1,721,117 research outputs found
Thalamus in flame: targeting of infectious agents to thalamic nuclei.
No full textThe involvement of the thalamus in infectious diseases of the nervous system has been hitherto rather neglected by investigators in clinical and basic neuroscience, despite numerous reports indicating that the thalamus, and territories within this region, can be attacked by different types of microbes. This topic is here reviewed. First, an overview is provided on general principles of spread of microbes to the brain (through peripheral nerves, or through the blood or cerebrospinal fluid) and their interactions with neurons and immune cells to cause acute, transient or persistent infections. Examples are given on how non-cytolytic infections can cause long-lasting disturbances in synaptic activities and neuronal networks as a result of a "hit-and-run" mechanism, or as an effect of factors released in the microenvironment to control the neuronal infection. Emerging data on how molecules functioning at the "immunological synapse" (the site of contact between immune cells and target infected cells) may affect nervous system synapses are pointed out. An account is then given of clinical and experimental infections of the thalamus caused by viruses (rabies and herpes viruses, influenza A virus, flaviviruses, HIV virus), the parasite Toxoplasma gondii , and prions. The implications and consequences of the attack of these microbes to the thalamus are discussed. Of special interest is the potential persistence of latent infections in thalamic neurons, which could cause disturbances of neuronal functions in the absence of overt structural lesions. Altogether these data recall attention on the pathogenesis and consequences of acute and persistent infections in the mammalian thalamus. © 2004 Elsevier Ltd. All rights reserved
The interrelations between cell groups in the caudal diencephalon of the rat projecting to the striatum and to the medulla oblongata
No full textIn order to investigate the topographical relationships between the caudal diencephalic cells of origin of ascending and descending projections in the rat, one fluorescent retrograde tracer was injected into the striatum and another into the medulla oblongata. The medullary injections were mainly centered in the inferior olive. Cells labeled from the striatal injections densely filled the thalamic parafascicular nucleus. Cells labeled from the medullary injections were seen ventrally to the fasciculus retroflexus in the subparafascicular nucleus. The two populations were mixed in a small area at the ventromedial border of the fasciculus retroflexus. No double labeled cells were observed. The present results indicate that caudal diencephalic cells which ascend to the striatum are different from those descending to the medulla oblongata and that they partially overlap
Nitric oxide synthase in the adult and developing thalamus: Histochemical and immunohistochemical study in the rat
No full textThe distribution of neuronal elements that express nitric oxide synthase (NOS), the synthetic enzyme of the free radical nitric oxide, was investigated in the adult and developing rat thalamus by means of NADPH-diaphorase (NADPH-d) histochemistry, which is a marker of NOS. Immunocytochemistry was also used to confirm the equivalence between the histochemical pattern of staining and the distribution of the expression of the neuronal NOS isoform. In the adult thalamus, NADPH-d-positive and NOS-immunoreactive perikarya were selectively concentrated along the midline (in the paraventricular, rhomboid, and central medial nuclei) and in the dorsal and ventral lateral geniculate nuclei. Isolated clusters of stained neurons were also observed in the lateral posterior nucleus, in the dorsal part of the medial geniculate nucleus, and in the ventromedial nucleus. Positive perikarya were either absent or very sparse in the other thalamic nuclei. Many thalamic domains were, however, characterized by distinct patterns of NADPH-d-positive fibers, preterminal and terminal-like elements. The highest density of stained neuropil was observed in the anteroventral and anteromedial nuclei, in several of the midline nuclei, in the anterior intralaminar nuclei, and in the lateral and medial geniculate nuclei. Although histochemical reactivity was observed in the thalamus at birth, the intensity and the pattern of distribution of staining observed in adulthood was not achieved until the end of the third postnatal week. The NADPH-d histochemical positivity followed discrete developmental schedules in various thalamic domains, and different areas reached a mature pattern at different ages. In addition, populations of transiently stained neuronal cell bodies were observed in the medial thalamus during the first two postnatal weeks. These results show discrete patterns of expression of NOS in the adult and developing thalamus and suggest that nitric oxide may be involved in selected physiological and developmental roles in different thala mic domains
Botulinum toxin induces nitric oxide synthase activity in motoneurons
No full textIntramuscular injections of botulinum toxin A were made into the snout of 3-month- and 3-week-old rats, resulting in transient paralysis of the facial muscles. Nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase histochemistry, which is a marker of nitric oxide synthase activity in fixed tissue and, in particular, in injured motoneurons, was studied in the facial nucleus. At variance with control injections of saline, the histochemical staining was found to be induced in facial motoneurons after botulinum toxin injection. The occurrence and persistence of the histochemical positivity in facial motoneurons paralleled that of muscle paralysis. These findings indicate that the enzyme of synthesis of the free radical nitric oxide can be induced in motoneurons after a functional disconnection from the target, which spares the axon and is associated with cell survival
Activation and response to axotomy of microglia in the facial motor nuclei of G93A superoxide dismutase transgenic mice
No full textMice over-expressing a human mutation of Cu2+/Zn2+ superoxide dismutase (SOD1) provide a model of amyotrophic lateral sclerosis. Using tomato lectin histochemistry, we analyzed microglia in the facial nuclei of SOD1(G93A) transgenic mice in the late stage of disease. In these animals, microglia was markedly activated, and ensheathed facial motoneurons as observed in wild-type mice 1 week after nerve transection. In the axotomized facial nucleus of transgenic mice at the same time point, microglia activation was enhanced and exhibited phagocytic features. The findings show that in the facial nucleus microglial cells react to motoneuron disease caused by the SOD1 mutation and to axotomy-induced damage of facial motoneurons. © 2000 Elsevier Science Ireland Ltd
The pioneering experimental studies on sleep deprivation
No full textThe experimental studies on sleep deprivation were initiated by the Russian physician and scientist, Mafie de Manaceine, who studied sleep-deprived puppies kept in constant activity. She reported in 1894 that the complete absence of sleep was fatal in a few days, pointing out that the most severe lesions occurred in the brain. In 1898, the Italian physiologists Lamberto Daddi and Giulio Tarozzi also kept dogs awake by walking them; the animals died after 9-17 days, and their survival was unrelated to food consumption. In the histological study performed by Daddi, degenerative alterations, mainly represented by chromatolytic changes, were observed in neurons of the spinal ganglia, Purkinje cells of the cerebellum, and neurons of the frontal cortex. Daddi ascribed these changes to a state of autointoxication of the brain during insomnia. In 1898, the psychiatrist Cesare Agostini, interested in the psychic phenomena caused by prolonged insomnia in humans, sleep deprived dogs by keeping them in a metallic cag e in order to avoid fatigue. The dogs survived about 2 weeks, and degenerative changes were observed in their brains. In these experimental paradigms, the effect of sleep loss was confounded by motor exhaustion and/or intense sensory stimulation. In spite of the absence of adequate controls, the pioneering studies performed at the end of the 19th century represented the first experimental attempts to relate sleep with neural centers and suggested that sleep is a vital function and that the brain may be affected by insomnia
Translation of the article “On the fine structure of the pes Hippocampi major (with plates XII-XXIII)”, by Camillo Golgi.
No full textWe have provided a translation of Golgi's original paper on the mammalian hippocampus (first published in 1883 and reprinted numerous times), along with a preface on its historical context. Golgi believed that this part of the cerebral hemisphere showed best the exact relationship between nerve cells and nerve fibers, the most important problem in 19th century neuroscience. Copyright © 2001 Elsevier Science Inc
The ependymal region of the thalamus. An electron microscopic study of the glial architecture and underlying labeled neurons of the rat paraventricular nucleus
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