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Ectopic neurons

In an analysis of six autism spectrum disorder (ASD) brains, Bailey et al. (1998) noted additional abnormalities in the brain stem. These included an unusually large arcuate nucleus in one brain and ectopic neurons on the lateral surface of the medulla in four brains. All the nine brains studied by Bauman and Kemper (2005) have shown abnormal superficial clustering of neurons in the inferior olive and in one brain there was an ectopic superficial cluster of neurons adjacent to the inferior... [Pg.69]

Jenner AR, Galaburda AM, Sherman GF (2000) Connectivity of ectopic neurons in the molecular layer of the somatosensory cortex in autoimmune mice. Cerebral Cortex 10 1005-1013. [Pg.80]

Murphey, R.K., Bacon, J.P. and Johnson, S.E. (1985) Ectopic neurons and the organization of insect sensory systems. J. Comp. Physiol. A -Sens. Neural Behav. Physiol. 156 381-389. [Pg.41]

Singh, S. C., Ectopic neurones in the hippocampus of the postnatal rat exposed to methylazoxymethanol during foetal development. Acta Neuropath. (Berl.), 1977, 40 111-116. [Pg.151]

Antiepileptics are used in neuropathic pain resulting from lesions to the peripheral (e.g., diabetes, heipes) or central nervous system (e.g., stroke). Such syndromes have been attributed to ectopic activity in sensitized nociceptors from regenerating nerve sprouts, recruitment of previously silent nociceptors, and/or spontaneous neuronal activity. This may result in sensitization... [Pg.77]

Extrahypothalamic OX-B-like immunoreactivity, reminiscent to that of CRF, has been described in clustered GABAergic neuronal populations, in the lateral division of central nucleus ofthe amygdala, the bednucleus of the stria terminalis, and in the hippocampus. Moreover, ectopic expression of preproorexin mRNA in the gut, ependymal cells, neuroblastomas, and of orexin receptors in adrenal gland, cancer and hematopietic stem cells suggests yet unexplored roles of orexins as paracrine factors controlling blood-brain barrier, and tumor or stem cell function. [Pg.911]

Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)... Fig. 4.1 Hypothetical model of pathogenesis of pain in DSP. (1) Injury of peripheral nerve fibers due to multifocal inflammation and secreted macrophage activation products results in abnormal spontaneous activity of neighboring uninjured nociceptive fibers ( peripheral sensitization ). (2) Furthermore, the aberrant inflammatory response in DRG leads to alterations in neuronal sodium and calcium channel expression and ectopic impulse generation. (3) This results in central remodeling within the dorsal horn due to A-fiber sprouting and synaptic formation with pain fibers in lamina 11, and maintenance of neuropathic pain ( central sensitization ). Reproduced with permission from (Keswani et al. 2002)...
A broad variety of diseases may cause neuropathic pain 935 Injured axons may develop spontaneous and repetitive firing known as ectopic activity 935 Sensory neurons transform their phenotype 936 Spinal disinhibition allows more nociceptive signal input 936 Peripheral nerve injury provokes a marked neuroimmune reaction 937... [Pg.927]

Spinal disinhibition allows more nociceptive signal input. Following peripheral nerve injury there is a reduction in the GABAergic component of postsynaptic inhibitory currents caused by a degeneration of GABAergic interneurons [24] (Fig. 57-6). This loss of inhibition (disinhibition) results in an overall increase in the excitability of dorsal horn neurons. The degeneration of inhibitory interneurons is due to an excitotoxic effect of primary afferent ectopic activity on dorsal horn neurons [26]. [Pg.936]

Sehgal According to some people, the per and timgal4 drivers are markers for all the neurons, or maybe even all the cells in the adult. I agree that they are not found everywhere, but the expression is widespread. One explanation is that the drivers are promiscuous. The other is that there are low levels of expression in these places that we don t detect any other way. I would think that this is kind of supported by some of the doubletime data, where, in a douhktime mutant we get per expression in ectopic locations. This would argue that per is synthesized in a lot of locations where you normally don t detect it because it is destabilized by doubletime. [Pg.233]

Delio DA, Reuhl KR, Lowndes HE. 1992. Ectopic impulse generation in dorsal root ganglion neurons during methylmercury intoxication An electrophysiological and morphological study. Neurotoxicol 13(3) 527-539. [Pg.596]

Gold Do you have data on the size distribution of neurons that show upregulation of brain 3, and does that correlate with what you would expect, at least in terms of the source of ectopic activity ... [Pg.53]


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See also in sourсe #XX -- [ Pg.69 , Pg.70 , Pg.103 ]




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