Organization of mitochondria in olfactory bulb granule cell dendritic spines.

In contrast to dendritic spines with only postsynaptic functions, the spines of olfactory bulb granule cells subserve both pre- and postsynaptic roles. In single sections these spines were previously seen to contain mitochondria, most likely needed to provide energy for presynaptic functions, but their frequency and distribution were unknown. In order to understand the organization of mitochondria in these specialized dendritic appendages, we have studied the geometry and cytoplasmic organization of granule cell spines with computer-assisted reconstructions of serial electron micrographs. The spine heads were seen to be elliptical in shape with a single pair of reciprocal synapses on the concave face apposed to the mitral/tufted cell dendrite. Mitochondria were found localized in the spine neck as well as the spine head and often extended between the two compartments. Based on their variable distribution it seems reasonable to suggest that these mitochondria are motile and move in and out of spine compartments from the parent dendrite. Spine apparatus was apparent in most of the spines as membrane bound cisterns of smooth endoplasmic reticulum located close to mitochondria. The possible role of spine apparatus in facilitating the movement of mitochondria in the necks and heads of granule cell spines in the absence of microtubules is discussed.

Differences in mortality rate between abrupt and progressive carotid ligation in the gerbil: role of endogenous angiotensin II.

Studies have shown that in comparison to rapid occlusion of a vessel, gradual occlusion produces less severe tissue ischemia due to a more effective development of collateral circulation. As other studies have shown that collateral circulation can be enhanced by stimulation of the endogenous renin-angiotensin II system, it was hypothesized that this system is involved in the mechanism of protection against ischemia that obtains during gradual vascular occlusion. To test this hypothesis, mortality rates were evaluated in gerbils subjected to gradual vascular occlusion by means of progressive carotid ligation while simultaneously infused with inhibitors of the renin-angiotensin II cascade--enalaprilat or saralasin. Groups of animals with either abrupt or progressive carotid ligation infused with saline served as controls. Results showed that (1) in saline-infused animals, there was a significant decrease in the mortality rate of progressive-ligated animals when compared to abrupt-ligated animals, and (2) administration of either enalaprilat or saralasin to progressive-ligated animals resulted in mortality rates that were indistinguishable from those of saline-infused abrupt-ligated animals. These results suggest that the endogenous renin-angiotensin system is indeed involved in an adaptive mechanism that occurs during progressive ligation of the carotid artery, and more specifically, that the relatively benign effect of progressive carotid ligation may be due to the action of angiotensin II to stimulate the development of collateral circulation and reduce the severity of focal brain ischemia.

Renin in angiolymphoid hyperplasia with eosinophilia. Its possible effect on vascular proliferation.

A hypertensive man became normotensive after the surgical removal of two subcutaneous masses of angiolymphoid hyperplasia with eosinophilia. To demonstrate that angiolymphoid hyperplasia with eosinophilia is a renin-producing pathologic condition, Bowie stain for juxtaglomerular cell granules and immunohistochemistry for human renin were used. Bowie stain was positive in cells showing cytoplasmic granules similar to those found in the juxtaglomerular cells of the kidney. Immunohistochemical staining using antiserum against human renin showed the presence of renin-containing cells. This staining was not seen after substitution of the specific renin antiserum by preimmune serum, by the renin antiserum preabsorbed with pure human renin, or with plasma from a patient with high-plasma renin activity. Renin-containing cells were located in areas surrounding vascular structures and were apparently neither endothelial, mast, nor lymphoid cells. Six of eight additional cases of angiolymphoid hyperplasia with eosinophilia were positive for renin-containing cells. Renin has been described in several other histologically highly vascularized tumors. Since a product of renin, angiotensin II, has been found to have angiogenic properties, it is possible to postulate that renin, through angiotensin II, may stimulate the proliferation of vessels and, therefore, may be involved in the pathogenesis of angiolymphoid hyperplasia with eosinophilia.