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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine if structural alterations of the bulk chromatin and the amount of protein associated with the nuclear matrix in cerebellar neurons depend on radiation dose and a cell's state of oxygenation. After irradiation with 2.5 to 25.0 Gy under both aerobic and anoxic conditions, the sensitivity of the neuronal chromatin to m. nuclease digestion increase linearly with dose up to about 5 Gy, beyond which there was no further increase. The same increase in accessibility of chromatin to micrococcal nuclease digestion was observed when neuronal nuclei were irradiated at 4 degrees C. Neuronal nuclei were stained with propidium iodide (PI) for DNA and with fluorescein isothiocyanate (FITC) for protein, both before and after complete digestion with DNase I, and analyzed by flow cytometry. There was no change in either the PI (P greater than 0.4) or the FITC (P greater than 0.9) fluorescence of undigested nuclei after irradiation. For the DNase I digested nuclei, the PI fluorescence was unchanged after irradiation (P greater than 0.4), but the FITC fluorescence increased significantly (P less than 0.02). This increase in the FITC fluorescence was linear with dose up to about 5 Gy, beyond which there was no further increase. The flow cytometry results from DNase I digested nuclei were identical for neurons irradiated under aerobic or anoxic conditions, indicating that this phenomenon is oxygen independent. This increase in FITC fluorescence after irradiation was inhibited at ice-cold temperatures and probably reflects an increase in protein content at the nuclear matrix that requires metabolism. This may explain our previously observed resistance of nuclear matrix-associated DNA to digestion by DNase I. This protein increase at the nuclear matrix appears to follow "saturation" kinetics identical to that previously reported for repair of DNA strand breaks in cerebellar neurons. However, the exact molecular nature of this process and its role in DNA repair or cell survival remains to be determined.
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PMID:Alterations of neuronal nuclear matrix and chromatin structure after irradiation under aerobic and anoxic conditions. 275 10

Benzodiazepine (BDZ) receptor binding was assayed in situ in dispersed cultures of fetal mouse cerebral cortex at 37 degrees C and at 0 degrees C and compared. Contrary to data obtained from disrupted tissues, receptor binding at physiologic temperature was reduced only to 40% of that observed in the cold when intact tissues were used for assay. Neuronal (clonazepam-displaceable) receptor binding was essentially unaffected by changes in temperature; however, non-neuronal (Ro5-4864-displaceable) binding was reduced to 25% of that of 0 degrees C. A relatively high-affinity (Kd approximately 24 nM) as well as a low-affinity (Kd approximately 200 nM) binding site were identified; the numbers of binding sites were only modestly reduced at physiologic temperature and probably reflect a predominant reduction in non-neuronal sites.
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PMID:Characteristics of benzodiazepine receptor binding in living cultures of mouse cerebral cortex at physiologic temperature. 299 14

The thermosensitivity of anterior hypothalamic-preoptic neurons was studied in cats during the waking-sleeping cycle. Direct cooling and warming of the anterior hypothalamic-preoptic region was accomplished with water-perfused thermodes. Neuronal thermosensitivity was determined by means of the linear regression analysis of firing rate changes vs anterior hypothalamic-preoptic temperature changes. A total of 117 neurons were classified as thermosensitive during wakefulness and synchronized sleep (20.1% of the studied neurons). Cold-sensitive neurons outnumbered warm-sensitive neurons by 3.7:1. The homeothermic states, wakefulness and synchronized sleep, are characterized by similar frequency distributions of neuronal thermosensitivity, although variable changes in single neuron thermosensitivity are state-dependent. Such changes underlie the quantitative differences in homeothermic regulation between these states. The impairment of thermoregulation during desynchronized sleep is characterized by a different frequency distribution of neuronal thermosensitivity resulting from both a drop in the responsiveness to thermal stimulation of a majority of neurons and a reversal in the sensitivity to cooling and warming of a minority of neurons. In conclusion, only the frequency distribution of thermosensitivity in the neuronal population is indicative of changes in the thermoregulation paradigm across behavioral states.
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PMID:Thermosensitivity of anterior hypothalamic-preoptic neurons during the waking-sleeping cycle: a study in brain functional states. 362 Sep 45

