Evidence for intraventricular secretion of angiotensinogen and angiotensin by the subfornical organ using transgenic mice.

Direct intracerebroventricular injection of angiotensin II (ANG II) causes increases in blood pressure and salt and water intake, presumably mimicking an effect mediated by an endogenous mechanism. The subfornical organ (SFO) is a potential source of cerebrospinal fluid (CSF), ANG I, and ANG II, and thus we hypothesized that the SFO has a secretory function. Endogenous levels of angiotensinogen (AGT) and renin are very low in the brain.

Ciliary Defects in a Mouse Model of Bardet-Biedl Syndrome are Selectively Pronounced in Brian Regions Involved in Cardiovascular Regulation.

Bardet-Biedl syndrome (BBS) is a human genetic disorder associated with several phenotypes including hypertension. Here we used the hypertensive Bbs4 knockout mouse model (Bbs4-/-) to test the hypothesis that areas of the brain involved in cardiovascular regulation (CVR) exhibit abnormalities in primary neuronal cilia (PNC) structure and density. We utilized immunocytochemical localization of adenylyl cyclase-III (ACIII), a specific marker for PNC, to identify the changes in PNC length and density in commissural nucleus of solitary tract (cNTS), area postrema (AP), rostroventrolateral medulla (RVLM) and subfornical organ (SFO).

Glutamatergic phenotype of glucagon-like peptide 1 neurons in the caudal nucleus of the solitary tract in rats.

The expression of a vesicular glutamate transporter (VGLUT) suffices to assign a glutamatergic phenotype to neurons and other secretory cells. For example, intestinal L cells express VGLUT2 and secrete glutamate along with glucagon-like peptide 1 (GLP1). We hypothesized that GLP1-positive neurons within the caudal (visceral) nucleus of the solitary tract (cNST) also are glutamatergic.

Ciliopathy is differentially distributed in the brain of a Bardet-Biedl syndrome mouse model.

Bardet-Biedl syndrome (BBS) is a genetically heterogeneous inherited human disorder displaying a pleotropic phenotype. Many of the symptoms characterized in the human disease have been reproduced in animal models carrying deletions or knock-in mutations of genes causal for the disorder. Thinning of the cerebral cortex, enlargement of the lateral and third ventricles, and structural changes in cilia are among the pathologies documented in these animal models.

Structural defects in cilia of the choroid plexus, subfornical organ and ventricular ependyma are associated with ventriculomegaly.

Background: Hydrocephalus is a heterogeneous disorder with multiple etiologies that are not yet fully understood. Animal models have implicated dysfunctional cilia of the ependyma and choroid plexus in the development of the disorder. In this report, we sought to determine the origin of the ventriculomegaly in four Bardet Biedl syndrome (BBS) mutant mouse strains as models of a ciliopathy.