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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The properties of periodontal mechanoreceptors innervating the lower canine teeth of cats have been determined 6 weeks and 1 year after sectioning the inferior alveolar nerve. Recordings were made from single fibres dissected from the nerve central to the injury site, whilst forces were applied at right angles to the long axis of the tooth. 2. The range of directions over which each mechanosensitive unit responded (are of sensitivity) was established. Forces were then applied in the direction of maximum sensitivity and the maximum discharge frequency, dynamic index, adaptation rate, and the force threshold at three rates of force application (0.25, 2 and 20 N s-1) were determined. 3. Data from 115 units characterized 6 weeks after nerve section revealed a significantly reduced mean dynamic index and raised mean force threshold to forces applied at 2 and 0.25 N s-1, when compared with the controls. These units were, however, more sensitive than those examined 12 weeks after nerve section in a previous study (Loescher & Robinson, 1989b). 4. Data from 158 units characterized 1 year after nerve section revealed a significantly narrower mean are of sensitivity, reduced mean maximum discharge frequency, lower mean dynamic index and raised mean threshold to forces applied at 0.25 N s-1, when compared with the controls. 5. Bone overlying the roots of the reinnervated teeth was removed in order to localize receptors in the underlying periodontal ligament. Forty-six units were localized 6 weeks after nerve section and thirty-eight 1 year after nerve section. The mean conduction velocity of these units was significantly reduced both 6 weeks and 1 year after nerve section compared to the controls. One unit was found which branched to innervate receptors at two locations within the ligament, and one unit was found which branched to innervate a receptor in the ligament and another in the overlying skin. 6. The higher level of sensitivity of receptors when first reinnervated than at later stages is attributed to their immaturity. This immaturity may also contribute to the paraesthesia which is experienced by patients at a corresponding stage in recovery from nerve injury. The persistent reduction in sensitivity of units 1 year after nerve injury suggests that changes occur which have a permanent effect on their properties.
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PMID:Properties of periodontal mechanoreceptors supplying the cat's lower canine at short and long periods after reinnervation. 182 67

The immature brain is considered relatively resistant to anoxia and ischemia. Although hypoxia without ischemia has not been considered to produce brain damage in immature rats as well as in adult rats (S. Levine, Anoxic-ischemic encephalopathy in rats, Am. J. Pathol., 36 (1960) 1-17 [8]; D.E. Levy, J.B. Brieley, D.G. Silverman, F. Plum, Brief hypoxia-ischemia initially damages cerebral neurons, Arch. Neurol., 32 (1975) 450-456 [9]; J.E. Rice, R.C. Vannucci, J.B., Brieriey, The influence of immaturity on hypoxic-ischemic brain damage in rat, Ann. Neurol., 9 (1981) 131-141 [14]), hypoxia in postnatal period is possible to cause a functional brain damage (T. Hender, P. Lundborg, Regional changes in monoamine synthesis in the developing rat brain during hypoxia, Acta. Physiol. Scand., 106 (1979) 139-143 [3]; W. Ihle, J. Gross, R. Moller, Effect on chronic postnatal hypoxia on dopamine uptake by synaptosomes from striatum of adult rats, Biomed. Biochem. Acta., 44 (1985) 433-437 [7]; A. Lun, J. Gross, M. Beyer, H.D. Fischer, C. Wustmann, J. Schmidt, K. Hecht, The vulnerable period of perinatal hypoxia with regard to dopamine release and behavior in adult rats, Biomed. Biochem. Acta., 45 (1986) 619-627 [10]). Using microdialysis, we studied the anoxic or hypoxic effect on catecholamine metabolism in immature rat brain by measuring extracellular concentrations of norepinephrine (NE), dopamine (DA), and its metabolites and also 5-hydroxyindole-3-acetic acid (5-HIAA), the serotonin metabolite. DA is a well established excitatory neurotransmitter (R.C. Vannucci, Experimental biology of cerebral hypoxia-ischemia: relation to perinatal brain damage, Pediatr. Res., 27 (1990) 317-326 [16]), and in the previous report using hypoxic 7-day-old rat pups increase of DA was not detected without additional stimulations (K. Gordon, D. Johnston, M.V. Robinson, T.E. Statman, J.B. Becker, F. Silverstein, Transient hypoxia alters striatal catecholamine metabolism in immature brain: An in vivo microdialysis study, J. Neurochem., 54 (1990) 605-611 [2]). Whereas recently in newborn piglets, hypoxic hypoxia produced increase of extracellular DA (C.-C. Huang, N.S. Lajevardi, O. Tammela, A. Pastuszko, Relationship of extracellular dopamine in striatum of newborn piglets to cortical oxygen pressure, Neurochem. Res., 19 (1994) 649-655 [6]; Olano, M., Song, D., Murphy, S., Wilson, D. F. and Pastuszko, A., Relationships of dopamine, cortical oxygen pressure, and hydroxyl radicals in brain of newborn piglets during hypoxia and posthypoxic recovery, J. Neurochem., 65 (1995) 1205-1212 [13]). We consider that hypoxic ischemic brain damage of human newborns that we can treat is a damage, which does not show overt neuropathological changes. We therefore tried to show that transient anoxia and hypoxia caused biochemical alteration if the exposure did not produce marked morphological changes. This rodent model is adequate to study perinatal asphyxia and alteration of monoamine level could be useful for evaluation of brain damage, even if it is not detected histologically.
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PMID:Anoxic and hypoxic immature rat model for measurement of monoamine using in vivo microdialysis. 997 39