Effect of preganglionic parasympathetic denervation on Nitric Oxide synthase in submandibular gland of adult albino rat

Adult albino rats were subjected to chorda tympani neurectomy on the right side and the left side served as the control. After different survival periods, the control and experimental submandibular glands were discected out and processed for histological and histochemical examinations. Chorda tympani neurectomy resulted in atrophic changes in about 90% of both seromucous acini and granular convoluted tubules of the submandibular gland. They showed statistically significant reduction in their mean diameters after denevation. The reduction in the diameter of the acini was more marked than that of the tubules. The atrophic acini became separated by wide spaces and their cells showed cytoplasmic vacuolation two weeks after chorda tympani neurectomy. At the third and the fourth weeks, an insignificant increase in the diameter was noticed in the tubules and acini. The interlobular striated ducts showed cytoplasmic vacuolation two weeks after denervation which became more prominent during the third and fourth week after chorda tympani neurectomy. After denervation, NADPH-d positive nerve terminals were absent around the majority of acini and the granular convoluted tubules and were seen around the remaining 7-10% of the acini and 10-23% of the tubules. Throughout the period of denervation, NADPH-d positive nerve terminals were found around the striated ducts, the interlobular ducts and the blood vessels. The majority of the NADPH-d positive nerve terminals around the acini and granular convoluted tubules are parasympathetic in origin derived from the chorda tympani. The origin of NADPH-d positive nerve fibers around some acini and granular convoluted tubules and in relation to the remaining duct system and blood vessels needs further investigation

Increased incidence of intranuclear rods and unusual cytoplasmic inclusions in clarke neurons in rats subjected to neonatal peripheral nerve injury: an ectron microscopic study

Clarke's nucleus of young adult rats whose right sciatic nerves were crushed in the first postnatal day was examined with the electron microscope and the ultrastructure of Clarke neurons was described on both the control [left] and experimental [right] ides. The general fine tructure of Clarke cells appeared quite similar to that of other neurons. Unlike other neurons. Clarke cells showed an eccentric nucleus and Nissl substance characterized by parallel cisternae of rough endoplasmic reticulum. Three types of intranuclear rods and two distinctive cytoplasmic inclusions, termed fibrillary inclusion bodies and nematosomes, have been identified in Clarke neurons on the experimental side. The nuclear rods consisted of microfilaments or microtubules and were called tubular, filamentous and filamentous.crystalloid rods. The fibrillary inclusion bodies appeared as balls of densely packed neurofilaments enveloped by a multiloculated membrane. The nematosomes consisted of a reticular network of filamentous strands, lacked a limiting membrane and were always present in ribosome-rich areas. On the control side, the cytoplasmic inclusion bodies were not seen, while the intranuclear rods were observed only in two clarke cells. Mother distinctive feature of Clarke cells on the experimental side was the presence of peculiar dendritie profiles packed with mitochondria and glyeogen particles

Ultrastructural dystrophic changes in central sensory synaptic terminals in clarke's nucleus neuropil after neonatal seiatic nerve crush

The present investigation demonstrates the long-term dystrophic changes in primary sensory terminals within Clarke's nucleus of young adult rats [12 weeks of age] whose sciatic nerves were subjected to crush injury at birth. Variable degrees of dystrophic changes were observed in the affected axon terminals. These changes included hyperplasia of neurofilaments, accumulation of electron-dense bodies, clustering of synaptic vesieles, distortion of mitochondria, collections of vesicular profiles and vacuoles and engulfment of some terminals by reactive glial cell processes. Accumulation of dense bodies and replacement of synaptic vesieles by neurofilaments were the most frequent features. In the control specimens of the same animals, dystrophie changes were rarely observed. These dystrophie changes are most probably due to transganglionic atrophy caused by defective axonal transport mechanisms from their hypoplastic perikarya in the dorsal root ganglia. Coupled with future studies on the axonal metabolism, these ultrastructural observations will contribute to the understanding of the alterations in the spinal cord synaptic transmission and of the abnormal sensory symptoms associated with peripheral nerve lesions

Prenatal development of the human parotid gland

The prenatal development of the human parotid gland has been investigated in 26 fetuses from the 10th week of gestation to full term. At 10-12 weeks, the gland was composed of primitive ducts and terminal buds of primitive acini surrounded by loose mesenchyme. The acini continued to increase in number and size till full term. At 16 weeks, the lobulation of the developing gland was recognizable together with differentiation of the primitive ducts into intra- and interlobular ducts. At 20 weeks, both intercalated and striated ducts were distinguished and their number increased gradually with age. At birth, the ducts and acini appeared fewer and less crowded than those of the adult and the gland appeared devoid of fat cells. PAS- and AB-positive secretory materials appeared in the epithelial cells of both ducts and acini and in their lumina during the 12th week. This secretory activity persisted throughout pregnancy. The functional significance of the secretory products is discussed