Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.9.3.1 (cytochrome oxidase)
 8,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The early development of the principal sensory nucleus of the trigeminal nerve (PSN) was examined to determine whether spatiotemporal patterns of synaptogenesis coincide with patterns in neuronal generation, migration, and death. The morphogenesis of PSN neurons during the period from G16 to P14 was studied with a Golgi method. Prenatally, PSN neurons had dendrites that extended into the sensory tract of the trigeminal nerve (s5), and from as early as G18, these dendrites were studded with spines. The dendrites in the s5 degenerated or regressed in the early postnatal period so that the s5 was free of dendrites by P14. The development of anti-synapsin I immunoreactivity was traced from G14 to P10. Immunoreactive puncta (synaptic boutons) appeared in the medial third of the s5 transiently between G18 and P5. On the other hand, puncta in the PSN did not appear until G20, at which time they were confined to the lateral margin of the PSN. By P0, puncta were distributed throughout the PSN. Cytochrome oxidase activity in the PSN was low and unpatterned prenatally. Postnatally, cytochrome oxidase activity intensified and a segmented pattern of barreloids appeared in the ventral PSN on the day of birth. By P5, the complete pattern of barreloids, spanning the full width of the ventral PSN, was evident. The development of cytochrome oxidase activity in the PSN followed the lateral-to-medial gradient of synaptogenesis revealed by the development of synapsin 1 immunoreactivity. This gradient is opposite of that for neuronal generation, migration, and death. Moreover, the s5 serves as a transient synaptic field.
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PMID:Development of the principal sensory nucleus of the trigeminal nerve of the rat and evidence for a transient synaptic field in the trigeminal sensory tract. 839 50

Studies were undertaken to determine whether neurons of the subplate layer represent a transient or stable population of cells in developing neocortex of rat. The first set of studies sought to determine the fraction of subplate neurons that is lost during early postnatal development. The optical dissector method was used to analyze fluorescently stained material in animals the age of postnatal day 0 (P0) to P40. These results demonstrate a reduction of slightly less than half of the total number of subplate neurons from P0 to P40. Counts of labeled cells in littermates at varied ages after [(3)H]thymidine or BRDU treatment on gestational day 14 (G14 - birthdate of occipital subplate neurons) or G18 (birthdate of layers III-IV neurons) demonstrate loss of approximately 50% of neurons in the subplate layer between P0 and P40, somewhat greater than the loss of neurons from cortical layers III-IV. The second set of studies investigated whether subplate neurons display cellular atrophy during postnatal development. Analysis of subplate neurons injected intracellularly with Lucifer yellow in fixed slice preparations indicates no reduction in soma size, number of dendrites, or extent of dendritic fields of subplate neurons taken from animals age P0 to P60. The third set of studies investigated whether functional markers of subplate neurons are reduced during postnatal development. Analysis of tissue stained histochemically for cytochrome oxidase or acetylcholinesterase, or stained immunocytochemically for GABA, somatostatin, or neuropeptide Y, demonstrate a remarkable loss of expression of staining patterns from late gestational ages to P20. These data demonstrate that, although subplate neurons seem not to be a transient population of cells in the usual sense of being eliminated by cell death or structural atrophy, the loss of histochemical and immunocytochemical markers indicates that they may be a functionally transient population of cells.
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PMID:Do subplate neurons comprise a transient population of cells in developing neocortex of rats? 1102 4