Home About us Contact | |||
Differential Vulnerability (differential + vulnerability)
Selected AbstractsDifferential vulnerability of propriospinal tract neurons to spinal cord contusion injuryTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2004Amanda C. Conta Abstract The propriospinal system is important in mediating reflex control and in coordination during locomotion. Propriospinal neurons (PNs) present varied patterns of projections with ascending and/or descending fibers. Following spinal cord contusion injury (SCI) in the rat, certain supraspinal pathways, such as the corticospinal tract, appear to be completely abolished, whereas others, such as the rubrospinal and vestibuospinal tracts, are only partially damaged. The amount of damage to propriospinal axons following different severities of SCI is not fully known. In the present study retrograde and anterograde tracing techniques were used to assess the projection patterns of propriospinal neurons in order to determine how this system is affected following SCI. Our findings reveal that PNs have differential vulnerabilities to SCI. While short thoracic propriospinal axons are severely damaged after injury, 5,7% of long descending propriospinal tract (LDPT) projections survive following 50 and 12.5-mm weight drop contusion lesions, respectively, albeit with a reduced intensity of retrograde label. Even though the axons of short thoracic propriospinal cells are damaged, their cell bodies of origin remain intact 2 weeks after injury, indicating that they have not undergone postaxotomy retrograde cell death at this time point. Thus, short PNs may constitute a very attractive population of cells to study regenerative approaches, whereas LDPT neurons with spared axons could be targeted with therapeutic interventions, seeking to enhance recovery of function following incomplete lesions to the spinal cord. J. Comp. Neurol. 479:347,359, 2004. © 2004 Wiley-Liss, Inc. [source] Differential vulnerability of cerebral visual functions in children born very prematurelyACTA PAEDIATRICA, Issue 2 2009Lorna S Jakobson No abstract is available for this article. [source] Differential vulnerability of propriospinal tract neurons to spinal cord contusion injuryTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2004Amanda C. Conta Abstract The propriospinal system is important in mediating reflex control and in coordination during locomotion. Propriospinal neurons (PNs) present varied patterns of projections with ascending and/or descending fibers. Following spinal cord contusion injury (SCI) in the rat, certain supraspinal pathways, such as the corticospinal tract, appear to be completely abolished, whereas others, such as the rubrospinal and vestibuospinal tracts, are only partially damaged. The amount of damage to propriospinal axons following different severities of SCI is not fully known. In the present study retrograde and anterograde tracing techniques were used to assess the projection patterns of propriospinal neurons in order to determine how this system is affected following SCI. Our findings reveal that PNs have differential vulnerabilities to SCI. While short thoracic propriospinal axons are severely damaged after injury, 5,7% of long descending propriospinal tract (LDPT) projections survive following 50 and 12.5-mm weight drop contusion lesions, respectively, albeit with a reduced intensity of retrograde label. Even though the axons of short thoracic propriospinal cells are damaged, their cell bodies of origin remain intact 2 weeks after injury, indicating that they have not undergone postaxotomy retrograde cell death at this time point. Thus, short PNs may constitute a very attractive population of cells to study regenerative approaches, whereas LDPT neurons with spared axons could be targeted with therapeutic interventions, seeking to enhance recovery of function following incomplete lesions to the spinal cord. J. Comp. Neurol. 479:347,359, 2004. © 2004 Wiley-Liss, Inc. [source] The sublethal effects of tebufenozide on the precopulatory and copulatory activities of Choristoneura fumiferana and C. rosaceanaENTOMOLOGIA EXPERIMENTALIS ET APPLICATA, Issue 3 2004Renée Dallaire Abstract The sublethal effects of tebufenozide, an ecdysone agonist, on the reproductive biology of Choristoneura fumiferana (Clem) and of Choristoneura rosaceana (Harris) (Lepidoptera: Tortricidae), treated during the larval stage, were evaluated using two treatment methods: the force-feeding method and the diet method. The percentage of mortality and the developmental time of survivors increased linearly with the concentration of tebufenozide used. This ecdysone analogue proved to be more toxic to C. fumiferana than to C. rosaceana. In C. rosaceana, the weight of males and females decreased proportionally with the dose ingested, but females were affected to a greater extent. This difference might be due to a greater consumption of the treated diet, or to a differential vulnerability to tebufenozide. Tebufenozide did not modify the pre-copulatory activities associated with chemical communication in the females. However, the consumption of tebufenozide delayed ovarian maturation, causing a reduction in the fecundity of females. Treated males had smaller spermatophores and fewer eupyrene sperms in their bursa copulatrix and spermatheca, along with lower mating success. In C. fumiferana, tebufenozide delayed the females' onset time of calling the first night after emergence, but did not affect the mean time spent calling or the production of the main component of the sex pheromone. The males showed significantly greater difficulty in executing oriented flight in a wind tunnel, although their mating success was not affected. We concluded that tebufenozide interferes with various aspects of the reproductive biology of males and females of C. fumiferana and C. rosaceana, including some pre-copulatory behaviors associated with sex pheromone communication. [source] Insensitivity to glutamate neurotoxicity mediated by NMDA receptors in association with delayed mitochondrial membrane potential disruption in cultured rat cortical neuronsJOURNAL OF NEUROCHEMISTRY, Issue 5 2008Yuki Kambe Abstract We have attempted to elucidate mechanisms underlying differential vulnerability to glutamate (Glu) using cultured neurons prepared from discrete structures of embryonic rat brains. Brief exposure to Glu led to a