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

In-utero alcohol exposure produces sensorimotor developmental abnormalities that often persist into adulthood. The rodent cortical barrel field associated with the representation of the body surface was used as our model system to examine the effect of prenatal alcohol exposure (PAE) on early somatosensory cortical development. In this study, pregnant female rats were intragastrically gavaged daily with high doses of alcohol (6 gm/kg body weight) throughout the first 20 days of pregnancy. Blood alcohol levels were measured in the pregnant dams on gestational days 13 (G13) and G20. The ethanol treated group (EtOH) was compared to the normal control chowfed (CF) group, nutritionally matched pairfed (PF) group, and cross-foster (XF) group. Cortical barrel development was examined in pups across all treatment groups from G25, corresponding to postnatal day 2 (P2), to G32 corresponding to P9. The EtOH and control group pups were weighed, anesthetized, and perfused. Brains were removed and weighed with, and without cerebellum and olfactory bulbs, and neocortex was removed and weighed. Cortices were then flattened, sectioned tangentially, and stained with a metabolic marker, cytochrome oxidase (CO) to reveal the barrel field. Progression of barrel development was distinguished into three categories: (a) absent, (b) cloudy barrel-like pattern, and (c) well-formed barrels with intervening septae. The major findings are: (1) PAE delayed barrel field development by one or more days, (2) the barrel field first appeared as a cloudy pattern that gave way on subsequent days to an adult-like pattern with clearly demarcated intervening septal regions, (3) the barrel field developed differentially in a lateral-to-medial gradient in both alcohol and control groups, (4) PAE delayed birth by one or more days in 53% of the pups, (5) regardless of whether pups were born on G23 (normal expected birth date for non-alcohol controls) or as in the case for the alcohol-delayed pups born as late as G27, the barrel field was never present at birth suggesting the importance of postnatal experience on barrel field development, and (6) PAE did not disrupt the normal barrel field pattern, although both total body and brain weights were compromised. These findings suggest that PAE delays the development of the somatosensory cortex (SI); such delays may interfere with timing and formation of cortical circuits. It is unknown whether other nuclei along the somatosensory pathway undergo similar delays in development or if PAE selectively disrupts cortical circuitry.
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PMID:Prenatal alcohol exposure delays the development of the cortical barrel field in neonatal rats. 1650 13