta c-a). In conscious rats, delta c-a was attenuated by administration of the angiotensin antagonist, saralasin, into the third cerebral ventricle. In rats with chronic electrolytic lesions of the anteroventral third ventricle (AV3V), delta c-a was abolished. Periventricular structures surrounding the third ventricle appear to mediate the central component of the pressor action of blood-borne angiotensin in the rat.

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