significant decrease in the mitochondrial activity in hippocampal neurons cultured for 9 or 12 days at 10 ,M to 1 mM with an apoptosis-like profile, without markedly affecting that in cortical neurons. Brief exposure to Glu also increased lactate dehydrogenase release along with a marked decrease in the number of cells immunoreactive for a neuronal marker protein in hippocampal, but not cortical, neurons. Similar insensitivity was seen to the cytotoxicity by NMDA, but not to that by tunicamycin, 2,4-dinitrophenol, hydrogen peroxide or A23187, in cortical neurons. However, NMDA was more efficient in increasing intracellular free Ca2+ levels in cortical neurons than in hippocampal neurons. Antagonists for neuroprotective metabotropic Glu receptors failed to significantly affect the insensitivity to Glu, while NMDA was more effective in disrupting mitochondrial membrane potentials in hippocampal than cortical neurons. These results suggest that cortical neurons would be insensitive to the apoptotic neurotoxicity mediated by NMDA receptors through a mechanism related to mitochondrial membrane potentials, rather than intracellular free Ca2+ levels, in the rat brain. [source] GABAA receptors in aging and Alzheimer's diseaseJOURNAL OF NEUROCHEMISTRY, Issue 4 2007Robert A. Rissman Abstract In this article we present a comprehensive review of relevant research and reports on the GABAA receptor in the aged and Alzheimer's disease (AD) brain. In comparison to glutamatergic and cholinergic systems, the GABAergic system is relatively spared in AD, but the precise mechanisms underlying differential vulnerability are not well understood. Using several methods, investigations demonstrate that despite resistance of the GABAergic system to neurodegeneration, particular subunits of the GABAA receptor are altered with age and AD, which can induce compensatory increases in GABAA receptor subunits within surrounding cells. We conclude that although aging- and disease-related changes in GABAA receptor subunits may be modest, the mechanisms that compensate for these changes may alter the pharmacokinetic and physiological properties of the receptor. It is therefore crucial to understand the subunit composition of individual GABAA receptors in the diseased brain when developing therapeutics that act at these receptors. [source] Hypothalamic-Pituitary-Adrenal Axis Abnormalities in Response to Deletion of 11,-HSD1 is Strain-DependentJOURNAL OF NEUROENDOCRINOLOGY, Issue 11 2009R. N. Carter Inter-individual differences in hypothalamic-pituitary-adrenal (HPA) axis activity underlie differential vulnerability to neuropsychiatric and metabolic disorders, although the basis of this variation is poorly understood. 11,-Hydroxysteroid dehydrogenase type 1 (11,-HSD1) has previously been shown to influence HPA axis activity. 129/MF1 mice null for 11,-HSD1 (129/MF1 HSD1,/,) have greatly increased adrenal gland size and altered HPA activity, consistent with reduced glucocorticoid negative feedback. On this background, concentrations of plasma corticosterone and adrenocorticotrophic hormone (ACTH) were elevated in unstressed mice, and showed a delayed return to baseline after stress in HSD1-null mice with reduced sensitivity to exogenous glucocorticoid feedback compared to same-background genetic controls. In the present study, we report that the genetic background can dramatically alter this pattern. By contrast to HSD1,/, mice on a 129/MF1 background, HSD1,/, mice congenic on a C57Bl/6J background have normal basal plasma corticosterone and ACTH concentrations and exhibit normal return to baseline of plasma corticosterone and ACTH concentrations after stress. Furthermore, in contrast to 129/MF1 HSD1,/, mice, C57Bl/6J HSD1,/, mice have increased glucocorticoid receptor expression in areas of the brain involved in glucocorticoid negative feedback (hippocampus and paraventricular nucleus), suggesting this may be a compensatory response to normalise feedback control of the HPA axis. In support of this hypothesis, C57Bl/6J HSD1,/, mice show increased sensitivity to dexamethasone-mediated suppression of peak corticosterone. Thus, although 11,-HSD1 appears to contribute to regulation of the HPA axis, the genetic background is crucial in governing the response to (and hence the consequences of) its loss. Similar variations in plasticity may underpin inter-individual differences in vulnerability to disorders associated with HPA axis dysregulation. They also indicate that 11,-HSD1 inhibition does not inevitably activate the HPA axis. [source] The dynamics of vulnerability: locating coping strategies in Kenya and TanzaniaTHE GEOGRAPHICAL JOURNAL, Issue 4 2005SIRI H ERIKSEN We investigate how smallholder farmers at two sites in Kenya and Tanzania cope with climate stress and how constraints and opportunities shape variations in coping strategies between households and over time during a drought. On the basis of this analysis, we draw out implications for adaptation and adaptive policy. We find that households where an individual was able to specialize in one favoured activity, such as employment or charcoal burning, in the context of overall diversification by the household, were often less vulnerable than households where each individual is engaged in many activities at low intensity. Many households had limited access to the favoured coping options due to a lack of skill, labour and/or capital. This lack of access was compounded by social relations that led to exclusion of certain groups, especially women, from carrying out favoured activities with sufficient intensity. These households instead carried out a multitude of less favoured and frequently complementary activities, such as collecting indigenous fruit. While characterized by suitability to seasonal environmental variations and low demands on time and cash investments, these strategies often yielded marginal returns. Both the marginalization of local niche products and the commercialization of forest resources exemplify processes leading to differential vulnerability. We suggest that vulnerability can usefully be viewed in terms of the interaction of such processes, following the concept of locality. We argue that coping is a distinct component of vulnerability and that understanding the dynamism of coping and vulnerability is critical to developing adaptation measures that support people as active agents. [source] |