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A Potempska

Publications and source records attributed to A Potempska.

24 records · Page 2Linked to original sources
PubMed1977

Relationship between changes in the content of acetylcholine and the activities of acetylcholinesterase and choline acetyltransferase in the hippocampus of the rat after septal lesions.

Changes in acetylcholine (ACh) content and acetylcholinesterase (AChE) and choline acetyltransferase (ChAc) activity in the hippocampus were compared after various septal lesions. With the use of a multiple regression model it was shown that the time course of the ACh and enzymic level changes is concordant after total destruction of the septum, but not always after partial damage. Septal lesions produced an effect mainly on bound ACh. The results suggest that the activity of AChE and ChAc is not the rate-limiting factor of the ACh level in the hippocampus. The involvement of other hippocampal neurotransmitters acting through the high-affinity uptake of choline is supposed to play an important role in ACh content regulation.

Acetylcholine↗
PubMedDate not supplied

Experimental maternal phenylketonuria: an examination of two animal models.

Two satisfactory rat models of maternal phenylketonuria (PKU) have been developed. Continuous subcutaneous infusion into pregnant rats from the 9th-20th day of gestation of either (1) phenylacetate (PA), to elevate plasma levels of unconjugated PA to 0.25-0.60 mumol/ml, or (2) a nontoxic dose (0.2 mumol/g/day) of p-chlorophenylalanine (pClPhe) with L-phenylalanine (Phe), to elevate plasma Phe levels at least 10-fold (1.7-2.3 mumol/ml) and unconjugated PA to at least 0.2 mumol/ml, produced the syndrome of untreated maternal PKU: spontaneous abortion, mortality rate greater than normal among the newborn, retarded growth of fetal body and brain, and a learning deficit among the progeny. From the plasma of rats infused with only pClPhe, a metabolite was isolated and identified as p-chlorophenylacetic acid. This compound, at a concentration greater than 0.15 mumol/ml plasma was found to retard fetal body and brain growth. In the pregnant rat, plasma levels of unconjugated PA, in the range observed in some PKU individuals on a normal diet, effectively induced a simulation of maternal PKU. The results of this investigation support our contention that PA, which is produced in excessive amounts in clinical PKU, is the primary cause of the brain dysfunction.

Animals↗