Explore chapters and articles related to this topic
Baroreceptor Reflex Components and Their Alteration in Hypertension
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Several investigators (Abraham, 1967; Aumonier, 1972) have described myelinated nerve bundles in the tunica adventitia of the vascular walls. These nerve bundles lose their myelin sheaths, branch profusely, and terminate in the form of rings and loops. Some of them display large compact endings, while others possess terminal fibrillar expansions. Ultrastructural studies on baroreceptors (Abdel-Magied et al., 1982; Bock and Gorgas, 1976; Knoche et al., 1980; Krauhs, 1979) indicate that unmyelinated axons form terminals and intercalated expansions of different sizes at the border of adventitia and media. Large terminals (5–8 μm) are located mainly in adventitia, whereas the small terminals (0.6–2 μm) are located between elastic fibers and muscle cells in the border region between tunica media and tunica adventitia. The terminal or intercalated expansion contains a mesaxon and is embedded in the cytoplasm of a specialized Schwann cell. The baroreceptors are either submerged into the surface of this cell or are surrounded by a thin cytoplasmic process of this cell (Knoche et al., 1980). The processes of the terminal cells are in contact with the elastic fibers, muscle fibers, and collagen. The receptor and the terminal cell form a functional unit. The presence of densely packed mitochondria and glycogen particles in these receptor terminals reflects the high metabolic demand due to repeated membrane activity in response to blood pressure pulsation. Because of high turnover and regeneration of axoplasm, abnormal organelles (notably myelin and dense bodies) are often present within baroreceptor endings. Active transport in response to fast turnover of axoplasm may explain the presence of abundant microtubules in these endings.
The leptin receptor mutation of the obese Zucker rat causes sciatic nerve demyelination with a centripetal pattern defect
Published in Ultrastructural Pathology, 2018
Jacques Gilloteaux, Kritika Subramanian, Nadia Solomon, Charles Nicaise
Low magnification demonstrates that all the samples from obese nerves have damaged nerve fibers shown with LM in a small branch of the sciatic nerve (Figures 4(a,b) and 5(a,b)). Among the smallest fibers alterations, some nerve fibers display defective myelin tight organization in the outer mesaxon of the SC cytoplasm where altered wrapping membrane can be seen while the axoplasm content seems untouched (Figures 4(b) and 5(c)–13). Further away from the perikaryon, internodal SC zones show other disruptions or anomalies in the outer and inner mesaxons with adjacent debris to the tight myelin (Figure 15) even though SCs appear to reveal typical nucleus with perikaryal organelles, clusters of dilated cisterns of rough and smooth endoplasmic reticulum, Golgi parts, intermingling polysomes, and mitochondria are recognized (Figure 6(c,d)). In Figure 6(c), an example of a lucky field of view displays an elongated deposit droplet (no limiting membrane) seemingly or faintly striated but of unclear nature can accompany other few endoplasmic cisterns where sometimes a fibril of collagen precursor (pro-collagen?) is viewed; one could interpret it to be later secreted as part of the basal lamina (Figure 6(d)). At all stages of damage, the nerve fibers show inner mesaxon changes or anomalies in alignment as well as for the adaxonal lining. The neuroplasm reveals swelling of the neuroreticulum but no apparent fibrillar or microtubular changes (Figures 4(b) and 9–13). Near one Golgi cistern, adjacent electron dense vesicles (lysosomes?) are noticed (Figure 6(d)). The basal lamina always tightly surrounds all SCs and does not appear with any discontinuities in all TEM views throughout the nerve. In the endoneurium, collagen eventually shows erratically organized fibers and bundles (Figure 4(b)).