Neuronal thermoresponsiveness in the preoptic and anterior hypothalamic (PO/AH) region of a bird and a mammal were compared in vitro by recording the activity of 48 units from ducks and 37 units from rats in tissue slices subjected to temperature changes. Warm-responsive units were found in similar proportions in duck and rat PO/AH slices. The average degrees of thermoresponsiveness did not differ between the two species. Neurons exhibiting thresholds of warm responsiveness had higher threshold temperatures (2P less than 0.01) in duck (38.8 +/- 0.2 degrees C) than in rat (37.4 +/- 0.4 degrees C) slices (means +/- standard errors). Firing rates at threshold temperatures and thermoresponsiveness below and above thresholds did not differ between ducks and rats. During synaptic blockade in a Ca2+-free/high-Mg2+ medium, warm-responsiveness was retained in 9 out of 13 units in duck slices and in 8 out of 13 units in rat slices. In two instances in ducks and in one case in rats positive temperature coefficients were converted into negative temperature coefficients. Among two cold-responsive units tested in duck slices one retained its cold-responsiveness. It is concluded that in vitro evaluation of PO/AH neuronal thermoresponsiveness in a bird and a mammal has not revealed differences at the single unit level which might explain the diverging contributions of the avian and mammalian hypothalamus to deep body temperature perception.
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PMID:Comparison between hypothalamic thermoresponsive neurons from duck and rat slices. 362 44

1. Ninety-six neurones in forty-six explant tissue cultures of rat medial basal hypothalamus (m.b.h.) and preoptic area (p.o.a.h.) were subjected to thermal stimulation. 2. Neuronal response to temperature was determined on the basis of an extrapolated Q10 calculated from the regression line relating mean spontaneous activity to bath temperature. 3. Thermal stimulation (28-41 degrees C) of p.o.a.h. cultures resulted in the identification of three distinct groups of neurones: (1) temperature-insensitive (0.5 less than or equal to Q10 less than or equal to 2), (2) warm-sensitive (Q10 greater than 2), and (3) cold-sensitive (Q10 less than 0.5). 4. No temperature-sensitive neurones were identified in m.b.h. cultures. 5. In the presence of a medium which effectively blocks synaptic transmission (12 mM-Mg2+ and 0.25 mM-Ca+) the sensitivity of both warm- and cold-sensitive neurones was preserved. 6. These data indicate that thermosensitivity is a characteristic not only of the preoptic neuronal network in vitro but also is an intrinsic characteristic of individual neurones.
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PMID:Electrophysiological analysis of neuronal thermosensitivity in rat preoptic and hypothalamic tissue cultures. 628 24

The effects of diode laser irradiation on peripheral nerves was examined by monitoring neuronal discharges elicited by application of various stimuli to the hind-paw skin of rats. Neuronal discharges elicited by brush, pinch, cold, and/or heat stimulation, as well as chemical stimulation by injection of turpentine (0.1 ml, SC) were recorded from L5 dorsal roots in urethane-anesthetized rats. Diode laser irradiation (830 nm, 40 mW, 3 min, continuous wave) of the saphenous nerve exposed from the muscle of the lower leg significantly inhibited neuronal discharges elicited by pinch (68.4 +/- 6.5%), cold (45.4 +/- 9.2%), and heat stimulation (49.2 +/- 11.3%). Neuronal discharges induced by brush stimulation (104.3 +/- 4.7%) were not affected by laser irradiation. Injection of turpentine, a chemical irritant, into the hind-paw skin (0.1 ml, SC) elicited neuronal discharges in the ipsilateral dorsal root, and these discharges were significantly inhibited or abolished by laser irradiation. In 6- to 7-week-old rats treated neonatally with capsaicin (10 mg/kg, SC), injection of turpentine into the hind-paw skin did not elicit neuronal discharges and laser irradiation did not affect the background discharges. These data suggest that laser irradiation may selectively inhibit nociceptive neuronal activities.
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PMID:Laser irradiation abates neuronal responses to nociceptive stimulation of rat-paw skin. 808 27

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.
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PMID:[A 75-year-old man with parkinsonism and sudden death]. 853 59

