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Experimental pineocytoma of the Syrian hamster induced by a human papovavirus (JC). A light and electron microscopic study.
The gross, light and electron microscopic features of a pineocytoma of the Syrian hamster (mesocricetus auratus) which had been induced by a human oncogenic virus (JC papovavirus) have been defined. For comparison, adult hamster pineal tissue was studied, and the literature was consulted in regard to other pineal parenchymal tumors, and to pineal cell differentiation during ontogeny and phylogeny. Many differentiated tumor cells contained organelles, such as vesicle-crowned lamellae (synaptic ribbons) and microtubular sheaves, as consistent with adult hamster pineocytes. Some cells showed rudimentary photoreceptor-like differentiation as consistent with fetal hamster pineocytes and with cells seen in the pineal systems of some lower vertebrate species. Such tumor cells had lumen-directed specialized cytoplasmic extensions which, by their richness in mitochondria and presence of centrioles and striated rootlets, resembled inner segments. Extending 9+0 cilia were accompanied by occasional lamellar whorls. Oncogenesis seems to have simulated different stages of hamster pineal ontogeny. This observation would support the theory that the secretory mammalian pineocyte derived phylogenetically from the true photoreceptor cell of the pineal system of fishes and amphibians. The possible influences of host and of virus in the accomplishment of tumor morphology were discussed. This tumor differed considerably in pattern and cell detail from the only other pineocytoma studied previously by electron microscopy. It is the first experimentally induced pineocytoma.
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Ultrastructure of neurons in the ventromedial nucleus or the hypothalamus in ovariectomized rats with or without estrogen treatment.
The fine structure of the ventrolateral and dorsomedial subdivisions of the ventromedial nucleus (VMN) of the hypothalamus was examined in ovariectomized/control and ovariectomized/estrogen-treated rats to compare neurons of these areas to other neurons (specifically the ventrolateral thalamus), and to determine the effects of estrogen on these cells. The neurons of the VMN contain a large nucleus with a prominent nucleolus, rough endoplasmic reticulum (RER), polysomes, a Golgi complex, coated, uncoated and dense-cored vesicles, lysosome-like bodies, inclusion bodies, multivesicular bodies whorl bodies and myelin figures. Similar organelles were present in the neurons of the ventrolateral thalamus, although polysomes wee more prominent, and the cells lacked dense-cored vesicles in the perikarya. Differences in the cells of the VMN between ovariectomized/control and ovariectomized/estrogen-treated rats included a more conspicuous stacking of the RER and greater number of dense-cored vesicles in the estrogen-treated group in both the ventrolateral and dorsomedial subdivisions. In both areas the differences were statistically significant, although more marked in the ventrolateral subdivision. In both VMN subdivisions, the increased stacking of the RER could be correlated with the greater number of dense-cored vesicles and may reflect increased biosynthesis of a secretory product.
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Electron microscopic autoradiography for demonstration of pineal serotonin in rat.
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Fine structure observations of the uptake of intravenously injected peroxidase by the rat choroid plexus.
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Development of the capillary system in the neurohypophysis of the rat.
The development of the vascular system in the neurohypophysis of the rat shows three periods of structural differentiation. The first period lasts until the 17th fetal day. During this period the superficial and the border plexuses are formed, and rapid vascularization of the neural lobe anlage takes place. The end of this period is marked by the formation of the perivascular space. The second period lasts from the 18th fetal day until the 10th day after birth. Its initial phase is characterized by the appearance of the first endothelial pores. During this period the formation of the internal capillaries proceeds, together with the maturation of the previously formed vascular elements. The third period lasts from the 10th postnatal day until the end of the first month after birth. At the end of this period the vascular net of the neural lobe has attained its fully developed state. The results of this study, together with data from previous investigations, lead to the conclusion that at the 18th fetal day the neural lobe displays signs of functional activity, and that the maturation of the vascular network in the neural lobe occurs more rapidly than the maturation of its other structural components.
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Synaptogenetic mechanisms during chick cerebellar cortex development.
Chick embryo cerebellar cortex development was analyzed in an attempt to visualize the fine ultrastructural changed involved in cortical synaptogenesis. Three major stages of synapses formation were detected during days 13 to 18 of maturation: intermembranous adherence, cytoplasmic recognition, and definitive synaptic formation period. The more primitive morphological event indicative of synaptic onset was the occurrence of external plaques; these plaques must have a negative charge since they accumulated cationized electron-dense tracers. These plaques favor the adhesions between parallel fibers and Purkinje cell dendrites. Once axonal and dendritic membranes adhered to form an adhesion contact, the dendritic half of this contact forms a pinocytic vesicle that incorporates part of the membrane of the axonic half of the contact. This particular pinosome delivers its content to different cytoplasmic organelles including the nucleus. At day 15 Purkinje cells significantly increase the number of dendritic-forming pinocytic vesicles; this phenomenon means that during this day a large amount of parallel fiber membrane is passed into the Purkinje cell cytoplasm. From day 15 to 16 postsynaptic densities begin to appear; ribosomes associated to these structures seem to be the origin of a progressively accumulated amorphous material composing the rare primitive postsynaptic densities. Some other morphological details related to these processes are given in the text.
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Projection of ventrolateral medullary (A1) catecholamine neurons toward nucleus tractus solitarii.
