Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pattern of ischemia-induced cell death was examined with histochemical methods in the striatum of adult gerbils 4 and 7 days after transient forebrain ischemia. The results showed a massive loss of immunoreactivity to enkephalin and tachykinins, peptides present in striatal efferent neurons. In contrast, neurons expressing acetylcholinesterase activity, or choline acetyltransferase immunoreactivity, as well as neurons immunoreactive for somatostatin, were relatively preserved in areas of severe neuronal loss. The selective vulnerability of subpopulations of striatal neurons to transient ischemia in the adult is similar to that observed in the neonate and after local injections of agonists of N-methyl-D-aspartate receptors, but not of agonists of other glutamate receptor subtypes. It also presents striking similarities to the pattern of neuronal death observed in Huntington's disease. The results further support a role for overstimulation of a subtype of excitatory amino acid receptor in ischemia-induced cell death and show that the selective sparing of subpopulations of striatal interneurons after ischemic injury is not related to immaturity of these neurons but also occurs in the adult.
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PMID:Ischemic damage in the striatum of adult gerbils: relative sparing of somatostatinergic and cholinergic interneurons contrasts with loss of efferent neurons. 197 9

Treatment of the cholinergic cell line NG108-15 with retinoic acid or cAMP results in an increase of choline acetyltransferase activity (ChAT) whereas none of these agents influences the amount of the vesicular acetylcholine transporter (VAChT) as judged from vesamicol binding and immunoblot studies. We suggest that immaturity of posttranslational events controlling the expression of VAChT protein is responsible for the apparent absence of coregulation of ChAT and VAChT protein expression.
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PMID:Influence of retinoic acid and of cyclic AMP on the expression of choline acetyltransferase and of vesicular acetylcholine transporter in NG108-15 cells. 978 41

Autonomic ganglia of the human pelvic plexus contain sympathetic and parasympathetic neurons which innervate the internal reproductive organs and the lower urinary tract while the urinary bladder also receives innervation from small intramural ganglia embedded in the detrusor muscle. Previous studies have used the immunocytochemical demonstration of tyrosine hydroxylase (TH), either alone or in combination with dopamine beta-hydroxylase, to identify noradrenergic neurons in these ganglia. However until recently a reliable marker for cholinergic neurons in the human autonomic nervous system was not available since antibodies to choline acetyltransferase do not react in this tissue. The present immunohistochemical study has used an antibody to human vesicular acetylcholine transporter (VAChT) to identify cholinergic neurons in the pelvic plexus and intramural bladder ganglia in a series of specimens from human male neonates and children. Immunostaining for TH was also carried out on the same sections and the results showed that while the vast majority of pelvic ganglion neurons were either cholinergic or noradrenergic (as seen by the presence of VAChT or TH respectively), approximately 50% of the neurons in the intramural ganglia were labeled with both immunomarkers. The presence of TH in cholinergic neurons may be due to the immaturity of the tissues examined since previous data on intramural bladder ganglia in the adult have shown that a much smaller proportion of the neurons contain TH than was observed in the present study. It is concluded that the presence of TH alone cannot be regarded as a specific marker for noradrenergic neurons in the genitourinary system of the human neonate and child.
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PMID:Tyrosine hydroxylase and vesicular acetylcholine transporter are coexpressed in a high proportion of intramural neurons of the human neonatal and child urinary bladder. 1062 37