Allergic rhinitis involves an early phase, largely mediated through mast cells, and a late phase which involves cellular infiltration and mediator release. In the early phase, mast cells release mediators as a result of antigen cross-linking adjacent immunoglobulin E molecules bound to mast cell surfaces. This results in an accumulation of histamine which gives rise to the characteristic symptoms of rhinitis--sneezing, itching, rhinorrhoea and congestion. The late phase of the allergic response (hours after challenge) involves infiltration of the nasal epithelium by eosinophils, basophils, monocytes and T-lymphocytes, which release leukotrienes, kinins, histamine and a host of other mediators. The most important part of the late-phase response is probably mediated via the production of cytokines (IL-4, IL-5, IL-6, IL-8, GM-CSF and RANTES) by mast cells, TH2 lymphocytes or epithelial cells. The infiltration of tissues by cells normally present only in the blood is brought about by the production of adhesion molecules, such as VCAM-1 and E-selectin, which cause circulating eosinophils, basophils and T-lymphocytes to adhere to endothelial cells before moving through the endothelium into the tissue (diapedesis). Neuronal reflexes also play a role in the allergic response, both by mediating local responses to mediators and possibly playing a part in the activation of T-lymphocytes. The allergic response has also been shown to be less intense in a hot, humid environment, and more marked in a cold, dry environment, possibly due to changes in osmolality of the nasal surface fluid. Similar factors may play a role in the aetiology of non-allergic rhinitis.
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PMID:Pathophysiology of perennial allergic rhinitis. 921 57

Neuronal hybrid cells established by somatic cell fusion are useful for studies of neuronal properties at the molecular level (Hammond, D.N., Lee, H.J., Tonsgard, J.H. and Wainer, B.H., Development and characterization of clonal cell lines derived from septal cholinergic neurons, Brain Res., 512 (1990) 190-200; Wainwright, M.S., Perry, B.D., Won, L.A., O'Malley, K.L., Wang, W.Y., Ehrlich, M.E. and Heller, A., Immortalized murine strial neuronal cell lines expressing dopamine receptors and cholinergic properties, J. Neurosci., 15 (1995) 676-688). The somatic cell fusion method requires a fusion partner which is unable to survive in the selection medium if it does not fuse with primary cells to isolate the hybrid cells. Hypoxanthine guanine phosphoribosyltransferase (HPRT)-deficient partner cells and hypoxanthine, aminopterin and thymidine (HAT) selection medium are commonly used for this procedure (Harlow, E. and Lane, D. (Eds.), Antibodies: a Laboratory Manual, Cold Spring Harbor Laboratory Publications, New York, 1988, pp. 139-243). The present method requires neither HPRT-deficient cells nor HAT medium. Primary neurons are fused with the C1300 neuroblastoma cells pretreated with emetine (Grollman, A.P., Inhibitors of protein biosynthesis, J. Biol. Chem., 243 (1968) 4089-4094), an inhibitor of ribosomes and actinomycin D (Perry, R.P., Selective effects of actinomycin D on the intracellular distribution of RNA synthesis in tissue culture cells, Exp. Cell Res., 29 (1963) 400-406), an inhibitor of ribosomal RNA (rRNA) synthesis, before fusion. By this treatment, we are able to isolate hybrid cells after fusion because non-fused C1300 cells die due to the loss of active ribosomes and protein synthesis, whereas C1300 cells fusing with primary cells survive due to the supply of intact ribosomes and rRNA from primary cells. This method produces neuronal hybrids at high efficiency.
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PMID:Method for production of neuronal hybridoma using emetine and actinomycin D. 938 57

Neuronal differentiation and function require extensive stabilization of the microtubule cytoskeleton. Neurons contain a large proportion of microtubules that resist the cold and depolymerizing drugs and exhibit slow subunit turnover. The origin of this stabilization is unclear. Here we have examined the role of STOP, a calmodulin-regulated protein previously isolated from cold-stable brain microtubules. We find that neuronal cells express increasing levels of STOP and of STOP variants during differentiation. These STOP proteins are associated with a large proportion of microtubules in neuronal cells, and are concentrated on cold-stable, drug-resistant, and long-lived polymers. STOP inhibition abolishes microtubule cold and drug stability in established neurites and impairs neurite formation. Thus, STOP proteins are responsible for microtubule stabilization in neurons, and are apparently required for normal neurite formation.
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PMID:STOP proteins are responsible for the high degree of microtubule stabilization observed in neuronal cells. 966 Aug 71


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