The distribution and interconnections of brainstem catecholamine cell groups thought to be important in cardiovascular control were studied using histochemical and ultrastructural techniques in the rabbit. Lesions and microinjections of horseradish peroxidase (HRP) were made in the nucleus tractus solitarii in the dorsomedial medulla, and in the ventrolateral medulla. After lesions of the dorsomedial medulla the fluorescence intensity of the A1-group of catecholamine neurons was increased, and swollen axons could be seen coursing from the ventrolateral medulla toward the lesions on the same side, but not the opposite side. Most of these axons ran in a band about 2 mm in width, centered at the level of the obex. Electron microscopically, specific cells, identified as A1-catecholamine neurons, showed evidence of chromatolysis after the dorsomedial lesions. Following injection of HRP into the nucleus tractus solitarii. A1-catecholamine cells in the ventrolateral medulla on the same side contained the reaction product. Lesions of the ventrolateral medulla did not produce evidence of a reciprocal projection of A2-catecholamine neurons toward the ventrolateral medulla. Thus axons of the A1-group of catecholamine neurons in the ventrolateral medulla project toward the ipsilateral nucleus tractus solitarii in a relatively compact band at the level of the obex. On the other hand, the A2-group of catecholamine neurons in the dorsomedial medulla does not appear to send projections toward the A1-group.
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The pineal gland of the gerbil, Meriones unguiculatus. I. An ultrastructural study.
Electron microscopy was employed in a study of the pineal gland of the Mongolian gerbil (Meiones unguiculatus). It was determined that the gerbil pineal gland contains pinealocytes and glial cells with the pinealocytes being the predominant cell type. The pinealocytes contain numerous organelles traditionally considered as being either synthetic or secretory in function such as an extensive Golgi region, smooth (SER) and rough (RER) endoplasmic reticulum, secretory vesicles and microtubules. Other cytoplasmic components are also present in the pinealocytes (synaptic ribbons, subsurface cisternae) for which no function has been assigned. Dense-cored vesicles are rare. Vacuolated pinealocytes are present and appear to be intimately associated with the formation of the pineal concertions. Evidence presented supports the proposal that the concretions form within the vacuoles. Once the concretions reach an enlarged state, the vacuolated pinealocytes break down and the concretions are thus extruded into the extracellular space where they apparently continue to increase in size. The morphology of the glial cells was interpreted as indicative of a high synthetic activity. The glial cells contain predominantly the rough variety of endoplasmic reticulum and form an expansion around the wide perivascular area.
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TDP-43 mediates SREBF2-regulated gene expression required for oligodendrocyte myelination.
Cholesterol metabolism operates autonomously within the central nervous system (CNS), where the majority of cholesterol resides in myelin. We demonstrate that TDP-43, the pathological signature protein for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), influences cholesterol metabolism in oligodendrocytes. TDP-43 binds directly to mRNA of SREBF2, the master transcription regulator for cholesterol metabolism, and multiple mRNAs encoding proteins responsible for cholesterol biosynthesis and uptake, including HMGCR, HMGCS1, and LDLR. TDP-43 depletion leads to reduced SREBF2 and LDLR expression, and cholesterol levels in vitro and in vivo. TDP-43-mediated changes in cholesterol levels can be restored by reintroducing SREBF2 or LDLR. Additionally, cholesterol supplementation rescues demyelination caused by TDP-43 deletion. Furthermore, oligodendrocytes harboring TDP-43 pathology from FTD patients show reduced HMGCR and HMGCS1, and coaggregation of LDLR and TDP-43. Collectively, our results indicate that TDP-43 plays a role in cholesterol homeostasis in oligodendrocytes, and cholesterol dysmetabolism may be implicated in TDP-43 proteinopathies-related diseases.
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NEDD4L induces mitochondrial dysfunction and neurodegeneration by promoting LIPT2 degradation in Huntington's disease.
Impairment of mitochondrial protein stability is associated with neurodegeneration in Huntington's disease (HD). However, the E3 ligase responsible for maintaining mitochondrial protein homeostasis in HD remains poorly understood. In this study, we demonstrate that NEDD4L protein levels are elevated in human striatal organoids (hSOs) derived from induced pluripotent stem cells of patients as well as in a mouse model of HD. Overexpression of NEDD4L leads to degeneration and cell death of medium spiny neurons (MSNs), along with a reduction in motor activities. Conversely, deletion of NEDD4L restores abnormal MSN morphology, corrects deficits in calcium signaling, alleviates neurodegeneration in HD-hSOs, and improves motor dysfunction observed in YAC128 mice. Mechanistically, NEDD4L disrupts mitochondrial function by binding to lipoyl(octanoyl) transferase 2 (LIPT2) and promoting its degradation through ubiquitination and lysosomal pathways. This process impairs lipoic acid biosynthesis and the lipoylation of E2 subunits of alpha-ketoglutarate dehydrogenase (α-KGDH E2). Furthermore, either overexpressing LIPT2 or administering lipoic acid mitigates neurodegeneration and rectifies deficits in motor coordination activity. These findings unveil a molecular mechanism underlying the regulation of lipoic acid metabolism and underscore the potential therapeutic role of protein lipoylation in the treatment of HD.