Mary Hasler

Characterization of the calcium-induced disruption of neurofilaments in rat peripheral nerve.

Transverse frozen sections of desheathed rat peripheral nerve were incubated in media of different composition prior to fixation and processing for electron microscopic examination. Neurofilaments remained intact when these tissues were incubated in calcium-free media. A loss of neurofilaments and their replacement by granular debris occurred in myelinated and unmyelinated fibers following incubation in media containing 2 mM calcium. The calcium-mediated disruption of neurofilaments was inhibited by preincubation or incubation with 1 mM p-chloromercuribenzoate (PCMB). The inhibition by preincubation with PCMB could be partially reversed by subsequent preincubation with 10 mM dithioerythritol (DTE). Calcium-mediated breakdown of neurofilaments did not occur after prolonged preincubation in calcium-free media, a finding which suggested that neurofilament disruption was dependent upon a tissue factor which could be lost or inactivated in frozen-sectioned nerve tissues. The findings of the present study provide morphological evidence that neurofilament disruption in mammalian peripheral nerve is mediated by a calcium-activated, PCMB-sensitive enzyme in the axoplasm of myelinated and unmyelinated nerve fibers.

ULTRASTRUCTURE OF ARTICULAR CARTILAGE OF MICE TREATED WITH SOMATOTROPHIN.

Administration of somatotropic hormone to newborn or weanling mice of strain C57BL Jax6 for one, two, or four weeks accelerated articular growth and development. The organelles were increased in number and the appearance of granular endoplasmic reticulum, Golgi vacuoles, multivesicular bodies, and glycogen was hastened. Toward the end of the developmental cycle, the chondrocytes swelled excessively and their plasmalemma ruptured without evidence of vascular erosion. After four weeks of treatment, there was premature breakdown of chondrocytes, their place being taken by fibrillar microscars. In the matrix, development of fibers was accentuated. The intensification of fibrillarity was followed by disorientation of the superficial collagen fibers with fraying of the articular covering. The functional significance of these findings, as well as their relation to aging changes in cartilage, is discussed.

Ultrastructure of articular cartilage of achondroplastic mice.

Articular chondrocytes of achondroplastic mice (cn/cn) resemble ultrastructurally those of their non-achondroplastic siblings (Cn/Cn or Cn/cn), except for premature deposition of glycogen and a tendency to undergo regression. The latter may be slight or extreme. The ultimate cause of the vulnerability of the chondrocytes and the cause of the heterogeneity of the reaction could not be determined with the method employed. Nevertheless, increased vulnerability accounts for cell death under conditions which are usually not injurious, and which may be either physiologic or altered by endogenous or exogenous factors.

Stimulation of Articular Cartilage of Young Adult Mice by Hormones

Young adult male mice of strain Cδ7Bl were treated with somatotrophin, thyroxine or estradiol benzoate and were observed for 24 h, 2, 4 days or 1 or 2 weeks. The articular cartil

Long spacing striated bodies in articular cartilage of mice.

Long spacing bodies with a characteristic pattern of striation were found in the articular cartilage of the femoral head of 1-year-old mice of strain C 57 B1. The structures were compared with similar ones found in tissues other than cartilage, and potential etiologic factors were discussed.

Stimulation of Articular Chondrocytes of Middle-Aged Mice by a Cartilage-Bone Marrow Extract

Articular chondrocytes of 1-year-old male mice of strain C57B1 were stimulated by injections of a cartilage-bone marrow extract to undergo hypertrophy, intensified organellar development and hyperplasia. This response was attenuated as compared with that of growing animals treated similarly. The morphological findings are consistent with some increase in synthetic activity on the part of the chondrocytes. The increased cell death observed was attributed to overstimulation and subsequent exhaustion, and was considered responsible for the prominence of microscars in the matrix.