Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The development of a second order structure in the olfactory pathway, the anterior olfactory nucleus, was examined in both normal rat pups and in subjects which underwent unilateral naris closure on postnatal day 1 (P1). Naris occlusion in neonatal rats produces a constellation of changes within the first relay in the pathway, the olfactory bulb, including a 25% reduction in total volume. Such large changes suggest that higher order structures might also be affected. Anterior olfactory nucleus development was quantified in several ways. Laminar volumes were computed by using serial section planimetry. In control animals differential development was observed, with regions extending most rostrally (e.g., pars externa and pars lateralis) exhibiting the least growth. The anterior olfactory nucleus on the "deprived" side of subjects with a single naris occluded was identical in size to that observed in controls, development within the pars lateralis was examined in control animals at
P10
, P20, P30, and adults. Developmental increases in numbers of both branches per cell and spines were noted, but mean branch length remained relatively constant. Finally, the effects of naris occlusion on histological patterns of
succinate dehydrogenase
(
SDH
) staining and 2-deoxyglucose uptake within pars lateralis were examined at P20 to test for more subtle effects of naris occlusion.
SDH
staining was quite similar in deprived and control rats at P20. However, 3H-2-DG uptake was decreased in rostral areas of the anterior olfactory nucleus ipsilateral to the deprived olfactory bulb, suggesting that naris closure does affect the structure.
...
PMID:Development of the anterior olfactory nucleus in normal and unilaterally odor deprived rats. 170 56
The time course and distribution of cell death in the trigeminal nuclear complex of the rat has been examined with the aid of sections stained for Nissl substance and
succinic dehydrogenase
activity. Pyknotic figure counts in the principal trigeminal nucleus and in each of the three spinal trigeminal subnuclei revealed that cell death commences at E19, in the region of the junction between the principal nucleus and the subnucleus oralis, close to the site of entry of trigeminal afferents into the brainstem. Cell death subsequently spreads rostrally and caudally into the rest of the principal and spinal trigeminal nuclei. Cell death ceases simultaneously, at about
P10
, in all parts of the trigeminal nuclear complex examined. Neurons could not be reliably distinguished from glial cells in prenatal animals, but data for neuronal numbers postnatally indicate that much of this cell death is indeed due to loss of neurons. The data suggest that, in the trigeminal nuclear complex, only half the number of neurons produced survive to maturity. These findings are of significance for those investigators using this system in studies of plasticity.
...
PMID:Cell death in the developing trigeminal nuclear complex of the rat. 172 12